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National Heart Foundation of Australia
Position statement on the relationships between
carbohydrates, dietary fibre, glycaemic
index/glycaemic load
and cardiovascular disease
Recommendations of the National Heart Foundation of Australia's
Nutrition and Metabolism Advisory Committee
Approved in November 2005
Published in February 2006
Contents
Page
Glossary of terms
4
Rationale
7
Objectives
7
Criteria for appraisal of evidence
8
Important findings
9
Dietary carbohydrates and cardiovascular disease endpoints
10
Conclusions
17
References
19
2
This position statement was prepared by Dr Manny Noakes, Chair of the National
Heart Foundation of Australia’s Nutrition and Metabolism Advisory Committee
(NMAC) and Barbara Eden, Executive Officer, National Nutrition Program, Heart
Foundation.
The members of the Heart Foundation’s NMAC during the development of this
paper were: Dr Manny Noakes, Prof Philip Barter, Prof Madeleine Ball, A/Prof David
Colquhoun, Prof David Crawford, Prof Len Kritharides, A/Prof Leon Simons, Ms
Margaret Miller, A/Prof Richard O'Brien, A/Prof David Sullivan, Dr David Topping,
Ms Susan Anderson, Ms Robyn Charlwood, Ms Cathy Cooper, Ms Ernestine
Thompson, Ms Barbara Eden, and Dr Peter Abernethy.
This position statement was developed from an evidence-based review of the
scientific literature prepared by the National Heart Foundation of Australia's
Nutrition and Metabolism Advisory Committee (NMAC), with the assistance of
Mr Bill Shrapnel who was contracted for this process. This position paper was also
informed by an addendum paper which examined studies published from December
2004 to June 2005.
The evidence-based review paper was developed through an extensive review and
consultation process. A Working Group consisting of the following members guided
the development of the review paper:
•
•
•
•
•
•
Dr Manny Noakes (NMAC member and Research Scientist, Health Sciences
and Nutrition, CSIRO)
Dr David Topping (NMAC member and Chief Research Scientist, Health
Sciences and Nutrition, CSIRO)
Prof Stewart Truswell, Academic Director, School of Molecular and Microbial
Biosciences , Sydney University, Sydney, NSW)
Bill Shrapnel (Contract Dietitian)
Toni Fear (Program Officer Nutrient Criteria/Regulations, Tick Program, National
Heart Foundation of Australia); and
Barbara Eden (Nutrition Manager NSW / Executive Officer, National Nutrition,
National Heart Foundation of Australia).
This paper underwent extensive internal consultation with staff and honoraries as
members of NMAC and external consultation with expert comments received from
Prof Jim Mann (Dept Human Nutrition, Otago University, New Zealand and Chair of
the NHFNZ Scientific Committee) and Prof Jennie Brand-Miller (School of
Molecular and Microbial Biosciences , Sydney University, Sydney, NSW).
It was also approved by the Heart Foundation’s Cardiovascular Health Advisory
Committee and the National Board.
3
Glossary of terms
In light of the complexity and controversies regarding definitions of carbohydrates,
the Heart Foundation’s evidence-based review did not rely on just one classification
of carbohydrates. Rather, it considered key studies that sought to answer
questions about whether the amount and source of carbohydrates and their
physiological effects influence the risk of cardiovascular disease. However, the
following definitions were found in the literature cited in the paper and have been
considered in developing the recommendations.
Body Mass Index
(BMI)
A calculated number used to identify and measure
under/overweight or obesity, calculated from a person’s height
and weight. BMI = weight in kg/(height in m)2. A BMI between
18.5 and 24.9 is recommended. (BMI values only apply to
adults aged 18 years and over, and are based on studies of
Caucasian populations.)
Carbohydrate refers to a complex range of compounds found
in food, including sugars, starches, oligosaccharides,
glycogen, maltodextrins, etc (FSANZ, 2005).
Carbohydrate
‘Available carbohydrate’ (including sugars and starches) is
carbohydrate, which after digestion in the body is able to be
used for energy (kilojoules).
A particular food is called a ‘carbohydrate’ food when
carbohydrate is the dominant or characterising nutrient in the
food. Examples are bread, pasta and cereals.
Cardiovascular
disease (CVD)
Cardiovascular disease refers to disease and conditions of the
circulatory system including heart, stroke and vascular
disease (NHFA, 2005).
Glycaemia
The level of the sugar, glucose, in the blood. Hyperglycaemia
occurs when there is too high a level of glucose (sugar) in the
blood.
Glycaemic index
(GI)
The glycaemic index (GI) of a carbohydrate containing food is
a standardised ranking of the blood glucose response to 50g
available carbohydrate from that food compared with 50g
carbohydrate from either glucose or white bread.
Carbohydrate from low GI foods is digested and absorbed
slowly, raising blood glucose levels gradually, whilst
carbohydrate from high GI foods raises blood glucose levels
quickly (Jenkins et al,. 1981; Brand-Miller et al, 1996).
Glycaemic load
(GL)
The glycaemic load (GL) of a food portion, meal or eating plan
is calculated by considering both the amount of carbohydrate
in the portion of the food consumed and the GI of that
individual food. The lower the GL of a food, meal or eating
plan, the lower the total impact on our blood glucose (BrandMiller et al, 2003).
4
Insoluble fibre
Insoluble fibre is the type of dietary fibre that does not dissolve
in water. It supports the plant structure, and is not as easily
digested. It is the hard, scratchy outer surfaces of roots,
grains, and seeds.
Insulin
resistance
This occurs when the body may produce enough insulin but
the body cells lose some of the ability to respond to the action
of the insulin. It occurs in non-insulin dependent diabetes,
because the person is usually older, overweight and has too
many fat cells.
Legumes
A legume, also known as a pulse, is the general name given
to beans, peas and lentils. Examples include dried peas (e.g.
split peas), dried beans (e.g. haricot beans, kidney beans),
canned beans (e.g. baked beans, three bean mix) and lentils.
Metabolic
syndrome
A clustering of risk factors incorporating central obesity and
any two of either raised triglyceride levels, reduced
HDL- cholesterol, raised blood pressure or raised fasting
plasma glucose (International Diabetes Federation, 2005).
Non-refined
carbohydrates
Non-refined, or unrefined, carbohydrate foods have had
limited processing, contain dietary fibre or have had dietary
fibre added during processing. They include foods like
wholegrain breads and cereals (e.g. oats, rice & pasta),
legumes, fruit, vegetables and dairy foods.
Plasma
cholesterol
Plasma cholesterol is a type of fat found in the blood. Low
Density Lipoprotein- (LDL) cholesterol is the ‘bad’
component of total cholesterol that increases the risk of
cardiovascular disease. High Density Lipoprotein- (HDL)
cholesterol or the ‘good’ component which helps protect
against cardiovascular disease.
Post-prandial
Occurring after food is consumed or after a meal.
Refined
carbohydrates
Refined carbohydrate foods have had the bran (outer layer)
and germ (inner layer) separated from the endosperm (middle
layer) of the grain during milling which results in lower levels of
dietary fibre, minerals, vitamins, phenols, phyto-oestrogens
and unsaturated fatty acids (Slavin et al,1997; Jacobs et al,
1998). Refined grain foods included sweet rolls and cakes or
desserts, white bread, pasta, English muffins, muffins or
biscuits, refined grain breakfast cereals, white rice, pancakes
or waffles, and pizza (Liu et al, 2003).
Soluble fibre
Soluble fibre is a type of dietary fibre that dissolves in water
and is more easily digested. It has a gel-like consistency and
is found in fruits, legumes (chickpeas, lentils, soybeans) and
cereals (oats and barley).
5
Triglycerides
(TG)
A type of fat found in the blood. The relationship between
high blood triglycerides and heart disease is less clear than for
blood cholesterol, however, there is evidence to suggest that
people with higher levels of blood triglycerides are at
increased risk of coronary heart disease.
Type 2 diabetes
Type 2 or adult onset diabetes is a condition involving the
relative or absolute lack of insulin which affects the way body
cells take up and use the carbohydrate (glucose) from the
blood. Diabetes increases the risk of developing
cardiovascular disease.
Wholegrains
Wholegrains are cereal foods that include all the parts of the
natural grain, including the endosperm (approximately 80%,
w/w), the germ and the bran of the grain (Anderson et al,
2000). Some studies have defined them as products
containing 25% wholegrain or bran by weight (Jacobs et al,
1998). Wholegrain foods included dark bread, wholegrain
breakfast cereal, popcorn, cooked oatmeal, wheat germ,
brown rice and other grains e.g. bulgur and couscous (Liu et
al, 2003).
Wholegrain in the Australian Food Standards Code means the
intact grain or the dehulled, ground, milled, cracked or flaked
grain where the constituents – endosperm, germ and bran –
are present in such proportions that represent the typical ratio
of those fractions occurring in the whole cereal, and includes
wholemeal (FSANZ, 2005).
6
Rationale
Dietary advice from the National Heart Foundation of Australia (NHFA) and most
other health authorities to reduce the risk of cardiovascular disease includes a
recommendation to reduce dietary saturated fatty acid intake in order to lower blood
cholesterol (NHFA, 1999). Carbohydrate and unsaturated fatty acids have been
recommended as suitable replacements. Concern about the rise in obesity rates in
many countries has favoured the use of carbohydrates as the replacement
(NHMRC, 1997), which leads to diets lower in total fat as well as saturated fat.
However, endorsement of low fat, high carbohydrate diets to lower cardiovascular
risk has not been universal. A recent review by the Heart Foundation found dietary
fat was not an independent risk factor for the development and progression of
overweight (NHFA, 2003). Furthermore, numerous short term studies have
indicated that diets high in carbohydrates increase serum concentrations of
triglycerides and decrease HDL-cholesterol. On these grounds it has been
suggested that high carbohydrate diets may be associated with increased risk of
cardiovascular disease (CVD) (Katan et al, 1997). Associations between glycaemic
load, coronary risk factors and increased coronary risk together with associations of
wholegrains, dietary fibre and lowered coronary risk, have raised further questions
about the potential role of both the amount and type of dietary carbohydrate in the
aetiology of cardiovascular disease.
Objectives
The objectives of the review of the relationship between carbohydrate, dietary fibre
and glycaemic load and cardiovascular disease are to:
•
Determine whether total dietary carbohydrate affects the risk of
cardiovascular disease with a focus on coronary heart disease (CHD) and
myocardial infarction (MI), blood lipid profiles, metabolic syndrome, insulin
resistance, type 2 diabetes and obesity.
•
Determine whether the source of dietary carbohydrate consumed affects the
risk of cardiovascular disease. The cardiovascular effects and mechanisms
associated with dietary fibre, wholegrains, fibre type, glycaemic index (GI)
and glycaemic load (GL) were also assessed in this review.
7
Criteria for appraisal of evidence
The following criteria were used to assess the evidence in this review
‘Good’ evidence
‘Moderate’ evidence
‘Some’ evidence
Level of
evidence
Consistency across
several study designs,
including long term
intervention studies
Inconsistency across
study designs; use of
surrogate measures;
limited number and
type of studies
Inconsistency
across study
designs; limited
number and type of
studies
Quality of
evidence
Measurement bias
adequately minimised
Limited in quality
Limited in quality
Statistically significant
Effect possibly due to
measurement bias
Effect possibly due
to measurement
bias
Metabolic studies in
humans
Metabolic studies in
humans
Lack of metabolic
studies
Size of effect
Mechanism
In light of the complexity and controversies regarding definitions of carbohydrates,
the Heart Foundation’s evidence-based review did not rely on one classification of
carbohydrates. Rather, it considered key studies that sought to answer questions
about whether the amount and source of carbohydrates and their physiological
effects influence the risk of cardiovascular disease.
8
Important findings
Based on the following discussion of the evidence, the Heart Foundation’s position
on dietary carbohydrate and cardiovascular disease concludes that:
Total carbohydrate
•
There is no evidence to support any significant association between total
carbohydrate and cardiovascular disease.
Glycaemic index/Glycaemic load
•
There is some evidence that dietary patterns high in refined carbohydrate
and high dietary glycaemic load are associated with an increased risk of
coronary heart disease which may be mediated by effects on Body Mass
Index (BMI) rather than by glycaemia.
Dietary fibre
•
There is moderate evidence that dietary patterns high in dietary fibre from
cereals and fruit are associated with a lower risk of coronary heart disease
and that wholegrains, independently of dietary fibre, also appear protective.
Triglycerides
•
There is good evidence suggesting that dietary patterns high in glycaemic
load raise serum triglyceride levels, particularly in those with elevated
triglycerides and a high BMI.
Total and LDL-cholesterol
•
There is good evidence that soluble fibre lowers plasma low density
lipoprotein- (LDL) cholesterol.
Insulin resistance – Metabolic syndrome and type 2 diabetes
•
There is no evidence that total carbohydrate intake significantly affects
insulin sensitivity or the risk of developing type 2 diabetes.
•
There is moderate evidence that eating patterns low in refined carbohydrate,
lower in sucrose or high in cereal fibre are associated with a lower risk of
type 2 diabetes and have beneficial effects on post-prandial glucose
profiles.
Obesity
•
There is moderate evidence that high carbohydrate eating patterns, high in
sucrose or fructose may increase the risk of excessive energy intake. This
may impact on the development of overweight and obesity, and indirectly on
the risk of type 2 diabetes and cardiovascular disease.
9
Dietary carbohydrate and cardiovascular disease endpoints
Total carbohydrate
There is no evidence to support any significant association
between total carbohydrate and cardiovascular disease.
Experimental studies in the literature are of insufficient length and sample size to
determine if total carbohydrate intake directly affects clinical outcomes in humans.
Few epidemiological studies have found that total carbohydrate intake is associated
with cardiovascular endpoints if adjustment is made for confounders including total
energy intake (Garcia-Palmieri et al, 1980; McGee et al, 1884; Liu et al, 2000a). An
arm of the Diet and Reinfarction Trial (DART) study (Burr et al, 1989) found total
carbohydrate intake had no significant effect on the risk of re-infarction after two
years. However, total carbohydrate intake has been associated with elevated risk
of hemorrhagic stroke in the Nurses Health Study where this was most evident
among women with a BMI =25 kg/m 2 (Oh et al, 2005).
Glycaemic index / Glycaemic load
There is some evidence that dietary patterns high in refined
carbohydrate and high dietary glycaemic load are associated with
an increased risk of coronary heart disease which may be
mediated by effects on Body Mass Index (BMI) rather than by
glycaemia.
The 10-year follow up of the Nurses Health Study was the first epidemiological
evidence that high glycaemic load directly increases the risk of coronary heart
disease (CHD) (Liu et al, 2000a). These findings were not supported by those from
a study of a smaller, older, male cohort (van Dam et al, 2000), nor was there a
significant relationship observed between dietary glycaemic load and the risk of
non-fatal myocardial infarction in an Italian case control study (Tavani et al, 2003).
More recent data from the Nurses Health Study (Liu et al, 2001; Liu et al, 2003)
found that diets high in refined carbohydrate were not only related to CHD risk but
that this was more pronounced in those with a higher Body Mass Index (BMI). It is
therefore possible that as a high refined carbohydrate intake is related to obesity
(Gross et al, 2004) the effects on CVD may be obscured by adjustment for BMI.
This is supported by evidence that weight gain is inversely associated with the
intake of high-fibre, wholegrain foods but positively related to the intake of refined
grain foods in men and women (Liu et al, 2003; Koh-Banerjee & Rimm, 2003).
In the Oh et al study (2005), dietary glycaemic load (GL) was also positively
associated with total stroke among only those with a high BMI. These findings
suggest that a high intake of refined carbohydrate is associated with haemorrhagic
stroke risk, particularly among overweight or obese women. In the same study,
high consumption of cereal fibre was associated with lower risk of total and
haemorrhagic stroke.
In terms of mechanisms whereby carbohydrate may impact on cardiovascular
disease, its role in raising post-prandial plasma glucose concentrations has been
10
implicated. Evidence has emerged suggesting two-hour post-challenge glycaemia
may be a more significant indicator of risk than either fasting blood glucose or
average hyperglycaemia, assessed by HbA1c (Balkau et al, 1998; deVegt et al,
1999; Coutinho et al, 1999; DECODE, 2001). Some epidemiological studies also
suggest there may be a relationship between plasma glucose levels and risk for
CHD (Stratton et al, 2000).
However, intervention studies have not demonstrated a convincing beneficial effect
of lowering blood glucose on cardiovascular outcomes (DCCT, 1993; UKPDS,
1998). Therefore, whether any measure of glycaemia is an independent risk factor
for cardiovascular disease remains unclear and possible benefits of reducing
dietary glycaemic load may be partly related to effects other than glycaemia.
Dietary fibre
There is moderate evidence that dietary patterns high in dietary
fibre from cereals and fruit are associated with a lower risk of
coronary heart disease, and that wholegrains, independently of
dietary fibre, also appear protective.
With respect to dietary fibre, a recent meta-analysis of dietary fibre and its subtypes
and risk of coronary heart disease was conducted using data from 10 prospective
cohort studies (Pereira et al, 2004). Over 6−10 years of follow-up and after
adjustment for potential confounders, each 10 g/day increment of total dietary fibre
was associated with a 14% lower risk for all coronary events and 27% lower risk of
coronary death. For all coronary events, cereal, fruit, and vegetable fibre intake
corresponding to 10 g/day were associated with 10%, 16% and 0% lower risk,
respectfully.
Of the individual prospective studies in the Pereira et al (2004) analysis, three
studies found cereal fibre to be more protective than fibre from fruits or vegetables
(Rimm et al, 1996; Pietinen et al, 1996; Wolk et al, 1999). Water-soluble fibre or
viscous fibre was more protective in two studies (Bazzano et al, 2003; Wu et al,
2003).
Studies further show an inverse association between wholegrains (defined as a
product that contained 25% wholegrain or bran by weight) and CVD–coronary
mortality (Jacobs et al, 1998), total CVD and all-cause mortality (Jacobs et al,1999;
Jacobs et al, 2000), and CHD (Liu et al, 1999). The mechanism is not known and
beneficial effects may be partially attributed to actions of dietary fibre on lipids or
other components associated with lower coronary risk.
How much wholegrain is recommended?
Significant associations between increasing consumption levels of wholegrain
cereals and a lower risk of CVD have been indicated by several studies including
Jensen et al (2004) who showed an 18% reduction in Hazard Ratio (HR) of CHD
between lowest median intake quintile (3.5 g/day) and highest median intake
quintile (42.4 g/day) of wholegrain consumption (95% CI, 0.70–0.96; P for trend
=0.01). Similarly, Mozaffarian et al, (2003) in their study found that after adjustment
11
for potential confounders, the consumption of cereal fibre intake resulted in an
overall reduction in CVD risk of 14% (HR 0.86, 95% CI, 0.075-0.99) when the 20th
percentile of cereal fibre intake of <1.7 g/day was compared to the highest quintile
of >6.3 g/day. The study found that most of this cereal fibre was predominantly
wholegrain intake with a reduced risk of 23% (HR 0.76; 95% CI, 0.64–0.90).
Other researchers have found positive associations between wholegrain cereals
and CVD, however limitations with assessing dietary fibre intake have been
suggested for their non-significance. Bazzano et al (2003) examining the National
Health and Nutrition Examination Survey (NHANES) data found a non-significant
20% reduction in CHD risk per 4.5 g cereal fibre per 1735 kcal/d (~7300 kJ/d) (RR
0.80, 95% CI, 0.63–1.01; P= .06 for trend). Similarly, Jacobs et al, (2000) showed
that women who consumed on average 1.9 g refined grain fibre/2000 kcal (~8200
kJ) and 4.7 g wholegrain fibre/2000 kcal (~8200 kJ) had a 17% lower all-cause
mortality rate (95% C,I 0.73–0.94) and a non-significant 11% lower CHD rate (95%
CI, 0.66–1.20) than women who consumed predominantly refined grain fibre (4.5
g/2000 kcal (~8200 kJ) but only 1.3 g wholegrain fibre/2000 kcal (~8200 kJ).
These studies suggest that a wholegrain fibre intake of at least 6 g/day may
contribute significantly to a lowering of CVD risk. In food items this
recommendation is equivalent to an intake of at least 100 grams of wholegrain
bread or its equivalent.
Dietary carbohydrate and cardiovascular risk factors - Triglycerides
There is good evidence suggesting that dietary patterns high in
glycaemic load raise serum triglyceride levels, particularly in
those with elevated triglycerides and a high BMI.
Epidemiological studies in women (Liu et al, 2001; Liu et al, 2003) suggest that total
carbohydrate as well as glycaemic index (GI) contribute independently to an
increase in fasting triglyceride (TG) concentrations as well as lowering HDLcholesterol. This seems more pronounced in those with higher BMI (Liu et al, 2001;
Liu et al, 2003).
In clinical studies, carbohydrates increase TG when they replace dietary fat or
protein (Parks & Hellerstein, 2000). The effects of these changes on cardiovascular
risk have been open to conjecture. Although the fasting serum TG response to high
carbohydrate diets is highly variable, larger increases in serum TG are generally
observed with greater increases in dietary carbohydrate (Retzlaff et al, 1995).
Furthermore, the larger the increase in dietary carbohydrate, the greater the
proportion of subjects experiencing elevated serum triglycerides (Frayn & Kingman,
1995).
Short term studies (Frayn & Kingman, 1995; Vidon et al, 2001; Bantle et al, 2000;
Hudgins et al, 1998; Marckmann et al, 2000; Raben et al, 2001) suggest the
amount carbohydrates increase serum triglycerides is in the order of fructose >
sucrose > starch. However, these studies have frequently used crystalline fructose
or glucose in large amounts (>15% energy) so that extrapolation to diets high in
sucrose from whole foods is problematic.
12
There is some conjecture as to whether the effects of carbohydrate on TG are
temporary. Some studies indicate increased serum TG in the short term (less than
six weeks) (Hudgins et al, 1998; Marckmann et al, 2000; Raben et al, 2001) or for a
14-week study of subjects with type 2 diabetes (Garg et al, 1994). Others found
that TG levels return to starting levels after initially increasing (Antonis & Bersohn,
1961). However, longer term studies (12 months) that have examined high
carbohydrate diets compared to very low carbohydrate diets have found that lower
carbohydrate eating patterns resulted in lower TG concentrations independently of
weight loss, suggesting that the effect is not transient (Foster et al. 2003).
Furthermore, a similar study by Samaha et al, (2003) in obese subjects with
diabetes or metabolic syndrome also suggests greater reductions in TG on a lower
carbohydrate diet after one year.
Other studies (Garg et al, 1988; Coulston et al, 1989; Garg et al, 1994) showing an
increase in TG and a fall in HDL-cholesterol concentration in type 2 subjects,
suggest high carbohydrate diets (>55%E) may exacerbate both components of the
dyslipidaemia associated with the metabolic syndrome. Although the evidence that
dietary modifications of serum TG and HDL-cholesterol impact on coronary risk is
weak, nevertheless it does suggest some caution should be exercised in relation to
high carbohydrate diets for people with elevated triglycerides unless energy
restriction is included as part of the dietary strategy. Although weight reduction will
ameliorate all the features of insulin resistance and metabolic syndrome, weight
loss dietary patterns lower in carbohydrate have shown greater improvements than
low fat, high carbohydrate weight loss patterns (Farnsworth et al, 2003; McAuley et
al, 2005).
A Cochrane review of fifteen randomised, controlled trials found no difference in
effect on serum triglyceride concentrations between low and high glycaemic index
(GI) diets (Kelly et al, 2004). Diets high in GL have resulted in serum TG
concentrations being 76% higher when the highest quintile of GL was compared to
the lowest (Liu et al,. 2001). In a multivariate analysis, GL predicted TG
concentrations independent of carbohydrate intake. The relation between GL and
fasting TG concentrations differed significantly by BMI. The dose-response
gradient was stronger in women with BMI >25 kg/m 2 (Liu et al, 2001).
Sloth et al (2004) investigated the effects of an ad libitum low fat, high carbohydrate
diet including high or low GI foods for 10 weeks in a parallel randomized,
intervention trial. Reductions in energy intake, body weight, and fat mass over time
were not significantly different nor were fasting serum insulin, TG or HDLcholesterol. However, a 10% decrease in LDL-cholesterol was observed with
consumption of the low GI diet as compared with the high GI diet. This study does
not support the contention that low fat low GI diets are more beneficial than high GI
diets with regard to appetite or bodyweight regulation. However, it confirms
previous findings of a beneficial effect of low GI diets on risk factors for ischaemic
heart disease.
13
Dietary carbohydrate and cardiovascular risk factors - Total and LDLcholesterol
There is good evidence that soluble fibre lowers plasma
LDL-cholesterol.
In controlled clinical studies, there has been no effect of total carbohydrate on
LDL- cholesterol directly, whereas there is good evidence that the replacement of
dietary saturated fatty acids with carbohydrate results in a fall in serum
LDL-cholesterol (Mensink et al, 2003; Clarke et al, 1997). Thus, carbohydrate has
been suggested as a replacement for saturated fatty acids as a means of lowering
coronary risk but it is not the optimal replacement for saturated fatty acids as the
replacement with unsaturated fatty acids has a more favourable effect on CVD
outcomes and lipid protein profile (NHFA, 1999). Furthermore, high carbohydrate
low fat diets even in healthy normolipidaemic men, induce changes in LDL particle
size which suggests that isoenergetic substitution of carbohydrates are indicative of
increased risk of coronary artery disease (Dreon et al, 1999).
Soluble fibres such as oats, psyllium, pectin and guar gum have been shown to
lower total and LDL-cholesterol (Truswell, 1995). A meta-analysis of 67 controlled
trials indicated that soluble fibre intake of 3 g/day was associated with small but
significant decreases in total and LDL-cholesterol and that the effects of soluble
fibre from oats, psyllium or pectin were not significantly different (Brown et al,
1999). Greater reductions in serum cholesterol concentrations have been observed
with higher intakes of fibre (Anderson et al, 2000). Serum TG and HDL-cholesterol
concentrations are not significantly influenced by soluble fibre. Water-insoluble
wheat fibre and cellulose have no independent effect on serum lipids (Truswell,
1995).
Dietary carbohydrate and cardiovascular risk factors - Insulin resistance :
metabolic syndrome and type 2 diabetes
There is no evidence that total carbohydrate intake,
independently from BMI, affects insulin sensitivity or the risk of
developing type 2 diabetes.
There is moderate evidence that eating patterns low in refined
carbohydrate, lower in sucrose, or high in cereal fibre are
associated with a lower risk of type 2 diabetes and have
beneficial effects on post-prandial glucose profiles.
Insulin resistance has been implicated as an important initiating factor in coronary
atherosclerosis and is independently associated with specific morphologic features
of atherosclerotic coronary arteries (Yoshitama et al, 2004). It results in a failure of
cellular receptors for insulin to respond correctly to insulin and the pancreas
responding by producing more insulin in an effort to keep blood glucose controlled.
Insulin resistance is thought to be central in the aetiology and clinical course of
hypertension, obesity, ischaemic heart disease, dyslipidaemia and type 2 diabetes
(Reaven, 1988).
14
Insulin resistance is often associated with the presence of a cluster of risk factors in
susceptible individuals. This has been termed the ‘metabolic syndrome’ and is
associated with substantially increased risks of CVD and type 2 diabetes (McNeill
et al, 2005).
According to the International Diabetes Federation’s (IDF, 2005) clinical practice
definition, for a person to be defined as having the metabolic syndrome, he/she
must have:
Central obesity (defined as waist circumference = 94cm for Europid men and
= 80cm for Europid women, with ethnicity specific values for other groups) plus
any two of the following four factors:
•
•
•
•
raised TG level: > 1.7 mmol/L, or specific treatment for this lipid
abnormality
reduced HDL cholesterol: < 0.9 mmol/L in males and < 1.1 mmol/L in
females, or specific treatment for this lipid abnormality
raised blood pressure: systolic BP = 130 or diastolic BP = 85 mm Hg, or
treatment of previously diagnosed hypertension
raised fasting plasma glucose (FPG) = 5.6 mmol/L, or previously
diagnosed type 2 diabetes
If above 5.6 mmol/L, an oral glucose tolerance test (OGTT) is strongly
recommended but is not necessary to define presence of the syndrome.
As the metabolic syndrome is characterized by a dyslipidaemia featuring elevated
serum triglycerides and low HDL-cholesterol, the optimal approach to dietary
management has focused on the quantity and quality of carbohydrate.
Epidemiological Evidence
There is no epidemiological evidence that total carbohydrate intake is associated
with the risk of type 2 diabetes if data is adjusted for BMI (Salmeron, 1997a;
Salmeron, 1997b). Similarly there has been no direct relationship between sucrose
or starch and CVD (Liu et al, 2000a) or between sucrose intake and CHD risk (Liu
et al, 1982; McGee et al, 1984; Kushi et al, 1985; Bolton-Smith & Woodward, 1994)
when BMI and other CVD risk factors are controlled.
However, higher consumption of sugar-sweetened beverages is associated with a
greater magnitude of weight gain and an increased risk for development of
type 2 diabetes in women, possibly by providing excessive energy (kilojoules) and
a large amount of rapidly absorbable sugars (Schulze et al, 2004). A diet high in
rapidly absorbed carbohydrates and low in cereal fibre is associated with an
increased risk of type 2 diabetes (Schulze et al, 2004). Diets with a high GL and
low cereal fibre content are also associated with increased risk of type 2 diabetes
in men (Fung et al, 2002).
Carbohydrates in the form of sugars and rapidly digested starch raise serum
concentrations of TGs when they replace other macronutrients in the diet. Fructose
has the strongest effect, followed by sucrose, then starch. Very high intakes of
sucrose (>35%E) and fructose (>18%E) are associated with elevated TGs.
The effects of more moderate intakes are unclear. However, as sucrose is
50% fructose, caution should be advised around eating patterns high in fructose
and sucrose.
15
Previous studies have found cereal fibre, but not total dietary fibre, to be inversely
associated with diabetes risk (Salmeron et al, 1997a; Stevens et al, 2002), while no
association between total dietary fibre intake and diabetes risk was found in the
Finnish and Dutch cohorts of the Seven Countries Study (Feskens et al, 1995).
An inverse association between wholegrain consumption and the risk of
type 2 diabetes has been shown to be consistent across a number of studies
(Liu et al, 2000b; Fung et al, 2002; Meyer et al, 2000; Montonen et al, 2003)
Several biological mechanisms that might explain a protective effect of wholegrains
or dietary fibre against diabetes have been suggested. One hypothesis suggests
that higher post-prandial levels of serum glucose may lead to ‘exhaustion’ of
pancreatic beta cells and the lower glycaemic response of wholegrain or fibre-rich
foods relative to refined cereal foods would therefore be expected to be protective
(Chandalia et al, 2000; Jang et al, 2001). Although it is thought that the plasma
glucose-lowering effects of fibre is primarily due to soluble fibre, findings from four
prospective cohort studies support a stronger association of insoluble fibre than of
soluble fibre with diabetes risk (Salmeron et al, 1997a; Salmeron et al, 1997b;
Meyer et al, 2000; Stevens et al, 2002), which suggests other mechanisms may be
more relevant.
There is suggestive evidence that dietary fibre or wholegrains may influence the
risk of type 2 diabetes through an effect on insulin sensitivity (Manolio et al, 1991;
Lovejoy & DiGiroloama, 1992; Feskens et al, 1994; Vitelli et al, 1996; Marshall et al,
1997; Pereira et al, 1998; Ludwig et al, 1999). However, this has not been
confirmed in clinical studies. In addition, dietary magnesium, as a component of
grains and the fibrous component of cereal plants, has been found to have an
inverse relationship with the incidence of diabetes (Meyer et al, 2000; Salmeron
et al, 1997a; Salmeron et al, 1997b; Lopez-Ridaura et al, 2004; Song et al, 2004).
Circulating C-peptide concentrations which are associated with insulin resistance
and the development of type 2 diabetes are associated with intakes of fructose and
high glycaemic foods whereas consumption of carbohydrates high in fibre, such as
wholegrain foods, is associated with lower C-peptide concentrations
(Wu et al, 2004).
Clinical evidence
It has been concluded that, in the absence of overweight, there appears to be no
adverse effects of high carbohydrate diets on insulin sensitivity (Daly et al, 1997).
However in relation to post-prandial glycaemic response, Gannon et al (1998) found
that the integrated 24-h plasma glucose and insulin area response was statistically
significantly smaller after ingestion of low starch low carbohydrate meals
(40% energy) compared with a high starch, high carbohydrate (55% energy) meals.
However if, weight loss is achieved on a high carbohydrate diet, glycaemic control
is improved (Gerhard et al, 2004).
16
Dietary carbohydrate and cardiovascular risk factors - Obesity
There is moderate evidence that high carbohydrate eating
patterns, high in sucrose or fructose, may increase the risk of
excessive energy intake. This may impact on the development
of overweight and obesity, and indirectly on the risk of
type 2 diabetes and cardiovascular disease.
Diets high in refined carbohydrate intake have been linked to obesity (Gross et al,
2004). Weight gain is inversely associated with the intake of high fibre, wholegrain
foods but positively related to the intake of refined grain foods in men and women
(Liu et al, 2003; Koh-Banerjee & Rimm, 2003).
In addition to the epidemiological evidence that high sucrose intake is associated
with higher body weight (Schulze et al, 2004), studies have attributed the greater
palatability of sucrose relative to starch as the mechanism for increased
consumption of energy from sucrose-rich diets (Raben et al, 1997). Excessive
consumption of sugar (sucrose and fructose) sweetened drinks has also been
associated with a higher daily energy intake and greater weight gain in children and
adults (Ludwig et al, 2001; Mrdjenovic & Levitsky, 2003; Bray et al, 2004).
In Australia, since the early 1980’s, the increase in obesity has been associated
with increasing dietary intakes of sugars, starch, total carbohydrate and total energy
(Australian Food & Nutrition Monitoring Unit, 2001), and overfeeding with various
carbohydrates as sugars or starch as well as fat has been shown to lead to an
increase in body weight (McDevitt et al, 2000).
Conclusions
Despite the current lack of evidence implicating total carbohydrate intake and CVD,
the source or type of the carbohydrate consumed does impact on the risk of
developing CHD and risk factors for CVD.
The evidence reviewed suggests that the consumption of eating patterns high in
rapidly absorbed carbohydrate and high in GL are associated with an increased risk
of CHD and CVD risk factors including obesity, elevated LDL-cholesterol and
TG levels, and type 2 diabetes. The consumption of different types of dietary fibre
has benefits for lowering the risk for CVD. There is evidence that consuming
wholegrain cereals lowers the risk of CVD and that the consumption of soluble fibre
is associated with lower plasma LDL cholesterol levels.
Implications
The protective nature of wholegrains, apart from the fibre content itself, indicates
that dietary recommendations around carbohydrate foods should particularly
emphasise the consumption of wholegrain cereals products as well as fibre from
fruit and vegetables. Overall dietary recommendations should limit the
consumption of highly refined carbohydrate foods and recommend eating patterns
with a low GL.
17
It is estimated that an intake of at least 6 g/day fibre from wholegrains may
contribute significantly to a lowering of CVD risk. This is equivalent to a daily intake
of at least 100 grams of wholegrain bread or its equivalent.
Further research
Further detailed studies are needed to clarify the mechanisms by which
wholegrains exert protective effects on CVD risk. Similarly, the influence of
carbohydrate type and amount on novel and emerging markers of cardiovascular
risk as well as harder endpoints are required in groups who have the metabolic
syndrome phenotype.
18
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