GI News—September 2013

• Why cheese doesn't have a GI value; 
• Nicole Senior checks out almonds - that great all rounder;  
• Make the most of almonds with recipes from Michael Moore and Anneka Manning;  
• Obesity and diabetes: the gene factor; 
• Obesity and diabetes on the up, downunder;  
• New GI values for Yoplait Petit Miam.  

GI News 
Editor: Philippa Sandall
Web management and design: Alan Barclay, PhD
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Food for Thought

Should you be eating that, it’s full of sugar? 
Last month one of our readers (a self confessed, long-time follower of the Montignac diet) was outraged that we had published a recipe that included sugar (by which she specifically means sucrose). Montignac does use sugar in his recipes – his sugar of choice is fructose (GI 19), not one with a lot of fans these days.

First of all, we like to provide readers with a range of recipes in each issue of GI News to appeal to a variety of tastes and to suit a variety of occasions. We also give a nutrient analysis with our recipes so people can make an informed choice. And we carefully control for portion size, especially with sweet treats.

Secondly, one of the happy spin-offs of over 30 years of glycemic index research has shown that most sugars in foods produce quite moderate blood glucose responses, lower than most refined starches. Why? Well sugars (including sucrose/table sugar GI 65) are a mixture of molecules, some of which have only a negligible effect on blood glucose levels. In addition, many scientific studies now very clearly show that a moderate amount of added sugar (for example 30–50 grams a day) does not lead to poor blood glucose control nor weight gain in people with diabetes. Keep in mind, however, that this moderate amount includes all sources of added refined sugar consumed that day – the sugar on your breakfast cereal (or already in your cereal), soft drinks, desserts, cookies, cake, snack foods, and the sugar in a cup of tea or coffee.

However, we are very aware that there’s a ‘sugar-free’ boom well underway fuelled by massive misinformation and fad diet solutions. It’s also become a significant profit centre for the food industry now busily adapting foods to make them ‘sugar-free’ or low sugar because it knows (through market research) that many consumers are convinced sugar is THE problem nutrient. Get rid of sugar and all will be well. Apparently. Certainly the technology is there – most sugars can be relatively easily replaced by oligosaccharides and starches – perhaps with a touch of aspartame, sucralose or stevia to boost sweetness. However, it is unlikely the net result will be of any nutritional benefit, as these oligosaccharides and starches are typically as refined and devoid of nutrients (other than calories) than the sugars they replaced – and they have a higher GI. Based on the events of the past few decades, we believe it’s highly likely that these sugar-free foods will continue to contribute to the global obesity and type 2 diabetes epidemic just like their low-fat and low-carb predecessors. History sadly has a tendency of repeating itself.



The real problem is the one-nutrient-at-a-time, fad diet approach. We don’t eat one nutrient at a time – we eat tasty meals that contain a wide variety of foods. This is why most people find it hard to stick to fad ‘quit this food’ diets. It doesn't fit in with their lifestyle – there are too many pressures and opportunities to enjoy a wide variety of flavoursome foods with family and friends. What's the solution?

Nutrients are by definition essential. It’s how we eat them (and how many of them we put on our plates) that ultimately counts. We think it is time to stop the individual nutrient blame game and focus on enjoying an overall low GI healthy eating pattern built around vegetables, fruits, nuts, seeds, legumes, lean meats/fish, minimally refined grains, yoghurt and other fermented dairy products, and oils (olive/peanut). And of course being more active.

And, when you want a little sweetness in your life, opt for nutritious foods that will provide more than calories – porridge with brown sugar, a dollop of jam on grainy toast, muesli with fruit yoghurt, a baked apple with a crumble filling. And enjoy a treat occasionally too, such as a couple of squares of good quality dark chocolate or one (1) of Anneka's gluten-free mandarin and roasted almond cakes.

What’s New?

Obesity and diabetes: The gene factor. 
Using careful definitions and measurements of body fatness, Professor Lesley Campbell and Dr Arthur Jenkins have shown that obesity that runs in families of people with type 2 diabetes is due to a large number of rare variants in many different genes. Their study was published in PLOS ONE.


Professor Lesley Campbell

Over the past 25 years, Campbell’s research has looked at people who are genetically at risk of developing type 2 diabetes and are overweight or obese before they get diabetes. Genes, she stresses, bring out underlying predispositions and there are fairly predictable interactions between genes and environment. She explains: ‘The reason we see so many people getting fat is that they carry strong hunger genes while the environment is maxed; it’s an obesogenic environment that rewards eating. People no longer have to go fishing, or hunting and gathering in order to eat. They just go to McDonald's, or KFC, or the freezer. The point is that people don’t have to expend any energy to get an abundance of food, often high in fat or sugar. We have shown in previous studies that people with diabetes in the family tend to be hungry more often, are able to eat more at a sitting, and will generally opt to eat high calorie foods. This does not mean they are greedy, it just means that their bodies are genetically driven to eat more. The same genes would serve these people well in times of food scarcity or famine. They would survive, while their leaner neighbours would perish.’

Obesity and diabetes: is the association as causal as we think asks Prof Garry Egger? 
‘The statistic that approximately 70–80 per cent of type 2 diabetes patients are overweight or obese led to the conclusion that there is a causal relationship between obesity and diabetes. However, the lock and key conclusions regarding the causality of diabetes are becoming questionable. It seems to be more complex than obesity alone, potentially influenced by a range of lifestyle factors. While the following facts are not conclusions in themselves, they imply that being overweight is not the sole cause of type 2 diabetes.

• Approximately 1 in 3 people with obesity have consistently shown to not have any risk factors for the dysmetabolism needed for diabetes. 
• Approximately 1 in 4 people with a healthy body weight display all the metabolic risks for diabetes, risks that would be typically expected in individuals with obesity. 
• According to the “obesity paradox”, overweight individuals are less susceptible to mortality from type 2 diabetes and other metabolic ailments than lean individuals.
•  A better understanding of adipocyte (‘fat cell’) physiology implies that triglyceride storage in adipocytes is healthy until excessive energy abnormally ‘outpours’ into the liver, muscles and blood. 

Extending upon the final point, in the body, fat storage increases via two processes, the first being hypertrophy, meaning expansion within the adipocyte, and the second being hyperplasia, in which new adipocytes are formed due to established cells being “full”. Undetermined genetic factors seem to reduce adipocyte hypertrophy. Once this hypertrophy has reached its limit, ectopic fat (for instance, as in fatty liver) occurs due to the “outpour”. Ectopic fat is toxic and results in oxidative stress and metaflammation, a low-grade form of systemic inflammation that correlates with a metabolic cascade resulting in insulin resistance.

What does this imply for diabetes management? There is the likelihood that weight loss is less of a priority than improving eating habits, exercising and sleeping more and managing stress. Mounting evidence is finding exercise to be one of the most effective individual changes, with recent research demonstrating that high intensity resistance exercise decrease IR-associated visceral fat.’
– Prof Garry Egger was a keynote speaker at the AustralAsian Academy of Anti-Ageing Medicine Conferenceheld in Melbourne, 24-25 August.  

Dementia risk and BGLs.  
Higher blood glucose levels are associated with higher dementia risk, even among people who do not have diabetes according to a study published in the New England Journal of Medicine. Reporting on more than 2,000 Group Health patients age 65 and older in the Adult Changes in Thought (ACT) study, the researchers found that blood glucose levels averaged over a five-year period were associated with rising risks for developing dementia. ‘The most interesting finding was that every incrementally higher glucose level was associated with a higher risk of dementia in people who did not have diabetes,’ said lead author Dr Paul K. Crane.

Organic labels and ‘health halo’ bias.   
A study by Cornell University's Food and Brand Lab researchers shows that an organic label can influence perceptions of taste, calories and value. The researchers recruited 115 people to take part in the study. Participants were asked to rate the taste and caloric content of 2 yoghurts, 2 cookies and 2 potato chip portions and say how much they would be willing to pay for them. One item from each food pair was labelled ‘organic’, while the other was labelled ‘regular’. In fact all were organic and the products were identical. What were the findings? The participants estimated the cookies and yoghurt had significantly fewer calories when labelled ‘organic’ and were willing to pay up to 23.4% more for them. They also reported that the ‘organic’ yogurt tasted ‘lower in fat’ and the ‘organic’ cookies and chips were more nutritious. In addition, ‘organic’, chips were perceived as being more appetizing and organic yogurt more flavourful. ‘Regular’ cookies however were reported to taste better than ‘organic’ – is this because people often believe healthy foods are not tasty?

Nicole's Taste of Health

Almond amore.  
I love almonds (and nuts in general actually) but I’m not the only one as these crunchy little numbers have been a delicacy throughout history. They originated in China before spreading throughout Europe. And speaking of loving almonds, the ancient Romans would give newlyweds almonds as a fertility charm. Even now sugar-coated almonds are given as bomboniere (gifts) to guests at Italian weddings and symbolise health, wealth, happiness and long life as well as fertility. I always thought the tooth-cracking coating spoiled a perfectly good almond but the sugar itself is also symbolic of wishing guests a sweet life.

Despite their charming reputation in times past, almonds – like all nuts – have been tarred by the fat-phobia brush, deeming them too naughty to enjoy because of their high oil content. However in the case of almonds and nuts in general, nutrition science is the bearer of glad tidings. The type of fat in almonds is ‘good’ fat, meaning it is mostly unsaturated and therefore good for health. And to make this story’s ending even happier, the good fats are combined with a super-healthy combination of protein, fibre, vitamins and minerals (particularly vitamin E, magnesium and potassium), and beneficial phytochemicals.

Almonds contain little carbohydrate so they can’t be tested for GI, however eating them with high GI foods will lower the GI of the meal or snack, which is great news and adds further to their charm. Even more exciting is the research indicating that not all of the calories (kilojoules) are fully absorbed from eating almonds, probably due to their physical structure that prevents some of the oil from being absorbed. While this does not represent a get-out-of-jail-free card for overeating, it does suggest we can relax a bit about the numbers and focus on eating almonds regularly for their many health benefits. To name a few, almonds have been shown to lower LDL (bad) cholesterol, improve insulin sensitivity and enhance satiety (feeling of fullness), all of which support sensible snacking and metabolic health.

Dietary surveys show most of us don’t eat enough nuts to obtain these health benefits but how much do we need? The scientific evidence suggests we aim for one to two handfuls (30–60g) a day of nuts which gives us plenty of opportunity to enjoy a variety of nuts including almonds. Eat them anyway you like - raw or roasted - but leave the chocolate-coated ones to special occasions and buy your almonds unsalted, and of course you get more fibre and phytochemicals eating the skin.

You can roast your own almonds quite simply (see Anneka's recipe). They’re great to eat on their own but they add wonderful flavour and crunch to stir-fries and salads, they provide real ‘oomph’ to trail mix and they’re so versatile as to be delicious in desserts too. Witness the delight of friand made with almond meal, or the gorgeous crunch of slivered almonds in a crumble. You can blanch your own almonds for making sweet treats by placing raw almonds in a bowl of boiling water for one minute, rinse under cold water, drain, dry and peel the skin off. These pale and naked beauties can be crushed, sliced or pulverised in a blender or food processor to make almond meal which you can then add to fruit smoothies or cookies, or use to make cakes and muffins.

And after all that effort it’s good to know you can freeze any unused almond meal for another day. Of course if you’re really keen you can make marzipan – the famously indulgent confection used to make sweets, hideous miniature faux fruits (sorry if you like them but I think they’re awful) or rolled out to make white icing for celebration cakes.

And after all that sweet talk you’re probably looking for a dietary ‘detox’. You may have heard the hype about activated almonds being the ultimate health food, but what are they? Essentially activated almonds are soaked overnight, rinsed and slow roasted on a low heat for several hours. Enthusiasts say this process deactivates enzyme inhibitors in the outer layer making the almonds more digestible and their nutrients more available. Looking at the science it becomes clear this is more a good story to justify charging a lot more money for them. Enjoy them by all means but I think I’ll stick to the regular lazy almonds.

Gosh, what a great all-rounder: taste, versatility, health, history and symbolism. I think I’ll go and have a handful now, and I’m definitely making Anneka’s cake!



Nicole Senior is an Accredited Practising Dietitian and Nutritionist, author, speaker, consultant, and commentator with an interest in how we can learn to love good food that's good for us.

In the GI News Kitchen

Here's how you can cut back on the food bills and enjoy fresh, easily, seasonal, satisfying and delicious low or moderate GI meals that don’t compromise on quality and flavour one little bit with our Money Saving Meals including chef Michael Moore’s Chilled apple, pear & quinoa porridge with raw almonds from Blood Sugar: the Family reprinted courtesy New Holland Publishers.

Chilled apple, pear and quinoa porridge with raw almonds. 
A little goes a long way says chef Michael Moore’s suggesting you add (or substitute) seasonal berries or the fruit of your choice. Serves: 4

1 1/3 cups skim milk
½ cup water
120g (4oz) quinoa (a slightly heaped ½ cup), rinsed
½ cup plain yoghurt
1 tbsp agave nectar/syrup
1 red apple, washed
1 green pear, washed
Pinch ground ginger
Pinch ground cinnamon
60g (2oz) raw almonds, skin on, chopped or finely sliced



Place the milk, water and quinoa in a small saucepan, bring to the boil then reduce to a simmer and cover. Cook, stirring occasionally for approximately 15 minutes until soft then allow to cool.
Place the cooked quinoa in a mixing bowl and stir in the yoghurt and agave nectar.
Grate the apple and pear into the bowl with a coarse cheese grater, including the juices. Mix together well. Add the spices to taste and adjust consistency with a splash of milk to your taste. Spoon into small serving bowls and sprinkle with chopped almonds.

Per serve 
1270 kJ/300 calories; 12g protein; 11g fat (includes 2g saturated fat); 38g available carbs; 5g fibre

Family Baking, Anneka Manning, author of Bake Eat Love. Learn to Bake in 3 Simple Steps and founder of Sydney’s BakeClub,  shares her delicious ‘better-for-you’ recipes for snacks, desserts and treats the whole family will love. Through both her writing and cooking school, Anneka teaches home cooks to bake in practical and approachable yet inspiring ways that assure success in the kitchen.

 

Gluten-free mandarin roasted almond cakes.
These cakes are a play on the original (and wonderful) Middle Eastern orange cake from the one-and-only Claudia Roden. Making use of seasonal mandarins (while they are still around), ground roasted almonds and with the addition of polenta this version is also flourless and gluten-free. The ground roasted almonds give this can a lovely ‘toasted’ flavour but you can substitute pre-ground almond meal if you prefer.
Makes: 12
Prep: 20 minutes (+ 30 minutes simmering and 15 minutes cooling time)
Bake: 15-18 minutes

2 large mandarins (about 110g/3½oz each)
Melted butter or olive oil spray, to grease
½ cup instant polenta
80g natural almonds, roasted, finely ground (see Baker’s tip)
½ tsp baking powder
3 eggs, at room temperature
3/4 cup raw caster sugar
2 tsp natural vanilla essence or extract
icing sugar, to dust (optional)



Put the mandarins (skin and all) in a small saucepan and cover with water. Bring to the boil and simmer for 30 minutes or until very soft when tested with a skewer. You may need to place a small saucer over the mandarins to keep them submerged. Remove from the water and set aside to cool slightly.
Meanwhile preheat the oven to 180°C. Brush a 12-hole 80ml (1/3 cup) muffin tin with the melted butter to grease.
Combine the polenta, roasted almond meal, and baking powder in a medium bowl and mix well to combine evenly.
Quarter the mandarins and remove and discard any centre core or seeds. Puree in a food processor or blender until smooth.
Put the eggs, sugar and vanilla in a medium mixing bowl and use an electric mixer with a whisk attachment to whisk until very thick and pale and a ribbon trail forms when the whisk is lifted. Add the mandarin puree and use a spatula or large metal spoon to fold in until just combined. Add the polenta mixture and fold together until evenly combined.
Divide the mixture evenly among the muffin holes (pouring the mixture from a jug or using a ladle works well).
Bake in preheated oven for 15-18 minutes or until the cakes are firm to the touch on the top and cooked when tested with a skewer. Remove from the oven and cool in the tin for 10 minutes. Use a palette knife to ease the cakes out of the tin and transfer to a wire rack. Serve warm or at room temperature dusted with a little icing sugar if you wish.

Baker’s tip

• To roast and grind the almonds, spread on an oven tray and place in an oven preheated to 180°C/350°F for 8-10 minutes or until aromatic. Cool on the tray before processing in a food processor until finely ground.

Per piece
560 kJ/ 130 calories; 3.5g protein; 5g fat (includes 1g saturated fat); 18.5g available carbs; 1g fibre

American dietitian and author of Good Carbs, Bad Carbs, Johanna Burani, shares favourite recipes with a low or moderate GI from her Italian kitchen. For more information, check out Johanna's website. The photographs are by Sergio Burani. His food, travel and wine photography website is photosbysergio.com.



Grilled shrimp over rucola salad. 
This dish is short on work but long on flavor.  Simple, fresh, unadulterated whole foods, marinated, grilled, then placed on a bed of fresh greens (I always use organic).  Add a glass of chilled Pinot Grigio and some sourdough crostini and you have a perfect meal – Italian style! Serves: 4 (2 skewers each)

20oz (600g) uncooked large shrimps (prawns), shelled and deveined
10oz (300g) baby bella mushroom caps
10oz (300g) large grape tomatoes
6oz (180g) rucola (arugula/rocket), washed and drained

For the marinade
¼ cup extra virgin olive oil
juice half lemon (about 1½ tbsp)
1 tbsp finely chopped fresh parsley
1 shallot, finely chopped
¼ tsp salt a few twists freshly ground pepper



Place all marinade ingredients in a medium bowl; mix well.  Add the shrimps and stir thoroughly to coat the shrimps evenly.  Cover and refrigerate for at least 1 hour, stirring a couple of times.
Wash the vegetables, pat dry and set aside.
Heat the grill according to manufacturer’s instructions. Using metal or wooden skewers previously soaked in water, alternately thread the mushrooms, shrimps and tomatoes. Grill the skewers 2 minutes per side, basting with the marinade for the first 2 minutes only.
Divide the rucola among the 4 dinner plates.  Place 2 skewers on each plate and serve.  This dish tastes best when the shrimps and vegetables are removed from the skewers and mixed in with the rucola.

Per serve (assumes 50% marinade consumption) 
250 calories/1040 kilojoules; 30g protein; 10g fat (includes 1.5g saturated fat); 14g available carbs; 2g fibre 

We Are What We Ate

Say cheese, but when? 
The processing of milk and particularly the production of cheese were critical in early agricultural societies as it allowed the preservation of milk in a non-perishable and transportable form and, of primary importance, it made milk a more digestible commodity for early prehistoric farmers.



However, while we do know a fair amount about the human diet, both past and present, we don’t actually know very much about how and where cheese making first happened. Recent research published in Nature provides unequivocal evidence that people in northern Europe were making cheese more than 7000 years.

By analysing fatty acids extracted from unglazed pottery pierced with small holes excavated from archaeological sites in Kuyavia (Poland) dating from around 7000 years ago, the researchers showed that dairy products were processed in these ceramic vessels. Using lipid biomarker and stable isotope analysis, researchers examined preserved fatty acids trapped in the fabric of the pottery and showed that the sieves had indeed been used for processing dairy products.  Milk residues were also detected in non-perforated bowls, which may have been used with the sieves.

By way of contrast, the analyses of non-perforated pottery (cooking pots or bottles) demonstrated that they were not used for processing milk.  The presence of ruminant carcass fats in cooking pots showed that they were likely used to cook meat, while the presence of beeswax in bottles suggests the sealing of the pottery to store water. The analyses thus showed that the people who lived here used different types of pottery in very specific ways – sieves (and maybe bowls) for cheese-making, cooking pots for cooking their meat and waterproofed bottles to store and carry water.

Mélanie Salque, a PhD student from the University of Bristol and one of the authors of the paper said: ‘Before this study, it was not clear that cattle were used for their milk in northern Europe around 7000 years ago.  However, the presence of the sieves in the ceramic assemblage of the sites was thought to be a proof that milk and even cheese was produced at these sites.  Of course, these sieves could have been used for straining all sorts of things, such as curds from whey, meat from stock or honeycombs from honey.  We decided to test the cheese-making hypothesis by analysing the lipids trapped into the ceramic fabric of the sieves.

‘The presence of milk residues in sieves (which look like modern cheese-strainers) constitutes the earliest direct evidence for cheese-making.  So far, early evidence for cheese-making were mostly iconographic, that is to say murals showing milk processing, which dates to several millennia later than the cheese strainers.’

Peter Bogucki one of the co-authors of this new study and proponent of the cheese strainer hypothesis nearly 30 years ago notes that: ‘As well as showing that humans were making cheese 7000 years ago, these results provide evidence of the consumption of low-lactose content milk products in prehistory.  Making cheese allowed them to reduce the lactose content of milk, and we know that at that time, most of the humans were not tolerant to lactose.  Making cheese is a particularly efficient way to exploit the nutritional benefits of milk, without becoming ill because of the lactose.’

GI Symbol News with Dr Alan Barclay

Dr Alan Barclay

Overweight, obesity and diabetes are on the up downunder. 
The latest results from Australia’s largest population health study, AusDiab, show that rates of diabetes continue to increase around the nation. When AusDiab began in 1999–2000, 8.5% of the adult population 25 and over had diabetes; in 2011–12 that number had increased to 12.0%. As is the case in other parts of the world, rates are higher amongst socially disadvantaged groups.

While by no means the only factor, increasing rates of overweight and obesity are likely partially responsible for the upward trend. Results from Australia’s most recent national health survey show that in 2011–12, 69.7% of men and 55.7% of women 18 and over were overweight or obese, and slightly more men (52% of all cases) have diabetes than women (48% of all cases). Overweight and obesity rates have increased from 56.3% of all adults in 1995.

Of greatest concern is the finding that young adults (25–34 years) are gaining more weight around the middle than any other age group – a 6.6cm increase over the 12-year follow-up period. Increased waist circumference is an independent risk factor for type 2 diabetes, independent of overall weight gain.



The ingenious use of accelerometers and inclinometers enabled AusDiab researchers to compare self-reported physical activity levels with those measured objectively with scientific instruments. Nearly two-thirds of participants were classified as sufficiently active (50 minutes of moderate-to vigorous-intensity physical activity per day) based on their self-reported physical activity. However, on average, participants engaged in 32 minutes of accelerometer-assessed moderate- to vigorous-intensity physical activity per day – a gap of 18 minutes. In other words, people overestimated their moderate-to vigorous-intensity physical activity by more than 50% each day. Arguably the most sobering finding was that on average, participants engaged in 523 minutes (8 hours and 43 minutes) of inclinometer-assessed sitting time per day.

The AusDiab researchers recommended a concerted effort to improve people’s physical activity levels, and perhaps more importantly to decrease their sitting time, to help reduce the rate of type 2 diabetes in Australia. Standing desks discussed in the April 2012 edition of GI News are a practical example of what can be done to help with this in the workplace environment.

A 10% ‘fat tax’ was also recommended. Australia’s current Goods and Services Tax (GST) already acts as a de-facto ‘fat tax’ in Australia as it is not levied on fresh fruit and vegetables or other core foods – only so-called ‘junk foods’ like soft drinks, chips, confectionery and fast foods attract the 10% GST. Overall, the evidence that a ‘fat tax’ will reduce levels of obesity and associated type 2 diabetes is limited. It is also regressive, affecting people from lower socio-economic groups the most. The evidence for the positive effects on dietary behaviours of tax subsidies for healthy foods like fresh fruits and vegetables is far stronger, and will conversely benefit people from lower socio-economic groups the most.

While it may sound like doom and gloom, it’s important to note that the increase in diabetes rates over the past 12 years in Australia are in line with AusDiab’s best case scenario – not worst. Australia's population is aging, and the risk of diabetes increases with age. Also, we are helping people with diagnosed diabetes manage their condition better, so they are living for longer with the condition. So at this point in time, an increase in diabetes prevalence may be seen as somewhat inevitable. The fact that prevalence has increased at a relatively modest rate in line with AusDiabs best case scenario indicates that as a community we must be doing something right to reduce the populations risk overall.

The GI Symbol, making healthy low GI choices easy choices



For more information about the GI Symbol Program

Dr Alan W Barclay, PhD
Chief Scientific Officer
Glycemic Index Foundation (Ltd)
Phone: +61 (0)2 9785 1037
Mob: +61 (0)416 111 046
Fax: +61 (0)2 9785 1037Email: alan.barclay@gisymbol.com
Website: www.gisymbol.com

GI Update with Prof Jennie Brand-Miller

Prof Jennie Brand-Miller answers your questions. 



Why doesn’t cheese have a GI value? Other dairy foods like milk and yoghurt and even ice cream do. 
The glycemic index (GI) is a ranking of carbohydrates on a scale from 0 to 100 according to the extent to which they raise blood glucose levels after eating. Only foods that are sources of carbohydrate can be GI tested. Milk and yoghurt are good sources of carbohydrate (and protein, too). For example, here in Australia a 200g/7oz tub of low fat plain yoghurt contains around 12g each of carbohydrate and protein. The carbohydrate comes from the milk sugar, lactose. (However, if the yogurt is sweetened, then it will contain other sugars in addition to lactose.) Cheese on the other hand is a good source of protein but has almost no carbohydrate because cheese is made from milk solids (curd); the lactose-rich whey has been drained off during the early stages of processing which is why people who are lactose intolerant can enjoy cheese but not milk.

Other foods that contain no carbohydrate, or so little that their GI can’t be measured, are meat, chicken, fish, eggs and nuts (well most nuts). If you come across a website that gives you a GI value for cheese (or meat, chicken, fish and eggs), then you know the testing has certainly not followed the international standard method and was probably done in a test tube (in vitro).

Following the international standard method, the GI value of a food is determined by feeding 10 or more healthy people a portion of the food containing 50 grams of digestible (available) carbohydrate and then measuring the effect on their blood glucose levels over the next two hours. For each person, the area under their two-hour blood glucose response (glucose AUC) for this food is then measured. On another occasion, the same 10 people consume an equal-carbohydrate portion of glucose sugar (the reference food) and their two-hour blood glucose response is also measured. A GI value for the test food is then calculated for each person by dividing their glucose AUC for the test food by their glucose AUC for the reference food. The final GI value for the test food is the average GI value for the 10 people.

Latest GI values from Fiona Atkinson at SUGiRS.  

Yoghurt, naturally low GI. 
Yogurt’s low GI values are thanks (mainly) to the combination of acidity and high protein and of course the fact that lactose, the sugar in milk, has a naturally low GI. Here’s why. Lactose is a disaccharide (double sugar) that needs to be digested into its component sugars before our bodies can absorb it. In our bodies, glucose and galactose, the two component sugars that make up lactose, compete with each other for absorption. Once absorbed, the galactose is mainly metabolised in the liver and produces very little effect on our blood glucose levels. The remaining sugar, glucose, is present in a small enough amount not to cause a spike in blood glucose.

Did you know that even if you are lactose intolerant, you can enjoy yoghurt? This is because the micro-organisms added to milk to make yoghurt are active in digesting lactose during passage through the small intestine, in other words, the ‘bugs’ help do the job of lactose digestion for you.

Yoplait Petit Miam: SUGiRS recently tested Yoplait Petit Miam 100g tubs – a calcium-rich, creamy tasting snack or dessert for babies (they say 1+ years on the label), toddlers and young children with 87 calories (364kJ), 14g available carbs and 3g protein in a tub. No arguments over who got the biggest serving because everyone gets their own little pot of yoghurt.

• Fruit Salad GI 41
• Strawberry & Banana GI 39
• Banana GI 39
• Strawberry GI 43
• Blueberry GI 43
• Mixed Berry GI 43
• Vanilla GI 38

GI testing by an accredited laboratory
North America
Dr Alexandra Jenkins
Glycemic Index Laboratories
20 Victoria Street, Suite 300
Toronto, Ontario M5C 298 Canada
Phone +1 416 861 0506
Email info@gilabs.com
Web www.gilabs.com

Australia
Fiona Atkinson
Research Manager, Sydney University Glycemic Index Research Service (SUGiRS)
Human Nutrition Unit, School of Molecular and Microbial Biosciences
Sydney University
NSW 2006 Australia
Phone + 61 2 9351 6018
Fax: + 61 2 9351 6022
Email sugirs@mmb.usyd.edu.au
Web www.glycemicindex.com

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