Sugar intake, serum insulin and platelet adhesiveness in men with and without peripheral vascular disease

Yudkin, John; Szanto, Stephen; Kakkar, Vijay V.

doi:10.1136/pgmj.45.527.608

Cited by 26 publications

(9 citation statements)

References 4 publications

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“…Whatever their intake of sugar, this would not affect their serum insulin levels, so that we would expect this group to show little or no relationship between the insulin level and sucrose intake. This prediction of the presence or absence of a relationship between insulin and sucrose intake in these two groups has already been tested, and the results are reported in the following paper (Yudkin, Szanto & Kakkar, 1969).…”

Section: Discussionmentioning

confidence: 99%

The effect of dietary sucrose on blood lipids, serum insulin, platelet adhesiveness and body weight in human volunteers

Szanto¹,

Yudkin²

1969

Postgraduate Medical Journal

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112

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Summary A study was made of the effect of high or low intake of sucrose for periods of 14 days in a group of nineteen apparently healthy men. The high sucrose diet produced no change in blood levels of cholesterol or phospholipids, or in glucose tolerance, but it produced a significant rise in triglycerides in all nineteen men. In six of them, there was in addition a rise in serum immunoreactive insulin, especially during the glucose tolerance test, and these same six subjects also showed a considerable increase in weight and a significant increase in platelet adhesiveness. There was no difference between the six subjects and the remaining thirteen in any of the other measurements, or in the diets they consumed during the experiment. The changes produced by sucrose had disappeared, or nearly so, after 14 days of normal diet. It is suggested that the effect of sucrose in producing hyperinsulinism may be more relevant to its possible role in the aetiology of ischaemic heart disease than its effect on blood lipids. It is further suggested that only some individuals are susceptible to the development of ischaemic heart disease by dietary sucrose, and that these may be identified as those that show ‘sucrose-induced hyperinsulinism’.

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Section: Discussionmentioning

confidence: 99%

The effect of dietary sucrose on blood lipids, serum insulin, platelet adhesiveness and body weight in human volunteers

Szanto¹,

Yudkin²

1969

Postgraduate Medical Journal

Self Cite

112

View full text Add to dashboard Cite

show abstract

“…47, 52 Both human and animal studies show various metabolic risk for CHD with high sugar diets (e.g., impaired glucose tolerance, insulin resistance, elevated uric acid level, and altered platelet function). 47, 52–54 All of these abnormalities can be reversed when reverting to a diet low in sugar. 54, 55 …”

Section: Sugar and Chd Risk Factorsmentioning

confidence: 99%

The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease

DiNicolantonio

Lucan

O’Keefe

2016

Progress in Cardiovascular Diseases

278

143

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Dietary guidelines continue to recommend restricting intake of saturated fats. This recommendation follows largely from the observation that saturated fats can raise levels of total serum cholesterol (TC), thereby putatively increasing the risk of atherosclerotic coronary heart disease (CHD). However, TC is only modestly associated with CHD, and more important than the total level of cholesterol in the blood may be the number and size of low-density lipoprotein (LDL) particles that contain it. As for saturated fats, these fats are a diverse class of compounds; different fats may have different effects on LDL and on broader CHD risk based on the specific saturated fatty acids (SFAs) they contain. Importantly, though, people eat foods, not isolated fatty acids. Some food sources of SFAs may pose no risk for CHD or possibly even be protective. Thus, advice to reduce saturated fat in the diet without regard to such nuance could actually increase people’s risk of CHD. When saturated fats are replaced with refined carbohydrates, and specifically with added sugars (like sucrose or high fructose corn syrup), the end result is not favorable for heart health. Such replacement leads to changes in LDL, high-density lipoprotein (HDL), and triglycerides that may increase the risk of CHD. Additionally, diets high in sugar may induce many other abnormalities associated with elevated CHD risk, including elevated levels of glucose, insulin, and uric acid, impaired glucose tolerance, insulin and leptin resistance, non-alcoholic fatty liver disease, and altered platelet function. A diet high in added sugars has been found to cause a 3-fold increased risk of death due to cardiovascular disease. But sugars, like saturated fats, are a diverse class of compounds. The monosaccharide, fructose, and fructose-containing sweeteners (e.g., sucrose) result in greater degrees of metabolic abnormalities than seen with glucose (either isolated as a monomer or in chains as starch) and may present greater risk for CHD. This paper reviews the evidence linking saturated fats and sugars to CHD, and concludes that the latter is more of a problem than the former. Dietary guidelines should shift focus away from reducing saturated fat, and from replacing saturated fat with carbohydrates, specifically when these carbohydrates are refined. To reduce the burden of CHD, guidelines should focus particularly on reducing intake of concentrated sugars, specifically the fructose-containing sugars like sucrose and high-fructose corn syrup in the form of ultra-processed foods and beverages.

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“…High intake of sugar increases insulin level in some individuals, but not all, and that these individuals are susceptible to the effect of sucrose for occlusive arterial disease. 155 Hyperglycemia in diabetes would produce ROS through various mechanisms already described in the section "glucose and generation of reactive oxygen species" of this review. ROS have been implicated in the development of atherosclerosis, which has been described in the section "atherosclerosis" of this review.…”

Section: Peripheral Arterial Diseasementioning

confidence: 96%

Oxidative Stress as a Mechanism of Added Sugar-Induced Cardiovascular Disease

Prasad

Dhar

2014

Int J Angiol

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Added sugars comprise of table sugar, brown sugar, corn syrup, maple syrup, honey, molasses and other sweeteners in the prepared and processed foods and beverages. Sugars (simple carbohydrates) refer to monosaccharides (glucose, galactose, and fructose) and disaccharides (sucrose [glucose þ fructose] found in sugarcane, beets, honey, and corn syrup; lactose [glucose þ lactose] found in milk products; and maltose [glucose þ glucose] found in malt). Complex carbohydrates are glucose-containing polysaccharides, that is, starch. The American Heart Association recommends six teaspoons (24 g) of added sugar per day for women and nine teaspoons (36 g) per day for men or in other words added sugar should provide 100 cal/d for women and 150 cal/d for men, respectively. 1 The American Heart Association recommends that not more than 5% of calories should come from sugar. 1 High consumption of added sugars has a higher risk of cardiovascular disease and the associated risk factors. 2,3 Benn et al, 4 have reported that elevation of nonfasting glucose is associated with an increased risk of ischemic heart disease (IHD) and myocardial infarction (MI). A high intake of sugar enhances the risk of coronary heart disease (CHD) in diabetic individuals using diuretics. 5 The International Study of Macro/Micronutrients and Blood Pressure reported that daily consumption of every extra sugar-sweetened beverage increased the systolic arterial pressure by 1.6 mm Hg and the diastolic pressure by 0.8 mm Hg. 6 The present review deals with the glucose and oxidative stress, cardiovascular disease, serum lipids, and inflammatory mediators, and the glucose-induced oxidative stress as a mechanism of cardiovascular diseases. A recent publication has shown that there is a significant correlation between the added sugar consumption and an increased risk of cardiovascular disease mortality. 7 Reactive Oxygen SpeciesThe formation of reactive oxygen species (ROS) is schematically depicted in ►Fig. 1 and has been described in detail Keywords ► added sugars ► reactive oxygen species ► atherosclerosis ► hypertension ► coronary artery disease ► peripheral vascular disease AbstractAdded sugars comprising of table sugar, brown sugar, corn syrup, maple syrup, honey, molasses, and other sweeteners in the prepared processed foods and beverages have been implicated in the pathophysiology of cardiovascular diseases. This article deals with the reactive oxygen species (ROS) as a mechanism of sugar-induced cardiovascular diseases. There is an association between the consumption of high levels of serum glucose with cardiovascular diseases. Various sources of sugar-induced generation of ROS, including mitochondria, nicotinamide adenine dinucleotide phosphate-oxidase, advanced glycation end products, insulin, and uric acid have been discussed. The mechanism by which ROS induce the development of atherosclerosis, hypertension, peripheral vascular disease, coronary artery disease, cardiomyopathy, heart failure, and cardiac arrhythmias have been discussed in detail....

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Sugar intake, serum insulin and platelet adhesiveness in men with and without peripheral vascular disease

Cited by 26 publications

References 4 publications

The effect of dietary sucrose on blood lipids, serum insulin, platelet adhesiveness and body weight in human volunteers

The effect of dietary sucrose on blood lipids, serum insulin, platelet adhesiveness and body weight in human volunteers

The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease

Oxidative Stress as a Mechanism of Added Sugar-Induced Cardiovascular Disease

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