Does added sugar in foods and drinks contribute to the development of
heart disease?

According to the Canadian Sugar Institute's FAQ, the answer is "No
evidence"!

QUOTE http://www.sugar.ca/
Q: "Should I avoid sugar if I'm worried about heart disease?"
A: "There is no evidence that sugar (sucrose) intake contributes to
the development of heart disease. Many genetic and lifestyle factors
are involved in the development of heart disease. The most important
dietary advice to help reduce the risk of coronary heart disease is to
increase the intake of carbohydrate-rich foods, especially grain
products, vegetables and fruit, decrease fat intake, and maintain a
healthy body weight."
UNQUOTE

BUT then, what about these articles about the consequences of
high-glycemic diets?

===

Asia Pac J Clin Nutr. 2004;13(Suppl):S3.

   Glycemic index in relation to coronary disease.

   Brand-Miller JC.

   Human Nutrition Unit, University of Sydney, NSW, 2006, Australia.

   In cardiovascular disease, dietary fat and blood lipids have
attracted the lion's share of attention. But carbohydrate, the
macronutrient that increases when fats are restricted, may not be the
totally desirable nutrient that we believe. The findings of the Lyon
Heart Study, one of the most important nutrition studies ever carried
out, emphasise that the 'prudent' high carbohydrate western diet is
not the best choice for reducing cardiovascular events. One
explanation is the potential to increase postprandial hyperglycemia,
an under-recognised risk factor for cardiovascular and total mortality
in the non-diabetic population. In the DECODE study and a host of
other large prospective cohort studies, high post-challenge blood
glucose was associated with 1.8 to 3 times greater relative risk of
death. The glycemic potential of carbohydrates is therefore relevant
to both prevention and management of coronary disease. Diets based on
high glycemic index (GI) carbohydrate foods have been shown to 1)
increase day-long blood glucose and insulin levels 2) exacerbate
insulin resistance in predisposed individuals 3) adversely affect
markers of the metabolic syndrome (triglycerides and HDL-cholesterol)
in intervention studies and 4) increase the risk of coronary disease
in a healthy population. How does high blood glucose increase the risk
of CVD? Laboratory studies have shown that high glucose levels even
within the normal range adversely affect endothelial function via a
multitude of mechanisms including oxidative stress, inflammatory
factors, protein glycation, LDL oxidation, pro-coagulatory and
anti-fibrinolytic activity. In intervention studies of men with
hyperlipidemia, Jenkins et al showed that a low GI diet was associated
with lower TG and LDL cholesterol levels compared with an otherwise
equivalent diet based on high GI carbohydrates. In women with a family
history of CVD following a low GI diet for 4 weeks, Frost et al found
increased insulin sensitivity after a glucose challenge and increased
glucose uptake in isolated adipocytes. Even in lean young adults, a
low GI diet reduced muscle triglycerides, a marker of insulin
resistance, despite no effect on insulin-stimulated glucose uptake.
Epidemiological studies provide further support. In the Nurses Health
Study, those in the highest quintile of GI and glycemic load (GI x
carbohydrate) had nearly double the relative risk of coronary infarct,
compared to those in the lowest quintile, after adjustment for known
risk factors, including fibre. In several observational studies of
healthy men and women, high GI diets have been consistently associated
with lower HDL levels. In post-menopausal women, high GI diets were
associated with higher C-reactive protein levels (a marker of low
grade chronic inflammation), high triglycerides and lower HDL levels,
all of which increase the risk of CVD. Low GI diets may also reduce
visceral fat deposition. In recent studies, we compared 4 weight loss
diets of differing glycemic load (GL). Compared to the conventional
low fat diet with a high GL, the reduced GL diets produced greater
rates of weight loss but only the low GI diet was associated with
significant reductions in LDL-cholesterol (unpublished data). Finally,
the STOP-NIDDM study using Acarbose (a drug which slows brush border
digestion of carbohydrates) provides direct evidence that reducing the
rate of carbohydrate absorption per se halves the risk of
cardiovascular events and hypertension. The use of naturally-occurring
'slow-release' or low glycemic index (GI) carbohydrates to achieve the
same end remains controversial.

   PMID: 15294465 [PubMed - in process]

===
Curr Opin Lipidol. 2005 Feb;16(1):69-75.    

   Glycemic index, postprandial glycemia and cardiovascular disease.

   Dickinson S, Brand-Miller J.

   Human Nutrition Unit, School of Molecular and Microbial
Biosciences, University of Sydney, NSW 2006, Australia.

   PURPOSE OF REVIEW: Several lines of evidence indicate that
exaggerated postprandial glycemia puts individuals without diabetes at
greater risk of developing cardiovascular disease. In large,
prospective observational studies, including meta-analyses, higher 120
min post-load blood glucose and glycated hemoglobin (a measure of
average blood glucose level over time) independently predict
cardiovascular mortality and morbidity in individuals without
diabetes. These findings imply that the glycemic nature of dietary
carbohydrates may also be relevant. We aim to provide a clearer
perspective on how the glycemic impact of carbohydrates may modulate
development of cardiovascular disease. RECENT FINDINGS: In ecological
studies, average dietary glycemic index (a measure of the postprandial
glycemic potential of carbohydrates) and glycemic load (average
glycemic index x amount of carbohydrate) predicts coronary infarct and
cardiovascular disease risk factors, including HDL cholesterol,
triglycerides and C-reactive protein. In short-term intervention
studies of overweight and hyperlipidemic patients, low glycemic index
diets lead to improvements in cardiovascular disease risk factors,
including reduced LDL cholesterol and improved insulin sensitivity, as
well as greater body fat loss on energy-restricted diets. Molecular
studies indicate that physiological hyperglycemia induces
overproduction of superoxide by the mitochondrial electron-transport
chain, resulting in inflammatory responses and endothelial
dysfunction. SUMMARY: Taken together, the findings suggest that
conventional high-carbohydrate diets with their high glycemic index
may be suboptimal, particularly in insulin-resistant individuals.
Because around one in four adults has impairments in postprandial
glucose regulation, the glycemic potential of carbohydrates warrants
further investigation in cardiovascular disease prevention.

   Publication Types:

       * Review

   PMID: 15650566 [PubMed - indexed for MEDLINE]

===

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=15049931&query_hl=5&itool=pubmed_docsum

Diabet Med. 2004 Apr;21(4):311-7.

   Effects of glycaemic control on cardiovascular disease in diabetic
American Indians: the Strong Heart Study.

   Lu WQ, Resnick HE, Jablonski KA, Jain AK, Jones KL, Robbins DC,
Howard BV.

   MedStar Research Institute, Hyattsville, MD, and Washington
Hospital Center, Washington, DC, USA.

   AIMS: Diabetes increases the risk of cardiovascular disease (CVD).
Only part of this excess risk is explained by diabetes-associated
hypertension, obesity, and lipid disorders. Poor glycaemic control may
help explain the residual CVD risk. The aim of this study was to
determine whether variations in glycaemic control are associated with
CVD risk in diabetic individuals. METHODS: We examined longitudinal
data from the Strong Heart Study, a population-based study of CVD and
its risk factors among American Indians (a population with a high
prevalence of diabetes). Diabetes was defined using the 1998 World
Health Organization criteria: fasting plasma glucose >/= 126 mg/dl or
2-h plasma glucose >/= 200 mg/dl. American Diabetes Association
guidelines for glycaemic control were used: good, A(1c) < 7%; fair,
7-7.9%; and poor, >/= 8%. The analysis was based on data from diabetic
individuals with no CVD at baseline. RESULTS: During 9 years of
follow-up, 494 of the 2011 diabetic participants developed CVD.
Although Cox multivariate regression modelling showed dose-response
effects of glycaemic control on overall CVD and coronary heart disease
(CHD) incidence, the relationships were weakened when adjusted for
confounding variables. Kaplan-Meier analysis, however, showed that
diabetic individuals with poor baseline glycaemic control had
significantly increased proportions of overall CVD and CHD (P = 0.001)
during the 9 years of follow-up, compared with those who had good or
fair control. CONCLUSIONS: These findings highlight the importance of
risk factors, such as high blood pressure and dyslipidaemia, in
increasing CVD risk in those with diabetes.

   PMID: 15049931 [PubMed - indexed for MEDLINE]

===

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=16277121&query_hl=10&itool=pubmed_docsum

1: Int J Circumpolar Health. 2005 Sep;64(4):365-86.    

   Cardiovascular disease and risk factors in three Alaskan Eskimo
populations: the Alaska-Siberia project.

   Ebbesson SO, Adler AI, Risica PM, Ebbesson LO, Yeh JL, Go OT,
Doolittle W, Ehlert G, Swenson M, Robbins DC.

   Department of Neurological Surgery, University of Virginia,
Charlottesville 22908-0212, USA. se6b@virginia.edu

   OBJECTIVES: To determine the prevalence of CVD and to identify and
characterize associated risk factors in three distinct Eskimo
populations. STUDY DESIGN: Cross-sectional. METHODS: A slightly
modified Strong Heart Study protocol was followed to examine 454
participants, aged 25-91, from four villages. RESULTS: Overall, 6% of
the participants under 55 years of age and 26% of those > or = 55
years of age showed evidence of CHD by ECG, or in patient records. The
prevalence of "definite coronary heart disease" (CHD) in women with
glucose intolerance (GI) was 21.0%, compared to 2.4% in those with
normal glucose tolerance (NGT). Men had comparable values of 26.7% and
6.3%. In addition, comparable values for "possible CHD" were 29.7% vs
6.0% for women and 21.4% vs 8.0% for men. GI was associated with
relatively higher prevalences of CHD in women than in men (prevalence
ratio = 8.5 vs 4.3). CHD was significantly related to age, glucose
intolerance and insulin. Hypertension and obesity were significantly
associated with CHD only in some ethnic groups. The prevalence of
current smokers was 56%. CONCLUSIONS: Recent changes in lifestyle and
diet of Alaskan Eskimos, leading to obesity, hypertension, insulin
resistance and DM, contribute to an increased risk for cardiovascular
disease.

   PMID: 16277121 [PubMed - indexed for MEDLINE]

===

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra
ct&list_uids=10199351&query_hl=13&itool=pubmed_docsum
Lancet. 1999 Mar 27;353(9158):1045-8.    

   Glycaemic index as a determinant of serum HDL-cholesterol
concentration.

   Frost G, Leeds AA, Dore CJ, Madeiros S, Brading S, Dornhorst A.

   Department of Nutrition and Dietetics, Hammersmith Hospitals NHS
Trust, London, UK. gfrost@rpms.ac.uk

   BACKGROUND: Diet influences the prevalence of coronary heart
disease (CHD). Insulin sensitivity and concentrations of HDL
cholesterol, two metabolic predictors of CHD, are also influenced by
diet. Dietary carbohydrates with a high glycaemic index cause a high
postprandial glucose and insulin response, and are associated with
decreased insulin sensitivity and an increased risk of CHD. This study
examined whether the glycaemic index of dietary carbohydrates is a
determinant of serum HDL-cholesterol concentrations. METHOD: Dietary,
anthropometric, and biochemical data from the 1986-87 Survey of
British Adults (n=2200) were reanalysed by a multiple regression
model, which examined the relation between serum total cholesterol,
HDL-cholesterol, and calculated LDL-cholesterol concentrations and
various dietary characteristics, including the type of carbohydrate,
the glycaemic index, and fat intake. FINDINGS: Among the 1420
participants with complete data, there was a significant negative
relation between serum HDL-cholesterol concentration and the glycaemic
index of the diet for both men (regression coefficient -0.00724 [95%
CI -0.0101 to -0.00434], p=0.02) and women (-0.01326 [-0.0162 to
-0.0102], p<0.0001). No other significant relation was found with
total cholesterol or LDL-cholesterol concentration or with any other
dietary carbohydrate or fat constituent. INTERPRETATION: In a
cross-sectional study of middle-aged adults, the glycaemic index of
the diet was the only dietary variable significantly related to serum
HDL-cholesterol concentration. Thus, the glycaemic index of the diet
is a stronger predictor than dietary fat intake of serum
HDL-cholesterol concentration.

   PMID: 10199351 [PubMed - indexed for MEDLINE]

===

http://www.ajcn.org/cgi/content/abstract/83/2/362
American Journal of Clinical Nutrition, Vol. 83, No. 2, 362-370,
February 2006
© 2006 American Society for Clinical Nutrition
ORIGINAL RESEARCH COMMUNICATION
Predictors of weight gain in a Mediterranean cohort: the Seguimiento
Universidad de Navarra Study 1 ,2 ,3
Maira Bes-Rastrollo1, Almudena Sánchez-Villegas1, Enrique
Gómez-Gracia1, J Alfredo Martínez1, Raquel M Pajares1 and Miguel A
Martínez-González1

1 From the Departments of Preventive Medicine and Public Health (MB-R,
AS-V, RM-P, and MAM-G) and Physiology and Nutrition (JAM), University
of Navarra, Pamplona, Spain; the Department of Clinical Sciences,
University of Las Palmas de Gran Canaria, Las Palmas de Gran Canaria,
Spain (AS-V); and the Department of Preventive Medicine and History of
Medicine, University of Málaga, Málaga, Spain (EG-G)

Background: High consumption of sugar-sweetened drinks has been
associated with weight gain and obesity in the United States. This
trend may also be affecting populations with different eating patterns
who increasingly are adopting typical US dietary patterns.

Objective: We assessed whether the consumption of sweetened drinks and
other food items increased the likelihood of weight gain in a
Mediterranean population.

Design: This was a prospective cohort analysis of 7194 men and women
with a mean age of 41 y who were followed-up for a median of 28.5 mo
with mailed questionnaires. Dietary exposure was assessed with a
previously validated semiquantitative food-frequency questionnaire.

Results: During follow-up, we observed that 49.5% of the participants
increased their weight (x weight gain: 0.64 kg; 95% CI: 0.55, 0.73
kg). In the participants who had gained ≥3 kg in the 5 y before
baseline, the adjusted odds ratio of subsequent weight gain for the
fifth quintile compared with the first quintile of sugar-sweetened
soft drink consumption was 1.6 (95% CI: 1.2, 2.1; P for trend = 0.02).
This association was absent in the participants who had not gained
weight in the 5-y period before baseline. The consumption of
hamburgers, pizza, and sausages (as a proxy for fast-food consumption)
was also independently associated with weight gain (adjusted odds
ratio for the fifth compared with the first quintile = 1.2; 95% CI:
1.0, 1.4; P for trend = 0.05). We also found a significant, but
weaker, association between weight gain and both red meat and
sweetened fruit juice consumption.

Conclusion: In a Mediterranean cohort, particularly in the
participants who had already gained weight, an increased consumption
of sugar-sweetened soft drinks and of hamburgers, pizza, and sausages
was associated with a higher risk of additional subsequent weight
gain.

===

X'Posted to: sci.med.nutrition,sci.med.cardiology