Here's a collection of studies and quotes about how excess amounts of carbohydrates (sugar, starch, etc) can cause health problems:
“The possibility that high, long-term intake of carbohydrates that are rapidly absorbed as glucose may increase the risk of type 2 diabetes has been a long-standing controversy. Two main mechanisms have been hypothesized, one mediated by increases in insulin resistance and the other by pancreatic exhaustion as a result of the increased demand for insulin. During the past decade, several lines of evidence have collectively provided strong support for a relation between such diets and diabetes incidence. In animals and in short-term human studies, a high intake of carbohydrates with a high glycemic index (a relative measure of the incremental glucose response per gram of carbohydrate) produced greater insulin resistance than did the intake of low-glycemic-index carbohydrates. In large prospective epidemiologic studies, both the glycemic index and the glycemic load (the glycemic index multiplied by the amount of carbohydrate) of the overall diet have been associated with a greater risk of type 2 diabetes in both men and women. Conversely, a higher intake of cereal fiber has been consistently associated with lower diabetes risk. In diabetic patients, evidence from medium-term studies suggests that replacing high-glycemic-index carbohydrates with a low-glycemic-index forms will improve glycemic control and, among persons treated with insulin, will reduce hypoglycemic episodes. These dietary changes, which can be made by replacing products made with white flour and potatoes with whole-grain, minimally refined cereal products, have also been associated with a lower risk of cardiovascular disease and can be an appropriate component of recommendations for an overall healthy diet.” Willett W, Manson J, Liu S. Glycemic index, glycemic load, and risk of type 2 diabetes. Am J Clin Nutr. 2002 Jul;76(1):274S-80S
“Hyperglycemia and hyperinsulinemia are central features of the metabolic syndrome and type 2 diabetes mellitus, which contribute to the pathogenesis of coronary heart disease (CHD). Recent data indicate that increased dietary glycemic load (GL) due to replacing fats with carbohydrates or increasing intake of rapidly absorbed carbohydrates (ie, high glycemic index ) can create a self-perpetuating insulin resistance state and predicts greater CHD risk. In this paper, we discuss the historic development of the GI and GL concepts and summarize metabolic experiments and epidemiologic observations relating to clinical utilities of these measures. On balance, increased consumption of low-GI foods leads to improvements in glycemia and dyslipidemia in metabolic studies, and a low-GL diet has been associated with lower risk of type 2 diabetes and CHD in prospective cohort studies. We conclude that decreasing dietary GL by reducing the intake of high-glycemic beverages and replacing refined grain products and potatoes with minimally processed plant-based foods such as whole grains, fruits, and vegetables may reduce CHD incidence in sedentary individuals and populations with a high prevalence of overweight. Because of advances in food-processing technologies and changes in ingredients in our food supply, the composition and physiologic effects of foods are likely to change over time. Future efforts should continue to quantify and monitor the metabolic impacts of different foods, and such information should be routinely incorporated into long-term prospective studies to allow for the assessment of the interactive effects of diets and other metabolic determinants on chronic disease risk.” Liu S, Willett WC. Dietary glycemic load and atherothrombotic risk. Current Atherosclerosis Report. November 2002;4(6):454-61.
Effects of a low-carb (ketogenic) diet vs. a high-carb (low-fat) diet on rats: “…studies showed that the ketogenic diet did not significantly alter regional brain glucose utilization. However, rats maintained on the high-carbohydrate diet had a marked decrease in their brain glucose utilization … However, even marginal protein dietary deficiency, when coupled with a carbohydrate-rich diet, depresses cerebral glucose utilization to a degree often seen in metabolic encephalopathies. Our results support the clinical contention that protein dietary deficiency coupled with increased carbohydrate intake can lead to CNS [central nervous system] dysfunction.” - al-Mudallal AS, Levin BE, Lust WD, Harik SI. Department of Neurology, Case Western Reserve University School of Medicine, Cleveland, OH, USA. Neurology 1995 Dec;45(12):2261-2265
“A diet high in carbohydrates with high glycemic indexes (GI) and glycemic load were linked to risk of coronary heart disease development in women in a large prospective study. Two cross-sectional studies showed that low-GI diets are associated with high HDL-cholesterol concentrations, especially in women. In a tightly controlled study of patients with type 2 diabetes, serum total cholesterol, LDL cholesterol, and apolipoprotein B concentrations fell more significantly after a low-GI diet than after a high-GI diet. In the same study, plasminogen activator inhibitor-1 concentrations were reduced by 58% after the low-GI diet. Insulin-stimulated glucose uptake by adipocytes was significantly higher in patients undergoing coronary artery bypass graft surgery after 4 wk of consuming a low-GI diet than after consuming a high-GI diet.” Leeds AR. Glycemic index and heart disease. Am J Clin Nutr. 2002 Jul;76(1):286S-9S.
“Although weight loss can be achieved by any means of energy restriction, current dietary guidelines have not prevented weight regain or population-level increases in obesity and overweight. Many high-carbohydrate, low-fat diets may be counterproductive to weight control because they markedly increase postprandial hyperglycemia and hyperinsulinemia. Many high-carbohydrate foods common to Western diets produce a high glycemic response [high-glycemic-index (GI) foods], promoting postprandial carbohydrate oxidation at the expense of fat oxidation, thus altering fuel partitioning in a way that may be conducive to body fat gain. In contrast … foods that produce a low glycemic response (low-GI foods) may enhance weight control because they promote satiety, minimize postprandial insulin secretion, and maintain insulin sensitivity. This hypothesis is supported by several intervention studies in humans in which energy-restricted diets based on low-GI foods produced greater weight loss than did equivalent diets based on high-GI foods. Long-term studies in animal models have also shown that diets based on high-GI starches promote weight gain, visceral adiposity, and higher concentrations of lipogenic enzymes than do isoenergetic, macronutrientcontrolled, low-GI-starch diets. In a study of healthy pregnant women, a high-GI diet was associated with greater weight at term than was a nutrient-balanced, low-GI diet. In a study of diet and complications of type 1 diabetes, the GI of the overall diet was an independent predictor of waist circumference in men. These findings provide the scientific rationale to justify randomized, controlled, multicenter intervention studies comparing the effects of conventional and low-GI diets on weight control.” Brand-Miller JC, Holt SH, Pawlak DB, McMillan J. Glycemic index and obesity. Am J Clin Nutr. 2002 Jul;76(1):281S-5S.
“Although the adverse effects of excess adiposity on health outcomes are widely recognized, there is no consensus regarding the most appropriate dietary strategies for managing obesity in youth. Recently, a novel dietary variable termed glycemic load has been postulated to influence hunger and body weight regulation. Glycemic load, a measure of the effects of a meal on blood glucose levels, is determined by the type and the amount of carbohydrate consumed. According to a hypothetical model, ingestion of high-glycemic load meals induces a sequence of hormonal changes that alter partitioning of metabolic fuels, exacerbate hunger, and over the long-term, promote weight gain. This chapter provides an overview of the available evidence suggesting that dietary glycemic load, and its related factor, the glycemic index, should be taken into consideration in the design of weight loss interventions.” Ludwig DS. Dietary glycemic index and obesity. Journal Nutrition 2000; 130(suppl):280S -- 3S.
“OBJECTIVE: The prevalence of obesity has increased dramatically in recent years. However, the role of dietary composition in body weight regulation remains unclear. The purpose of this work was to investigate the acute effects of dietary glycemic index (GI) on energy metabolism and voluntary food intake in obese subjects. METHODS: Twelve obese teenage boys were evaluated on three separate occasions using a crossover study protocol. During each evaluation, subjects consumed identical test meals at breakfast and lunch that had a low, medium, or high GI. The high- and medium-GI meals were designed to have similar macronutrient composition, fiber content, and palatability, and all meals for each subject had equal energy content. After breakfast, plasma and serum concentrations of metabolic fuels and hormones were measured. Ad libitum food intake was determined in the 5-hour period after lunch. RESULTS: Voluntary energy intake after the high-GI meal (5.8 megajoule [mJ]) was 53% greater than after the medium-GI meal (3.8 mJ), and 81% greater than after the low-GI meal (3.2 mJ). In addition, compared with the low-GI meal, the high-GI meal resulted in higher serum insulin levels, lower plasma glucagon levels, lower postabsorptive plasma glucose and serum fatty acids levels, and elevation in plasma epinephrine. The area under the glycemic response curve for each test meal accounted for 53% of the variance in food intake within subjects. CONCLUSIONS: The rapid absorption of glucose after consumption of high-GI meals induces a sequence of hormonal and metabolic changes that promote excessive food intake in obese subjects. Additional studies are needed to examine the relationship between dietary GI and long-term body weight regulation.” Ludwig DS, Majzoub JA, Al-Zahrani A, et. al. High glycemic index foods, overeating, and obesity. Pediatrics. 1999 Mar;103(3):E26.
“AIM: The intent of this review is to critically analyze the scientific evidence on the role of the glycemic index in chronic Western disease and to discuss the utility of the glycemic index in the prevention and management of these disease states. BACKGROUND: The glycemic index ranks foods based on their postprandial blood glucose response. Hyperinsulinemia and insulin resistance, as well as their determinants (eg high energy intake, obesity, lack of physical activity) have been implicated in the etiology of diabetes, coronary heart disease and cancer. Recently, among dietary factors, carbohydrates have attracted much attention as a significant culprit, however, different types of carbohydrate produce varying glycemic and insulinemic responses. Low glycemic index foods, characterized by slowly absorbed carbohydrates, have been shown in some studies to produce beneficial effects on glucose control, hyperinsulinemia, insulin resistance, blood lipids and satiety.” Augustin LS, Franceschi S, Jenkins DJ, et. al. Glycemic index in chronic disease: a review. European Journal Clinical Nutrition. November 2002;56(11):1049-71
“The glycemic index has particular relevance to those chronic Western diseases associated with central obesity and insulin resistance. Early studies showed that starchy carbohydrate foods have very different effects on postprandial blood glucose and insulin responses in healthy and diabetic subjects, depending on the rate of digestion. A range of factors associated with food consumption was later shown to alter the rate of glucose absorption and subsequent glycemia and insulinemia. At this stage, systematic documentation of the differences that exist among carbohydrate foods was considered essential. The resulting glycemic index classification of foods provided a numeric physiologic classification of relevant carbohydrate foods in the prevention and treatment of diseases such as diabetes. Since then, low-glycemic-index diets have been shown to lower urinary C-peptide excretion in healthy subjects, improve glycemic control in diabetic subjects, and reduce serum lipids in hyperlipidemic subjects. Furthermore, consumption of low-glycemic index diets has been associated with higher HDL-cholesterol concentrations and, in large cohort studies, with decreased risk of developing diabetes and cardiovascular disease. Case-control studies have also shown positive associations between dietary glycemic index and the risk of colon and breast cancers.” Jenkins DJ, Kendall CW, Augustin LS, et. al Glycemic index: overview of implications in health and disease. Am J Clin Nutr. 2002 Jul;76(1):266S-73S.
“…Dr. Kenneth Vickery, who since the mid-1950's has written repeatedly of the dangers of refined carbohydrate foods in human nutrition, especially in connexion with the giving of cane-sugar in milk feeds to babies, and the ever-earlier introduction of refined farinaceous foods into the diet of infants. He has considered that such additions not only are the direct cause of dental decay and ever-more-frequent obesity in young children, but also probably lay the foundation for other conditions in later life, such as coronary thrombosis.” - from The Saccharine Disease: Conditions Caused by the Taking of Refined Carbohydrates, such as Sugar and White Flour, by Surgeon–Captain T.L Cleave, M.R.C.P., Director of Medical Research, Institute of Naval Medicine, London, 1974.
“Inquiry into the dietary history of patients diagnosed as schizophrenic reveals the diet of their choice is rich in sweets, candy, cakes, coffee, caffeinated beverages, and foods prepared with sugar. These foods, which stimulate the adrenals, should be eliminated or severely restricted." - Allan Cott, in Orthomolecular Approach to the Treatment of Learning Disabilities.
"Let us go to the ignorant savage, consider his way of eating and be wise … Let us cease pretending that toothbrushes and toothpaste are any more important than shoe brushes and shoe polish. It is store food that has given us store teeth." - Harvard professor Ernest Hooten, Ph.D. in Apes, Men, and Morons.
“The neutrophils that we rely on to kill any invading bacteria and viruses form 60% - 70% of the white blood cells in our bodies. They are generally much more active than any other blood cell. It can be disastrous to our health, therefore, if their effectiveness is compromised in any way. But this is exactly what happens if we eat too much carbohydrate and too much Sugar in particular. By 'sugar' I do not mean just the white, granulated stuff we serve from a bowl on the table; this is called 'sucrose' but the term Sugar applies to glucose, fructose (fruit sugar), maltose (grain sugar), honey (a mixture of glucose, fructose, sucrose and dextrin). … In a 1973 study, after an overnight fast and after their leucocytes had been tested for phagocytosis activity and their leukocytic index (LI) had been recorded, subjects were fed 100 grams of a specific carbohydrate (a sugar or starch). … all forms of carbohydrate - starch as well as sugars - reduced the neutrophils' effectiveness at destroying bacteria and other micro-organisms. (2) This study was confirmed in 1976 by Ringsdorf, et al. (3) They tested the effect of sugar (sucrose) by giving their subjects 24 ounces of sugar sweetened Cola. In this test the leucocytic index of all their subjects was reduced by 50%. In other words, the ability of their disease-fighting blood cells was halved.“- Barry Groves, PhD.
“This is the state of mind I imagine that mainstream nutritionists, researchers and physicians must inevitably take to the fat-versus-carbohydrate controversy. They may come around, but the evidence will have to be exceptionally compelling. Although this kind of conversion may be happening at the moment to John Farquhar, who is a professor of health research and policy at Stanford University and has worked in this field for more than 40 years. When I interviewed Farquhar in April, he explained why low-fat diets might lead to weight gain and low-carbohydrate diets might lead to weight loss, but he made me promise not to say he believed they did. He attributed the cause of the obesity epidemic to the ''force-feeding of a nation.'' Three weeks later, after reading an article on Endocrinology 101 by David Ludwig in the Journal of the American Medical Association, he sent me an e-mail message asking the not-entirely-rhetorical question, ''Can we get the low-fat proponents to apologize?''” – Gary Taubes, What if It’s All Been a Big Fat Lie?, New York Times, July 7, 2002.
“David Ludwig, the Harvard endocrinologist, says that it's the direct effect of insulin on blood sugar that does the trick. He notes that when diabetics get too much insulin, their blood sugar drops and they get ravenously hungry. They gain weight because they eat more, and the insulin promotes fat deposition. The same happens with lab animals. This, he says, is effectively what happens when we eat carbohydrates - in particular sugar and starches like potatoes and rice, or anything made from flour, like a slice of white bread. These are known in the jargon as high-glycemic-index carbohydrates, which means they are absorbed quickly into the blood. As a result, they cause a spike of blood sugar and a surge of insulin within minutes. The resulting rush of insulin stores the blood sugar away and a few hours later, your blood sugar is lower than it was before you ate. As Ludwig explains, your body effectively thinks it has run out of fuel, but the insulin is still high enough to prevent you from burning your own fat. The result is hunger and a craving for more carbohydrates. It's another vicious circle, and another situation ripe for obesity.” … “It is also undeniable, note students of Endocrinology 101, that mankind never evolved to eat a diet high in starches or sugars. ''Grain products and concentrated sugars were essentially absent from human nutrition until the invention of agriculture,'' Ludwig says, ''which was only 10,000 years ago.'' This is discussed frequently in the anthropology texts but is mostly absent from the obesity literature, with the prominent exception of the low-carbohydrate-diet books.” – Gary Taubes, What if It’s All Been a Big Fat Lie?, New York Times, July 7, 2002.
“'... Benedict and Carpenter. These workers determined the minimum (basal) oxygen requirements of normal human subjects and then measured the oxygen consumption of these subjects after various test meals of sugar, starch, protein, and fats, alone and in combination. After a protein meal they observed a marked rise in oxygen absorption (consumption), a phenomenon called "the specific dynamic action" of protein and which is regarded as highly beneficial to the body. After a fat meal there was a slight rise in oxygen absorption or none at all. After sugar and starch they found a slight initial rise followed by a fall in oxygen absorption in some experiments, and in other experiments they observed a consistent fall in oxygen absorption, with no initial rise. Benedict and Carpenter were unable to explain this fall in oxygen absorption after sugar and starch. They were much surprised to discover that the ingestion of sugar and starch actually could cause a Depression of total bodily oxygen absorption below basal requirements.” – Benjamin P. Sandler, M.D., 1951.