Sugar, Diabetes and Insulin Resistance
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WSRO POSITION STATEMENT
Sugar, Diabetes and Insulin Resistance
Updated December 2013
Background
Diabetes mellitus (DM), more commonly referred to as diabetes, is a metabolic
disorder characterized by raised blood glucose levels. Diabetes occurs when the
pancreas fails to produce enough of the hormone insulin, or the body fails to respond
adequately to the amount of insulin released. Insulin is a hormone produced by the
pancreas, mainly in response to raised blood glucose from ingestion and absorption
of dietary carbohydrates, but also to ingestion and absorption of other nutrients such
as amino acids from dietary protein. Insulin increases glucose uptake into skeletal
muscle and adipose tissue, increases glycogen formation, fat storage and amino
acid uptake into cells, and decreases glucose release from the liver. Diabetes often
follows a period of insulin resistance, in which the body fails to respond adequately
to normal levels of insulin, resulting in excessively high insulin release for a given
increase in blood glucose, and ultimately failure in blood glucose control (Tabak et
al. 2009). Insulin resistance is one of the characteristics of the metabolic syndrome
which, together with diabetes, carries increased risk of cardiovascular disease
(CVD).
There are 2 main types of diabetes, Types 1 and 2. Type 1 DM typically occurs in
young people, and in this case the insulin producing cells of the pancreas have been
destroyed by the body’s own immune system. It is treated with regular injections of
insulin and an appropriate diet. No nutrition recommendations can be made for
preventing Type 1 DM (Bantle et al. 2008) but careful control of the diet is essential
to the management of the condition (Evert et al. 2013) . Type 2 DM typically occurs
in older adults (less often in younger people) and is characteristically observed in
sedentary and overweight people. However, it should be noted that not all people
with Type 2 diabetes are overweight (unexplained rapid weight loss is a symptom of
untreated Type 2 diabetes). This type of DM is treated by diet, a combination of diet
and blood glucose lowering medication or insulin injections, together with increased
physical activity levels.
The risk of insulin resistance and Type 2 DM is associated with obesity, particularly
central obesity (where fat is deposited at subcutaneous and intra-abdominal sites),
and physical inactivity. Since DM is associated with obesity, and people with
diabetes need to control blood sugar (plasma glucose) levels, it is often assumed
that dietary sugar intake is important in either the prevention or management of the
condition.
Sugar and risk of Type 2 Diabetes
A number of expert reports have considered the possible role of sugar in the
causation of diabetes. The notion that sugar directly causes diabetes dismissed in
the 1980’s in the Report of the Food and Drug Administration’s Sugars Task Force
(Glinsmann, Irausquin & Park 1986) and by the UK Government’s COMA Committee
1(1989). In addition, there is no evidence that sugar uniquely contributes to obesity
(see Position Statement on ‘Sugar and Obesity’), nor indirectly causes diabetes.
The European Food Safety Authority (EFSA) has indicated that “the available
evidence is insufficient to set an upper limit for sugars based on their effects on type
2 diabetes risk” (EFSA 2010). Neither of the recent expert reports published by the
WHO or FAO have implicated sugars as being directly involved in the aetiology of
Type 2 DM (FAO/WHO 1997, WHO/FAO 2003). The current evidence-based
recommendations for prevention of Type 2 DM in high-risk groups from Diabetes
UK and the American Diabetes Association comprise lifestyle interventions of energy
restriction, a low fat diet and increased physical activity (Bantle et al. 2008, Dyson et
al. 2011).
Studies in animals have suggested that very high doses of sugar, often within a
hypercaloric diet, predispose to insulin resistance (Storlien et al. 2000). However,
intervention studies in humans employing more reasonable doses of sugar for
relatively short durations (up to 6 weeks) within isocaloric diets have shown more
variable results. These studies have either reported no effect upon (Black et al.
2006, Dunnigan et al. 1970, Lewis et al. 2013), or improved indices of insulin
resistance (Anderson, Herman & Zakim 1973, Brynes et al. 2003, Mann, Truswell
1972, Raben et al. 2001). Only one study has reported adverse effects from very
high doses of sugar, suggesting reduced insulin sensitivity, in subjects who were
hypertriglyceridaemic and possibly “carbohydrate sensitive” at the start of the study
(Reiser et al. 1979).
The results of intervention studies are normally considered the most reliable form of
evidence on diet and health risk. However, most of the intervention studies
undertaken to date in humans examining the effect of sugar on indices of insulin
resistance have been for relatively short durations (up to 6 weeks). In contrast, the
6-month CARMEN trial, examining the effect of low-fat diets high in simple sugars or
complex carbohydrates, revealed no differential effects on fasting blood glucose or
insulin (Saris et al. 2000). Prospective cohort studies may be regarded as reflecting
the effects of long-term dietary habits on health. However, the numerous limitations
of prospective cohort studies, including inadequate dietary recording and adjustment
for confounders, render their results unreliable and their intrinsic design can only
demonstrate associations and does not allow inference of causation. Nevertheless,
results of prospective cohort studies are frequently referred to in reviews and by
organisations issuing dietary guidelines. A number of prospective cohort studies
have not associated sucrose intake (apart from a slight negative association in one
study) with incidence of Type 2 DM (Meyer et al. 2000, Janket et al. 2003, Montonen
et al. 2007, Sluijs et al. 2013, Ahmadi-Abhari et al. 2013, Colditz et al. 1992).
Similarly, total sugars intake has either been inversely associated (Hodge et al.
2004), or not associated (Ahmadi-Abhari et al. 2013), with risk of Type 2 DM.
However, until supported by more direct, and more reliable, evidence these
prospective studies are unsuitable as a basis for advice on public health.
Sugar and management of persons with Diabetes
For people with Type 1 DM, the focus of management is the control of blood glucose
levels by balancing carbohydrate intake with insulin treatment (Dyson et al. 2011).
2The main purpose of management of Type 2 DM is to improve glycaemic control,
and reduce risk of diabetic complications and CVD. For overweight or obese
persons with Type 2 DM, the main nutrition strategy is weight management, with the
focus on total energy intake, together with regular physical activity. In addition, a low
glycaemic diet (GI) may be beneficial (Dyson et al. 2011, Evert et al. 2013). It should
be noted that, contrary to popular belief, sucrose is only of moderate GI.
Recommendations from recognised organisations for the dietary management of
people with Type 2 DM are inconsistent:
Older recommendations, from the European Association for the Study of
Diabetes, advised moderating the intake of free sugars for people with
diabetes (where free sugars were defined as all added mono- and
disaccharides, plus sugars naturally present in honey, syrups and fruit juices)
(Mann et al. 2004).
With respect to more recent recommendations
o Diabetes UK, focus on total carbohydrate and energy intake, and
weight control in those who are overweight (Dyson et al. 2011). The
UK recommendations did not consider it appropriate to make specific
recommendations for single nutrients, including added sugars;
o The American Diabetes Association (ADA) suggests minimizing
substitution of sucrose-containing foods for isocaloric amounts of other
carbohydrates (Evert et al. 2013). In making this recommendation, the
ADA acknowledged that dietary sucrose, in comparison to other
carbohydrates, does not appear to exert any deleterious effects on
indices of glycemic control. Instead, this recommendation was based
on advice for the general US population (USDA/HHS 2010) which
recommends people to ‘reduce’ or ‘limit’ intake of added sugars.
Sugar in Drinks*
High consumption of sugar-sweetened beverages (SSBs) has been suggested to
contribute to the increased risk of DM. A number of prospective cohort studies
employing food frequency questionnaires have examined the association between
SSB consumption and risk of subsequent DM. These were reviewed in a recent
meta-analysis by Malik et al., (2010). The review reported a 26% greater risk (4 of
the 8 studies were significant) of developing Type 2 DM in the highest compared to
lowest quartile of SSB intake. However, only 3 studies corrected for weight or
adiposity measures, 1 did not adjust for physical activity, and only 3 adjusted for
energy intake – all of which could be major determinants of DM risk. High SSB
consumption may be associated with other behaviours that alter the risk of diabetes.
(Pearson, Biddle 2011, Cohen, Curhan & Forman 2012, Munoz-Pareja et al. 2013).
Inadequate adjustment for these other confounding factors complicates interpretation
of the evidence. Risk of DM has also been reported to be higher for consumption of
diet sodas (Nettleton et al. 2009) (although this may reflect intention to lose weight)
and has even been shown for consumption of water (de Koning et al. 2011).
The question of SSB consumption and obesity has been reviewed within the WSRO
Position Statement on ‘Sugar and Obesity’ with no convincing evidence to support
the widely held view that sugar, including sugar in drinks, is particularly responsible
for obesity.
3The recent guidelines from the American Diabetes Association for people with
diabetes propose limiting or avoiding intake of SSBs to reduce risk of weight gain
and worsening of cardiometabolic risk factors (Evert et al. 2013). This
recommendation was based on the aforementioned review by Malik et al., (2010)
and on a single intervention study where subjects were asked to consume excessive
amounts of SSBs (providing 25% total energy intake) for 10 weeks (Stanhope et al.
2009). However, other intervention studies, which did not observe negative effects,
did not appear to be considered in making the recommendations. A 6-month
intervention in overweight subjects, which provided an additional litre of SSB daily
(>400 kcal/d), did not find effects on insulin sensitivity when compared with equal
volumes of milk, diet cola or water (Maersk et al. 2012); and two 3-week intervention
studies in normal-weight males, each providing >300 kcal/d of SSBs, did not observe
negative effects on insulin sensitivity with drinks containing sucrose (Aeberli et al.
2011, 2013).
CONCLUSIONS
Over-consumption of food energy, whatever its macronutrient composition, and
inadequate physical activity may lead to body weight gain and increase risk of Type
2 DM. There is no convincing evidence that sugar is responsible for increasing risk
of diabetes directly or indirectly via obesity.
STATEMENT
WSRO considers that the available evidence does not support that specific
recommendations need to be made for sugar intake in relation to either the
risk or management of diabetes. Sugar is a type of carbohydrate and moderate
intake of sugar can be included as part of the overall carbohydrate content in
the context of a healthy balanced diet. Any form of excessive energy intake or
inadequate physical activity may encourage weight gain and increase the risk
of Type 2 DM.
* “Sugar-sweetened beverages” may contain a variety of sugars, including sucrose,
glucose and fructose. In North America the majority of these beverages currently
contain high-fructose corn syrup (HFCS), which is a mixture of glucose and fructose,
and not sucrose. Furthermore, ‘sports’ or ‘energy’ drinks, which may be included in a
study on ‘sugar sweetened beverages’, contain a variety of other carbohydrates as a
source of energy and/or sweetness. Thus, the composition of these beverages may
differ between studies, making it difficult to make comparisons and draw firm
conclusions.
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