As the focus of public health nutrition switches from fats to carbohydrates there is uncertainty about how carbohydrates actually affect the risk for chronic diseases, such as type 2 diabetes and coronary heart disease. Early dietary advice on fats was based on effects on blood cholesterol but what mechanisms are driving the risk associated with carbohydrate?
Glycaemic response or fructose?
One view is that the key driver of carbohydrate-related risk is glycaemic response i.e. the degree to which carbohydrates raise blood glucose and insulin levels. If glycaemic response is the critical factor then the dietary measure of interest would be glycaemic load, which takes into consideration both the amount of carbohydrate consumed and its potential to raise blood glucose.
An alternative view is that fructose drives the chronic disease risk associated with dietary carbohydrate. If so, we should expect fructose or perhaps sucrose (the major dietary source of fructose) to be associated with risk for chronic disease in large population studies. And, importantly, glycaemic load would not be linked with risk.
Let’s look at the epidemiology and see if it supports one argument or the other.
Glycaemic load and coronary heart disease risk
Four meta-analyses of prospective cohort studies of glycaemic load and risk for coronary heart disease have been published in the last couple of years (Dong 2012, Fan 2012, Ma 2012, Mirrahimi 2012). The findings are essentially the same – glycaemic load is associated with heart disease in women but not men. In two of the meta-analyses the links between glycaemic load and heart disease were stronger in overweight subjects. Fan (2012) also found an association with stroke incidence, as did Sieri (2013) in a recent cohort study. In all four meta-analyses the relative risks for heart disease in men were positive – they just failed to reach statistical significance, perhaps due to smaller numbers.
A study in a Chinese cohort published last year found glycaemic load was associated with coronary heart disease risk in both genders (Yu 2013). Compared to studies in western populations carbohydrate intake was high (68% of calories) but sugar intake was relatively low. Most of the carbohydrate was starch, 87% of which came from white rice and refined wheat products.
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Fructose or sucrose and coronary heart disease risk
There are virtually no prospective cohort studies that find a significant association between fructose intake and risk for coronary disease. The few studies that have looked at total sugars and heart disease risk generally find no association (Beulens 2007, Sieri 2013). A recent exception found an association between ‘added sugars’ and cardiovascular disease in a study in the United States (Yang 2014).
There are few data about the consumption of sugar-sweetened beverages and risk for coronary heart disease. And the findings are mixed – Fung (2009) found a positive association but this was not confirmed by Eshak (2012). Eshak (2012) and Larsson (2014) found links with stroke, albeit inconsistent between genders.
Glycaemic load and risk for type 2 diabetes
In the last three years at least four meta-analyses of cohort studies have considered whether glycaemic load affects the risk for type 2 diabetes, the latest published this year by the Harvard team (Bhupathiraju 2014). All four meta-analyses found that high glycaemic load increases risk for type 2 diabetes.
A recent meta-analysis found that consumption of white rice, a high GI food, was associated with increased risk for type 2 diabetes in Asian populations where it is by far the major contributor to glycaemic load (Hu 2012). The association was also positive in western populations but failed to reach significance.
Fructose or sucrose and risk for type 2 diabetes
No meta-analysis of studies into whether fructose or sucrose affects risk for type 2 diabetes has been published and there are just a few cohort studies to go on. The findings are mixed. In a small cohort Montonen (2007) found intake of glucose and fructose combined, but not sucrose, was associated with increased risk of type 2 diabetes whereas in the large EPIC cohort sucrose, glucose and fructose were not associated with diabetes risk in men or women.
A couple of months ago a meta-analysis of studies into sugar-sweetened beverages and risk for type 2 diabetes and found a positive association (Greenwood 2014). Interestingly, the same study also found a positive association between non-sugar beverage consumption and diabetes. This raises questions about whether these links are causal or alternatively whether soft drink consumption is a marker for other lifestyle behaviours that are associated with risk.
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Glycaemic load or fructose?
Given the public debate about fructose and sucrose the paucity of data linking these sugars with risk for type 2 diabetes and coronary heart disease risk comes as a surprise. It is clear that glycaemic load is a more consistent predictor of risk for these conditions than fructose or any individual sugar or total sugars or added sugars. This doesn’t let sugars off the hook but rather suggests that the risk for chronic disease posed by sugars should be seen in the context of their contribution to glycaemic load.
The significant contribution of sugar-sweetened beverages to glycaemic load in western diets has an interesting parallel in Asian diets – white rice, a high GI, starch-rich food. Both are also nutrient-poor. Some dietary recommendations in Australia still encourage the replacement of sugars with starch but the rationale for this is lacking if limiting glycaemic load is the most effective means of lowering carbohydrate-related risk.
Poor quality carbohydrate is not a narrow concept. It’s broad and includes some traditional foods currently recommended for healthy eating.
So selling cookbooks where fructose is replaced with glucose/dextrose or Rice Malt Syrup (GI 98 almost same as glucose) isn’t an improvement?
But my guru said??!!
Beware gurus bringing dietary advice down from the mountain top! I’ll take reasoned scientific argument thank you. Regards, Bill
hahaha good one! I was thinking of the same cook book & author… Wider reading for the brainwashed anti-fructose sugar activists is needed, maybe we should post them a link to this blog post lol
Going low carb reversed my metabolic syndrome and stopped me becoming a Type 2 diabetic. My doc put me on a low carb program and now I eat a low carb version of paleo which basically keeps me away from the foods I can’t eat (coeliac) and the foods I have allergies and intolerances to. I am now well and not suffering from any sort of grain deficiency (lol), although I ocassionally have a little bit of white rice just to be social!
Great work for changing your diet and improving your health status. There is nothing better than being healthy!
Cutting all the [rubbish] out of your diet certainly improves the quality of the diet. However people forget that they get carbohydrate from a wide variety of foods not those we traditionally associated with carbohydrate.
Depending on your interpretation of the Paleo diet, which is so diverse these days on what is excluded or included and generally not that strict as in the traditional times but ” Eating Real Food’, carbohydrate can come from other cereal grains slightly less processed like quinoa, amaranth etc , so many vegetables but often more associated to the starchy vegetables like peas, parsnips, corn and pumpkin to mention a few , legumes, and lentils if these are included, milk/yoghurt , nuts, seeds and whole fruit if any of these foods are regularly into the diet. And when this is all added up the carbohydrate content in your diet is not always that low but fits well within the 45-65% of energy eaten, which is recommended for health especially those with T2 diabetes. It’ s just now coming from more whole than processed foods in a diet which I imagine the energy intake has been significantly reduced because of the more bulky foods eaten. And this lower energy and possibly weight loss has the most impact on metabolic syndrome, reducing your processed carbohydrate in your diet helped you achieve this..
I actually think that carbohydrate intakes below the range of 45-65% are quite OK, provided the quality of the carbohydrate-rich foods in the diet is good. In particular, nutrient-rich carbohydrate foods should be emphasised if overall intake of carbohydrate is low, just to ensure that the diet has enough of the micronutrients carried by carbohydrate-rich foods.
I get a bit nervous recommending healthy diets with up to 65% of calories coming from carbohydrate. You can do it but, again, carbohydrate quality needs to be high. And this time the emphasis needs to be on high fibre and low glycaemic index foods, which sits comfortably with the idea of eating whole foods or ‘real’ foods.
Overall, the total amount of carbohydrate in the diet doesn’t matter that much – it’s the quality that counts. Regards, Bill
I’ve tracked mine and I do fine hovering around 20%!
It all depends on what is replacing the carbohydrate when it is this restricted (<45%), often this is fat.
So for long term health benefits,the fat needs to be less saturated more poly/mono, and omega 3. We know in the short term carbohydrate restricted diets <45% may improve glycemic control but not blood lipids, so what happens in the long term is an area of interest. Also it is more challenging to get sufficient vitamins, minerals and fibre especially soluble fibre on such a restricted diet required for other areas of health for example gut health, often seen in those with coeliac disease.
However is it really necessary to restrict this low when good BGL control and better blood lipids can be achieved with carbs up to 60% of energy , as part of mixed meals, of good nutritional value and low GI. There are many fit healthy individuals with diets having carbohydrates that are at this level with and without diabetes who have a healthy body weight, but of course for long term health this needs to be of good nutritional value, lower GI and part of mixed meals, remain active and maintain a healthy body weight. I think the range 45-65% carbs/energy is entirely reasonable to meet many different lifestyle and nutritional needs.An individual approach is required in the end.
Nutritional guidelines are for all groups of people not just the 60% who are inactive and overweight or at risk of being overweight and developing lifestyle diseases which I understand is the main focus of your article.
There is no way I would even consider going that high! Low carb stabilises me and keeps me off the blood sugar rollercoaster!
Great post, Bill. Too often you see people on blogs citing studies in which large amounts of pure fructose are used, and then using the results of those studies to condemn moderate amounts of fructose/glucose combinations. The obsession with sugar is bizarre.
Hi Shane. The anti-fructose thing seems to be based on (1) studies in which vast amounts of fructose have been fed (25% of calories), (2) overfeeding with fructose (where the overfeeding is actually the major problem) and (3) the misconception that all fructose consumed is immediately metabolised to fat in the liver – it isn’t.
I spoke to a fellow recently whose wife had just recommenced eating fruit after nine months on a strict no-sugars diet. Apparently she had started to feel quite unwell.
How do we encourage moderation in a time when dietary extremes are pushed so hard by people who haven’t really got a clue what they are talking about? Regards, Bill
Bill, I’m curious. Where is Fructose metabolised if not in the liver? Any information I’ve found on the topic states that fructose is almost totally metabolised by the liver.
Hi Denis
Fructose is metabolised in the liver. The key question is: what is fructose metabolised to?
In pop nutrition circles we often here that ‘fructose turns to fat’ i.e. that fructose is converted to free fatty acids in the liver, contributing to fatty liver and high blood triglycerides. This can happen but it doesn’t happen very much – it appears that only 1-5% of dietary fructose has this fate. Most of the fructose we eat is converted to something else.
About 25% of fructose is converted to lactate, but by far the majority of fructose (about two-thirds) is converted to glucose. Most of this appears in the bloodstream in the six hours following consumption of fructose; some is stored as glycogen.
So the mantra should be ‘fructose turns to glucose’, not fat.
If you would like to read about this from a world expert I would recommend you look at the work of Professor Luc Tappy (http://physrev.physiology.org/content/90/1/23.long).
Regards, Bill
Thanks for the insight Bill. I too now wonder if soft drink consumption could be a marker of other behaviours related to diabetes risk, or if there is potentially a causal link with non-sugar sweetened beverages.
Hi Sean. Findings that both sugar-sweetened soft drinks and non-sugar soft drinks are associated with risk crop up several times in the literature.
Did you see this study in the three Harvard cohorts in relation to soft drinks and hypertension? http://www.ncbi.nlm.nih.gov/pubmed/22539069
As both types of drinks are associated with hypertension it’s had to argue that fructose or sugar is driving the problem. And it seems unlikely that some other aspect of these drinks is the cause, though it’s not impossible. Alternatively, it may just be due to confounding. We do need to be mindful of the shortcomings of observational studies. Regards, Bill