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  • From ‘Good Calories, Bad Calories’: Carbohydrates cause heart disease due to insulin

    Posted by .(JavaScript must be enabled to view this email address)
    Friday, September 28, 2007 9:40 am Email this article
    "Carbohydrates do [cause heart disease], because of their effect on the hormone insulin," according to the new book "Good Calories Bad Calories" by Gary Taubes. "The more easily-digestible and refined the carbohydrates and the more fructose they contain, the greater the effect on our health, weight, and well-being."

    I am waiting for a review copy of the book.

    The information above is from information “About The Book” provided by the publisher located here.


    Taubes G. Good Calories, Bad Calories : Challenging the Conventional Wisdom on Diet, Weight Control, and Disease. New York: Knopf, 2007.

    Articles on the same subject can be found here:


    On Oct 05, 2007 at 5:34 am David Brown wrote:

    . . . . .

    One of the best books I've read discussing the effects of fructose on metabolic activity is Nutrition Against Disease by Roger J. Williams, PhD. Here is an excerpt with notes:

    Excerpt from Nutrition Against Disease by Roger J. Williams, PhD, 1971, pp 85-86.

    In England recently, evidence has been put forth by Yudkin and his coworkers that excess sugar consumption is statistically associated with atherosclerosis and heart attacks. 64 On the basis of their studies Yudkin states: ?It would mean, for example, that a person assessed by our dietary history as taking more than 110 grams of sugar a day (4 ounces) was perhaps five or more times as likely to develop myocardial infarction as one taking less than 60 grams a day.?65
    Since Americans are estimated to consume about 140 grams of sugar per day (including syrups), one may not safely dismiss sugar consumption as a factor in heart disease. In another study, it was reported that on a statistical basis, sugar consumption (in which sugar is often used) was not so correlated. 66
    Sugar seems to have deleterious effects in addition to its being a source of naked calories, in that its consumption appears to be more conducive to atherosclerosis than is starch consumption. 67 At least partial explanation of this finding is to be found in the excellent work emanating from the University of Pennsylvania. 68
    Here it was found that fructose is highly distinctive metabolically as compared with glucose. Since starch yields glucose only and sugar yields fructose as well as glucose, it follows that starch and sugar are not nutritionally equivalent. Kuo and his coworkers found that the liver tissue of individuals with high blood fat levels took up fructose five times as rapidly as individuals whose blood-fat levels were lower. Fat tissue from individuals with high blood fat levels also took up fructose seven to eight times more rapidly than the fat tissues of individuals with low blood fat levels. This shows how biochemical individuality comes into the problem and gives us a lead as to how some individuals may be adversely affected by the fructose content of sucrose.

    References and Notes

    64. Yudkin, J. ?Diet and coronary thrombosis.? Lancet, 2:155, 1957; Ibid. 2:4, 1964.
    65. Yudkin, J. ?Dietary fat and dietary sugar in relation to ischemic heart-disease and diabetes.? Lancet, 2:4 1964.
    66. Yudkin, J., and Morland, J. ?Sugar intake and myocardial infarction.? Am. J. Clin. Nutr., 20:503; 1967.
    67. Kaufman, N. A., et al. ?change in serum lipid levels of hyperlipemic patients following the feeding of starch, sucrose, and glucose.? Am. J. Clin. Nutr., 18:261, 1966; Kuo, P. T., and N. N. Huang. J. Clin. Invest., 44:1924, 1964; Antar, M. A. Fed. Proc., 22:327, 1963; Hodges, R.E. Fed. Proc., 22:209, 1963.
    For other excellent reports on the subject of sugar and starch consumption and atherosclerosis, see the special symposium issue of the American Journal of Clinical Nutrition, 20, 1967.
    68. Kuo, P. T., et al. ?Dietary carbohydrates in hyperlipemia (hyperglyceridemia); hepatic and adipose tissue lipogenic activities.? Am. J. Clin. Nutr., 20:116, 1967.
    In this intensive study, the authors were endeavoring to ascertain the specific mechanism in the body by which sugar-induced hyperlipidemia is produced. They pointed out that the carbohydrate-induced hyperglyceridemia is relatively common and is most often in association with atherosclerosis. Its chief features are (1) the concentration of low density beta lipoprotein compounds in the serum, compounds with a large cargo of triglyceride, and is directly related to excess sugar intake; (2) elevated blood triglycerides (hyperglyceridemia) occurs when the subject eats his ordinary diet; (3) when the patient is maintained on a high carbohydrate diet, marked fluctuations occur to the serum triglyceride levels, with radical elevations occurring at times of the largest ingestion of sugar.
    In their study of eight ?hyperlipidemic? patients, Kuo and colleagues found that dietary sugar (sucrose) administered to patients causes blood fats to increase, while starch tends to lower them. They found that individuals who had low blood fat levels were relatively resistant to the effects of sugar, and that 85 to 90 percent of the total calorie intake in sugar was required to produce hyperglyceridemia.
    In eight hyperlipidemic patients maintained on special feeding periods from three to six weeks, Kuo and his coworkers found that when sugar was substituted for starch, three blood lipid levels were raised; conversely, when starch replaced sugar, serum lipid levels were lowered toward normal values.
    Kuo and his team then undertook an intensive investigation of the possible mechanism (s) involved in the production of high serum cholesterol/triglyceride concentrations in hyperlipidemic individuals. Lipid synthesis from carbohydrate is believed to take place chiefly in the liver. Studies have also suggested that the adipose tissues are involved. Kou and colleagues studied the respective roles of hepatic and adipose tissues of endogenous lipogenesis from glucose, sucrose, and acetate precursors in six normal and fourteen hyperlipidemic subjects.
    From their carefully conducted studies, they ascertained first, and to their surprise, that in both normal and hyperlipidemic subjects, 97.5 to 99.7 percent of all labeled fructose, glucose, and acetate carbons are incorporated by the liver into phospholipid, chiefly lecithin. While the liver tissues of the hyperlipidemic subjects synthesized fructose and acetate into lipids other than phospholipids more actively that than the livers of normal individuals, it did not account for the high blood lipid levels.
    These investigators then found that the adipose tissue of hyperglyceride patients incorporated labeled fructose carbon into lipids seven to eight times faster than the tissue of normal individuals. On the other hand, glucose was incorporated into lipids by the adipose tissue at a much slower rate in both groups. Since starch, by hydrolysis, yields only glucose molecules, these observations by Kuo and his coworkers together with the data obtained from fructose, sucrose, and glucose feeding experiments in animals and man partly explain why sucrose causes a rise in blood lipids while starch lowers them.
    Moreover, Kuo and colleagues found that the fat tissue of normal subjects converted much of the carbohydrate precursors into water soluble moieties of the lipid molecule, particularly phospholipids, while the tissue of hyperlipidemic subjects incorporated major parts of the precursors into fatty acids. Also, the lipolytic or triglyceride breakdown was greatly accelerated from as much as sixteen to forty-five times higher in the adipose tissues of hyperlipidemic fasting patients.
    The fat tissues of the hyperlipidemic subjects were highly active in synthesizing lipids from simple sugars and in releasing free fatty acids. The high influx of free fatty acids from fat tissue are transported to the liver, explains Kuo et al,; there they are incorporated into triglyceride and then released into the blood stream as low density lipoproteins, producing hyperglyceridemia.
    Finally, Kuo et al. point out that these data suggest ?an abnormality in phospholipid metabolism.? Whereas the fat tissues of normal individuals convert most carbohydrate precursors into water-soluble moieties of the phospholipids, the fat tissues of hyperlipemic subjects divert these precursors into accelerated production of free fatty acids, to be eventually incorporated into low density lipoproteins via the liver.

    Dave's comment:
    One can see from the above that people differ in their responses to fructose intake. Over the years, the sugar industry has used these observed differences to suggest that sugar intake is not related to obesity. The logic goes something like this. Since fat people consume more sugar than skinny people, sugar does not cause overweight.

    On Oct 05, 2007 at 6:21 am Larry Hobbs wrote:

    . . . . .


    Thank you for the wonderful information. Great stuff.

    I read Williams' book about 25 years ago and still have it on my shelf.

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