GI Symbol News with Dr Alan Barclay

Dr Alan Barclay

New American Diabetes Association (ADA) nutrition guidelines for adults with diabetes. 
The ADA has published its latest edition of the Nutrition Therapy Recommendations for the Management of Adults With Diabetes, the first major update in 5 years. Perhaps unsurprisingly, they are evolutionary rather than revolutionary. One of the more important aspects of the ADA guidelines is their Goals of nutrition therapy. While they importantly set targets for common diabetes complications risk factors, they equally importantly put these into the context of the cultural aspects of food, eating and mealtimes.

• “To address individual nutrition needs based on personal and cultural preferences, health literacy and numeracy, access to healthful food choices, willingness and ability to make behavioural changes, as well as barriers to change.” 
• “To maintain the pleasure of eating by providing positive messages about food choices while limiting food choices only when indicated by scientific evidence.” 
• “To provide the individual with diabetes with practical tools for day-to-day meal planning, rather than focusing on individual macronutrients, micronutrients, or single foods.” 

After all, food is one of life’s pleasures whether you have diabetes or not – there is absolutely no point in avoiding any particular food or drink unless there’s good evidence to do so.

One of the most debated issues over the past few millennia has been how much carbohydrate (sugars and starches), fat and protein can or should a person with diabetes eat? In line with its broader goals, the ADA states that:

• “Evidence suggests that there is not an ideal percentage of calories from carbohydrate, protein, and fat for all people with diabetes; therefore, macronutrient distribution should be based on individualized assessment of current eating patterns, preferences, and metabolic goals.” 

In practice, this means that a person with diabetes should work with their dietitian and other members of their health-care team to nut out what is best for them as an individual, rather than follow the latest fad diet.

Recommendations for saturated (less than 10% of kilojoules/calories) and trans fat (as little as possible) and sodium (less than 2,300 mg/day) are the same as those for the general population.

Importantly for readers of GI News, the latest ADA Guidelines now incorporate specific recommendations for use of the glycemic load (GL = GI x grams available carbohydrate per serve) for the management of diabetes. This means that all of the evidence-based recommendations for the management of diabetes from the major diabetes organisations around the globe now advise people to use of the GI or GL as part of the nutritional management of diabetes, including the Canadian Diabetes Association and Diabetes UK.

Although it is possible to lower the GL of your diet by either eating a low carb diet, or by eating a moderate or even high carb diet but with more low GI foods, the scientific evidence about the benefits of low GL diets is based on studies where people ate moderate amounts of healthy low GI foods – carbohydrates were about 40–50% of their total calories (kilojoules).

Here’s how you can enjoy a low GL diet. Simply use the low GI swap it approach. Choose the food/drink within each food group/category that has the lowest GI value (and that is a healthy choice overall, of course). Because foods within a group/category by definition have similar macronutrient (carbohydrate, fat and protein) contents, by choosing the food with the lowest GI, in most cases you are also choosing the food with the lowest GL. You can use our new Simple Low GI Swaps tool on our updated website www.gisymbol.com.



The GI Symbol helps you identify healthy foods and drinks with both a lower GI and GL.

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 1037
Email: alan.barclay@gisymbol.com
Website: www.gisymbol.com

GI Update with Prof Jennie Brand-Miller

Prof Jennie Brand-Miller answers your questions. 



I know that type 2 diabetes is one of the fastest growing chronic diseases worldwide. Do we know why this is so and what people like me (it runs in my family) can do to prevent getting it? 
The global increase in the prevalence of type 2 diabetes is being driven by the rise in overweight and obesity in all age groups. The reasons behind our weight gain creep are complex but include a simultaneous increase in global food abundance together with increased sedentariness and decreased physical activity during both work and possibly leisure time. Recent studies have also indicated that a deviation from the normal sleeping pattern of 7–8 hours sleep per night, particularly short duration of sleep, increases appetite and promotes obesity and its related diseases (e.g. type 2 diabetes and cardiovascular disease).

There are two ways to prevent type 2 diabetes: by preventing weight gain in the first place and by preventing people who already have pre-diabetes from progressing to diabetes with weight loss and maintenance. The main drivers in both situations are changes in dietary and physical activity patterns, but we also need to address disturbed sleep patterns and workplace stress. Unfortunately, despite convincing evidence from clinical trials that type 2 diabetes can be prevented or delayed through intensive lifestyle interventions resulting in weight loss, the reality is that weight regain and incremental weight ‘creep’ are very common. It is possible that this may jeopardise diabetes prevention and it remains to be seen the effect of a longer period of weight maintenance on prevention.

The recent Diogenes Study (Diet, Obesity and Genes) identified two dietary factors associated with shorter-term prevention of weight regain after prior weight loss: higher protein intake and lower glycaemic index (GI). The findings showed that overweight and obese participants assigned to the combination of modestly higher protein and lower GI ad libitum had significantly better completion rates and weight maintenance after six months as compared with the official dietary guidelines. Indeed, those consuming the high protein-low GI combination diet continued to lose weight during the weight maintenance phase and were twice as likely to have maintained a 5% weight loss compared to the other groups.

Here at the University of Sydney we are one of eight sites around the world taking part in the 3-year international PREVIEW Study. Its primary goal is to identify the most efficient lifestyle intervention pattern for the prevention of type 2 diabetes in people who are pre diabetic overweight or obese individuals (i.e. those at high risk of diabetes). The aim of this study is to find out the best methods (through diet, exercise and behavioural modification) of maintaining weight loss and keeping diabetes at bay. Individuals taking part in this study will have their own team of professionals dedicated to their weight loss and weight loss maintenance, all free of charge. We are recruiting participants now. If you are:

• Between the ages of 25–45 or 55–70 years 
• Overweight 
• Have a blood relative with diabetes 
• Been told you have pre-diabetes or impaired glucose tolerance you may be eligible to participate. 

This brochure will tell you about the study and how you can take part if you are eligible.

New GI Values from SUGiRS
Sustagen® Diabetic now has the GI Symbol 
Sustagen has been around a long time. It is a supplement designed for people finding it difficult to meet their nutritional requirements through regular food alone. There are a variety of products for specific purposes. Nestle Health Science have just launched Sustagen® Diabetic (vanilla flavour), specifically formulated to be low GI (34) for people with diabetes or pre-diabetes (type 1 or type 2) who are not eating well, or have a poor appetite, or are ill or recovering from illness. It provides essential nutrition without negatively impacting blood glucose levels. To be used under medical supervision.

• To make 1 serving, mix 7 level of scoops with 210ml water (or milk), stir and serve chilled or warmed (210ml is about ¾ cup).
• Nutrition information for 1 serving mixed with water: 25g carbohydrate and 8g fibre, 11g protein, 11g fat
• Glycemic load (GL) 1 serving = 3 
• For more information: www.sustagen.com.au 

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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GI News—October 2013

•  Sleep and diabetes risk;
•  Is insulin response more important than the GI value?
• Tomato Magic with Nicole Senior;  
• Four recipes including Wonton asparagus soup and Anneka's Baked eggs in nests with tomato and spinach;  
• The difference in being rich or poor in gut bacteria;  
• Dr David Katz new book: Disease Proof;   
• China's diabetes epidemic, Dr Alan Barclay reports.    

GI News 
Editor: Philippa Sandall
Web management and design: Alan Barclay, PhD
Contact email (for questions or permission to reproduce stories from this newsletter): info@gisymbol.com for technical problems or faults please contact smb.ginewstech@sydney.edu.au

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Food for Thought

Sugar, diabetes and why the state of our health is not about any one thing. 
Many of the nutrition studies we share with GI News readers are prospective studies. Looking at large groups of people over a period of time (usually many years), the researchers mine the data (rather like gold prospectors) looking for links between diet (e.g., consumption of fruit or vegetables or red meat or whole grains or sugar) and health. What you need to remember when you read (or watch) headline-hitting health stories featuring research findings from such studies is that the correlations or associations they find don’t actually establish causation. Prof David Katz comments on a recent study in Plos One using econometric models of repeated cross-sectional data of the association between sugar intake and diabetes around the world. Here is an edited summary of his Huffington Post piece reproduced with permission. 


Dr. David Katz

‘The study itself, published in the journal Plos One, is excellent overall. This kind of ecological evaluation – looking at an association between X and Y at the population level is certainly of some value. But it is absolutely not the “closest thing to causation” – in fact, it is among the least reliable forms of evidence. At the population level, the presence of a Bentley in the driveway, or a high-speed Internet connection in the home, is profoundly associated with reduced likelihood of malaria (or tuberculosis, or leprosy, etc.). This is absolutely not because Bentleys or the Internet protect against leprosy or malaria. Rather, affluent people with expensive cars and high-speed Internet access are much less likely to encounter malaria or leprosy than the poor for reasons having nothing to do with horsepower, or bandwidth.

Fundamentally, Dr Basu’s team found that the greater the availability of daily calories from sugar around the world, the more diabetes. I’m having some trouble figuring out what is supposed to be surprising about this. If people add sugar calories to their diets, they are getting both more sugar, and more calories, and those exposures alone and together are well known to contribute to diabetes risk. If they are adding sugar calories in place of other calories, then the percentage of total daily calories coming from sugar is going up, and the overall quality of diet is going down. Again, this pattern is pretty well linked to diabetes risk (and other chronic disease risk, for that matter) already.

To some extent, the Basu study was a self-fulfilling prophecy. It’s true the researchers looked at other associations between diet and diabetes. But consider that one food category was “meat,” which presumably lumped together everything from salmon to salami. Some such “meats” likely defend against diabetes, while others would likely increase risk. Lumped together, nothing much would be visible. Similarly, there was a category of “cereals,” but with no distinction between whole grains and refined starch. Putting everything from steel-cut oats to Cap’n Crunch in one category would not facilitate keen insights. The authors did not look at nuts and seeds, despite numerous studies – including one just published in the Journal of Nutrition – demonstrating that higher intake of walnuts and other nuts is associated with reduced diabetes risk.

Since Dr Basu’s methods involved looking at sugar dose available in the food supply per person per day, and the prevalence of diabetes in the population, there is nothing in the data to prove that those who ate the most sugar were most likely to develop diabetes – although one may infer that. Rather, as countries make more sugar calories available each day (i.e., become more like the US), their populations have more diabetes. Again, this is not terribly surprising.

But it’s more than a little wrong to conclude that since sugar intake contributes to diabetes risk, nothing else matters. In fact, Dr Basu and colleagues state explicitly that increasing sugar availability accounts for roughly one-quarter of the global rise in diabetes rates between 2000 and 2010. This clearly implies that something other than sugar accounts for almost 75 percent of that increase.

The reality, alas, is that the state of our health is not about any one thing. We can cut fat, and get fatter and sicker – by eating more starchy, sugary junk. We can cut carbs by switching from beans to baloney, and get fatter and sicker. And we can cut sugar and consume ever more artificially-sweetened, starchy, fatty junk – and get fatter and sicker. We clearly like little bits of truth we find easy to digest. But none of these is the whole truth, and when bits of truth are mistaken for the whole – they might just as well be falsehoods.’

About Dr David Katz
Known internationally for expertise in nutrition, weight management, and chronic disease prevention, Katz is the founding director of Yale University's Prevention Research Center. He is the founder and President of the non-profit Turn the Tide Foundation, and a blogger/medical review board member for The Huffington Post. 
www.davidkatzmd.com

What’s New?

Dementia risk and BGLs. 
Blood sugar levels averaged over a five-year period were associated with rising risks for developing dementia, according to the findings of a recent study published in the New England Journal of Medicine. For example:

• In people without diabetes, risk for dementia was 18% higher for people with an average glucose level of 115 milligrams per deciliter (6.4 mmol/L) compared to those with an average glucose level of 100 mg/dl (5.6 mmol/L)
• In people with diabetes, whose blood sugar levels are generally higher, dementia risk was 40% higher for people with an average glucose level of 190 mg/dl (10.6 mmol/L) compared to those with an average glucose level of 160 mg/dl (8.9 mmol/L).

The measurements included blood glucose (some fasting, some not) and glycated hemoglobin (also known as HbA1c).


Dr Paul Crane

‘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 first author Dr Paul K. Crane. ‘There was no threshold value for lower glucose values where risk leveled off.’ However, he emphasized that these results come from an observational study: ‘What we found was that people with higher levels of glucose had a higher risk of dementia, on average, than did people with lower levels of glucose,’ he said. ‘While that is interesting and important, we have no data to suggest that people who make changes to lower their glucose improve their dementia risk. Those data would have to come from future studies with different study designs.’

GI News's Dr Alan Barclay stated that it is good to see Dr Crane emphasising the point that the results are from an observational study and as such do not prove causality; just an association. At this point in time, we don’t know if reducing glucose will reduce dementia risk. We need to conduct a randomised controlled trial to test that hypothesis.

Catching up on sleep.  

Dr Peter Liu

Men who lose sleep during the working week may be able to lower their risk of developing Type 2 diabetes by getting more hours of sleep, according to research findings presented at The Endocrine Society’s 95th Annual Meeting in San Francisco. ‘We all know we need to get adequate sleep, but that is often impossible because of work demands and busy lifestyles,’ said Dr Peter Liu an LA BioMed lead researcher. ‘Our study found extending the hours of sleep can improve the body’s use of insulin, thereby reducing the risk of type 2 diabetes in adult men.’

Liu and researchers from the University of Sydney studied 19 non-diabetic men, with an average age of 28, who for six months or longer (average, 5 years) self-reported inadequate sleep during the work week – around 6 hours a night. But they regularly caught up on their sleep on the weekends, getting at least a third more sleeping time a night. Their reported sleep times were verified by actigraphy, in which each man wore a small device on his wrist that monitored sleep-wake cycles. The men spent three nights in a sleep lab on each of two separate weekends and each individual had the same food intake during the study visits, so that diet would not influence the results. When the men slept 10 hours a night on each of three nights of catch-up sleep, their insulin sensitivity was much better than when they had persistent sleep restriction. Their insulin resistance test score also improved (decreased) with sleep extension.

Being rich or poor in gut bacteria. 
A study in Nature reports that people with fewer bacterial species in their intestines may be more likely to develop cardiovascular disease and diabetes. The researchers examined the intestinal flora of 169 obese Danes and 123 non-obese Danes using an analytical approach called quantitative metagenomics. When comparing the two groups, they discovered that people with a low richness microbiota have more body fat and less healthy; they are more resistant to the action of insulin, have unfavorably altered blood lipids and show increased blood levels of inflammation markers and white blood cells, bringing them at increased risk of type 2 diabetes and cardiovascular disorders. They also observed that obese people from the low richness group gained on average significantly more weight than the high richness one during the past nine years.

The gut is like a rainforest says Oluf Pedersen. It appears that the richer and more diverse the composition of our intestinal bacteria, the stronger our health. The bacteria produce vital vitamins, mature and strengthen our immune system and communicate with the many nerve cells and hormone-producing cells in the intestinal system. And, not least, the bacteria produce a wealth of bioactive substances which penetrate into the bloodstream and affect our biology in countless ways.

Is stomach damage why diets are doomed to fail?  


Associate Professor Amanda Page
The way the stomach detects and tells the brain how full the body is becomes damaged in obese people, but does not return to normal once they lose weight, according to findings of a mouse study published in the International Journal of Obesity. The nerves in the stomach that signal fullness to the brain appear to be desensitised after long-term consumption of a high-fat diet. Researchers believe this could be a key reason why most people who lose weight on a diet eventually put that weight back on.

‘The stomach’s nerve response does not return to normal upon return to a normal diet,’ said Associate Professor Amanda Page from the University of Adelaide’s Nerve-Gut Research Laboratory and the study’s lead author. ‘This means you would need to eat more food before you felt the same degree of fullness as a healthy individual. In normal conditions, leptin (a hormone) acts to stop food intake. However, in the stomach in high-fat diet induced obesity, leptin further desensitises the nerves that detect fullness. These two mechanisms combined mean that obese people need to eat more to feel full, which in turn continues their cycle of obesity,’ she said. The researchers said there were not yet sure whether the desensitisation of the stomach nerves is a permanent effect, or just a long-lasting one. ‘We know that only about 5 per cent of people on diets are able to maintain their weight loss, and that most people who’ve been on a diet put all of that weight back on within two years.’

What’s new?
Disease-Proof. DNA is not destiny.



Abundant scientific evidence shows that not smoking, eating well, being active, and maintaining a healthy weight play an enormous role in our health. Drawing upon the latest scientific evidence and decades of clinical experience, Dr. Katz arms us with the skills to make lasting changes in each of these areas. Disease-Proof equips readers with the knowledge to manage weight, improve immune function, reprogram our genes, and prevent and reverse life-altering illnesses. DNA is not destiny. To a much greater extent, choices under our control determine our fate. We have scientific evidence to show that if we change our own behavior, we change the behavior of our genes. We can nurture nature. The relevant skills aren’t trivial, but they aren’t really hard, either. You can have them -- but you have to go get them. Remember you once had to learn how to ride a bike. But then... you’ve known how ever since. Without the right skill set, health is elusive.

Nicole's Taste of Health

Tomato magic.
‘Knowledge is knowing a tomato is a fruit. Wisdom is not putting it in fruit salad.’ 
This is one of my favourite quotable quotes and refers to one of the many botanical versus culinary inconsistencies in the world of food. Olives and avocadoes are the other obvious examples of fruits that we usually eat as vegetables. If you’re botanically inclined, tomatoes are a fruit because they form from the flower, and the seeds are inside. But it’s also obvious when you taste a really good one because they taste so deliciously sweet. Much like other fruits, they’re also rich in vitamin C.



‘You say to-may-to, I say to-mah-to, let’s call the whole thing off.’ 
The widely popular ruby fruit also features in this famous song lyric, although unlike Louie Armstrong and Ella Fitzgerald, everyone agrees tomatoes are great. The tomato is iconic to Italian cuisine and integral to many other Mediterranean countries as well. The beautiful balance of sweetness, zingy acidity and natural saltiness makes it the perfect partner for just about everything including pasta and pizza. Can’t come at legumes? Try them in a tomato ragu and voila: totally yum. Can’t take to green beans? Cook them up in tomato passata and you’ll be converted. Turn your nose up at eggplant or zucchini (courgette)? You’ll change your tune when they make sweet music with tomato in a ratatouille (great kids movie too). And don’t fret about the cooking or processing of tomatoes because their antioxidants including the red pigment lycopene actually become more available to the body when pureed and cooked with oil; what a bonus! And this enhanced absorption also applies to tomato juice found in Bloody Marys (although Virgin Marys sans alcohol are healthier of course). You might have heard that lycopene may reduce the risk of prostate cancer in men but studies have also shown benefits for cholesterol and protecting skin against UV damage.

Most commercially produced tomatoes have compromised flavour for hardness that allows them to be transported more easily but tomatoes are fairly easy to grow yourself either in the garden or in a pot, and the itty-bitty cherry varieties are both hardy and prolific. I’d go as far as to say they’re better for flavour as well. There is now a trend toward old fashioned heirloom varieties however these are still hard to find in the shops so grow your own: once you’ve tasted a really good tomato it’s hard to go back. And for any tomato it’s always better to eat them at room temperature. For a truly gorgeous feast for the eyes as well as the mouth, simply roast a whole sprig of cherry tomatoes drizzled in olive oil and bejewel your plate with culinary treasure. If your harvest cup runneth over, preserve your delights for later by making your own passata (which can be bottled or frozen) or slow roast them and store under oil in the fridge. Slow roasted tomatoes look a shadow of their former selves but beautiful on the inside with concentrated flavour. Use them on sandwiches, wraps, pizza, salads or stirred through pasta (but ensure you enjoy some hot with a dash of balsamic vinegar).

Speaking of harvest cups running over, you will no doubt have heard of the mad Spaniards in the town of La Tomatina and their annual organised mega food-fight where they throw 90,000 pounds of squashed, inedible tomatoes at each other. Now we can add ammunition and entertainment to an already bulging list of talents for this ever-versatile fruit/vegetable. That’s what I call tomato magic.


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

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.

 

Baked eggs in nests with tomato and spinach.
This delicious combination of egg, spinach and tomato is held within a clever individual bread basket and then baked – perfect for breakfast or a light lunch it will be popular with both kids and adults alike. Makes: 4 Preparation time: 20 minutes Baking time: 15-20 minutes

Olive oil, to brush or olive oil spray
4 slices good-quality mixed-grain bread, crusts removed
16 baby spinach leaves
160ml (2/3 cup) homemade tomato sauce (see recipe below)
4 eggs
20g finely shredded vintage cheddar or parmesan
1 tbs chopped flat-leaf parsley
Freshly ground black paper, to taste
Extra homemade tomato sauce (optional), to serve



Preheat the oven to 180°C/350°F.
Use your fingertips to flatten the bread slices slightly. Brush both sides of the slices lightly with the olive oil or spray lightly with the olive oil spray. Press each into a 3/4 cup muffin tin hole to line.
Place the spinach leaves into the bread cups to line and then top each with a tablespoon of homemade tomato sauce. One-by-one break an egg into a ramekin or small dish and then slide into the bread cups. Sprinkle with the cheese, top with another tablespoonful of the sauce. Sprinkle with the parsley and season well with the pepper.
Bake in preheated oven for 15 minutes for a soft yolk or 20 minutes for a hard yolk. Serve warm with extra sauce if desired.

Homemade tomato sauce.
This versatile, fresh-flavoured sauce will become a staple – perfect tossed through pasta, spread over pizzas and served as an accompaniment it is well worth making double and storing it the freezer for another time. Makes: about 1-1/4 cups Preparation time: 10 minutes Cooking time: 35-40 minutes

1 tbs olive oil
1 small brown onion, finely diced
1 garlic clove, crushed
1⁄4 tsp dried oregano
400g/14oz tin diced tomatoes
1⁄2 tsp sugar, or to taste
salt (optional) and freshly ground black pepper, to taste

Put the olive oil and onion in a medium saucepan over medium heat and cook, stirring occasionally, for 8 minutes or until the onion is tender.
Add the garlic and oregano and cook for 1 minute or until aromatic. Add the tomatoes and bring to the boil.
Reduce the heat to low and simmer for 25-30 minutes, stirring occasionally, or until thickened to a thick sauce consistency.
Remove from the heat and season with sugar, salt and freshly ground black pepper, to taste. Set aside to cool. Any leftover sauce will keep in an airtight container in the fridge for up to 4 days or in the freezer for up to 3 months.

Per serve 
1085 kJ/ 260 calories; 16 g protein; 14 g fat (includes 4 g saturated fat); 16 g available carbs; 4 g fibre

Here's how you can cut back on the food bills and enjoy fresh-tasting, easily prepared, 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 this wonton soup.

Wonton soup.
Now in season in Australia, asparagus is one of the best dietary sources of inulin an indigestible part of food that enters the large bowel to become food for the healthy bacteria that happily reside there. For that reason it is called a prebiotic (a food for bacteria). This recipe is reproduced courtesy the Australian Asparagus Council www.asparagus.com.au Serves 4

6 cups salt reduced chicken stock
1 tbs ginger matchsticks
1½ tbs light soy sauce
1 tsp caster sugar
¼ tsp sesame oil
300g (10oz) prawn or shitake wontons
1 bunch asparagus, woody ends trimmed
100g (3½oz) fresh snow peas
1 long red chilli, finely sliced
Vietnamese mint and coriander leaves, to serve
¼ tsp garlic infused olive oil



Place the stock in a large saucepan and bring to the boil. Reduce heat to a simmer and stir in the ginger, soy sauce, sugar and sesame oil. Add the wontons into the stock and cook for 3 minutes. Add the asparagus and snow peas, and cook a further 2 minutes.
Ladle the soup into serving bowls, and garnish with the chilli and herbs, then drizzle with the garlic oil.

Per serve 
995 kJ/ 240 calories; 9 g protein; 3.5 g fat (0.5 includes g saturated fat); 38 g available carbs; 5 g 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.



Oaty apple muffins
I’ve never found oat bran in any Italian supermarket, specialty shop or health food store. Even oats are less ubiquitous there. That’s why when I go to Italy, I fill my suitcase with boxes and bags of this wonderful grain and make these oaty muffins to share with my neighbors, friends and family. If they’re interested, I explain that the soluble fiber in the oats helps to lower cholesterol. They love the taste and I love seeing them eating something that’s good for them. In this recipe the muffin size is deliberately small because of the high fiber content. Chopped fresh fruit or nuts can be added. Makes 24

4 cups unprocessed oat bran
½ cup brown sugar
4 tsp baking powder
1½ tsp ground cinnamon
2 cups skim milk
1 whole egg plus
2 egg whites 1 cup unsweetened applesauce



Heat oven to 425°F (220°C). Place paper baking cups in 24 muffin molds or spray the mold bottoms with non-stick cooking spray.
Mix the oat bran, sugar, baking powder and cinnamon in a medium mixing bowl. Combine the remaining ingredients in a separate bowl, mix well.
Combine wet ingredients with the oat bran mixture and pour batter into prepared muffin tins. Bake 15 minutes.

Per serve: 1 muffin 
326 kJ/ 78 calories; 4g protein; 1g fat (includes 0g saturated fat); 12g available carbs; 2g fibre 

We Are What We Ate

The evolution of dietary recommendations for diabetes.   
They knew about diabetes in ancient Egypt. Physician Hesy-Ra of the 3rd Dynasty describes various diseases including a polyuric syndrome, presumably diabetes, in what is now known as the Ebers papyrus (1500BCE). Ancient Ayurvedic texts from India go further describing two types of diabetes-like conditions – congenital and late onset – and noting the relationship of diabetes to heredity, obesity, sedentary life and diet. Talk about the wisdom of the ancients. Today research has completely confirmed that relationship – diabetes risk comes from a combination of diet and lifestyle factors and not from any single nutrient or food (such as sugar or soft drinks) and also tends to run in families. Over the years, people with diabetes have been forced to undergo a number of very challenging dietary regimens. Here we summarise.



1797 Scottish physician John Rollo prescribes an ‘animal diet’ for his patients of ‘plain blood puddings’ and ‘fat and rancid meat’ so to manage the disease with foods their bodies could assimilate.
1871 French physician Apollinaire Bouchardat notices the disappearance of glycosuria (sweet urine) in his diabetes patients during food rationing under the Siege of Paris in the Franco-Prussian War, and formulates individualised diets to treat the condition.
1916 Boston pathologist Elliott Joslin compiles 1000 of his own cases and creates the textbook The Treatment of Diabetes Mellitus. In it he reports that ‘the mortality of patients was approximately 20 per cent lower than for the previous year’, due to ‘the introduction of fasting and the emphasis on regular exercise’.
1919 Dr Frederick Allen of the Rockefeller Institute in New York publishes his Total Dietary Regulations in the Treatment of Diabetes that introduces a therapy of strict dieting – dubbed the ‘starvation treatment’ – as a way to manage diabetes.

1921 Insulin was discovered by Canadians Dr Frederick Banting and Charles Best and became commercially available towards the end of 1922 revolutionising the management of diabetes throughout the world. The refusal to patent insulin but to share this miraculous therapy freely with the world will remain an outstanding example of unreserved generosity towards mankind in the history of medical disease. Banting’s colossal contribution has been globally recognised by the declaration, since 2007, of his birthday (14th November) as World Diabetes Day. 

1923 Dr H. Rawle Geyelin demonstrated that a higher carbohydrate diet did not upset blood glucose levels as long as enough insulin was supplied.
1950 The American Diabetic Association and American Dietetic Association developed and published the first set of carbohydrate exchange lists.
1970s Major diabetes organisations review their dietary recommendations due to the increasing number of deaths of people with diabetes from heart and blood vessel diseases. Recommendations for dietary fat dropped to less than 35% calories and carbohydrate recommendations went up to 55–60% of calories. Researchers found that the nutritional status of patients improved with a higher carbohydrate intake, and their insulin sensitivity improved as well.
1981 Dr David Jenkins, Dr Tom Wolever and colleagues develop the concept of the glycemic index (GI) of foods and publish their findings, A physiological basis of carbohydrate exchange, in the American Journal of Clinical Nutrition
1994 The American Diabetes Association completed a major revision of its dietary guidelines for people with diabetes acknowledging that there was no one right diet and dropping specific recommendations to limit the amount of simple sugars.
1997 World Health Organization/Food and Agriculture Organization recommended using the GI as the best guide to the effect of carbohydrate foods on blood glucose levels.
2008 A systematic review Glycemic index, glycemic load, and chronic disease risk–a meta-analysis of observational studies was published reporting that those eating the highest GI diet had a 40% higher risk of type 2 diabetes than those with the lowest GI diet. When it comes to diet and diabetes risk, the researchers found that the overall glycemic load of the diet (i.e. the total amount of carbohydrate x GI) is the biggest potential problem.

GI Symbol News with Dr Alan Barclay

Dr Alan Barclay
Diabetes and pre-diabetes epidemic in China.  
China is now the global epicentre of diabetes and pre-diabetes according to new research in the Journal of the American Medical Association. Nearly two out of three Chinese adults has diabetes or prediabetes. In 2010, a survey of Chinese adults found that 11.6%, equivalent to a staggering 113.9 million people, had diabetes, and unfortunately only one in three were aware that they had the condition. In addition, just over half (50.1%) of all Chinese adults had prediabetes, equivalent to an even more staggering 493.4 million people.

Perhaps surprisingly, unlike other countries with similarly high diabetes prevalence rates, the average adult in China is not nearly as overweight as their Western counterparts. It’s thought that poor nutrition during pregnancy and the early life of the child, combined with over-nutrition in later life, may be contributing to the accelerated epidemic of diabetes in China. In addition, rapid economic growth and associated industrialization, urbanization, and lifestyle changes (increased high-calorie diets high in refined carbohydrates and fats and decreased physical activity) are taking their toll.

Traditionally, Chinese people consume a high carbohydrate diet, with a very high proportion of their calories coming from white rice. While they were physically active and relatively lean, this was not a major health issue, but as they have become more sedentary, and adopted more Western foods into their diets, the high glycemic load may be contributing to the development of type 2 diabetes.

 

The good news is that there is strong evidence that at least 50% of people with pre-diabetes can prevent or delay its progression to type 2 diabetes through regular physical activity (at least 30 minutes a day), modest weight reduction (5-10% of initial body weight) moderate calorie restriction (eating 500 less calories a day), and eating a diet low in saturated fat (less than 10% of calories) and high in fibre (25-30 g a day).

As regular readers know, there is also very good evidence that lowering the glycemic load of the diet will also reduce the risk of type 2 diabetes. In China, there are a number of staple foods with a high glycemic load such as rice, noodles, bread, and potatoes. There are low GI versions of these foods so swapping high for healthy low GI varieties is one strategy to help reduce body weight and the associated diabetes risk. Healthy swaps include:

• Rice: SunRice Low GI White Rice and Low GI Brown Rice; Moolgiri 
• Noodles: Rice, udon and mung bean 
• Bread: Dense wholegrain (e.g., Burgen varieties) and authentic sourdough 
• Potatoes: Carisma 

While these varieties and brands of staples are not available yet in China, we know that work is well underway to make them more widely available. Stay tuned.

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 1037
Email: alan.barclay@gisymbol.com
Website: www.gisymbol.com

GI Update with Prof Jennie Brand-Miller

Prof Jennie Brand-Miller answers your questions. 



Isn’t the insulin response more important than the GI value? Wouldn’t it be better to have an insulin index of foods? 
The insulin demand exerted by foods is indeed important for long-term health, but it doesn’t necessarily follow that we need an insulin index of foods instead of a glycemic index. When they have been tested together, the glycemic index is extremely good at predicting a food’s insulin index. (In other words, a low GI food has a low insulin index value and a high GI food has a high insulin index value.) There are some instances, however, in which a food has a low GI but a high insulin index value. This applies to dairy foods and to some highly palatable, energy-dense ‘indulgence foods’. Some foods (such as meat, fish and eggs) that contain no carbohydrate, just protein and fat (and have a GI of essentially zero), still stimulate significant increases in blood insulin. We don’t currently know how to interpret this type of response for long-term health. It may be a good outcome, because the increase in insulin has contributed to the low level of glycemia. On the other hand, it may be less than ideal, because the increased demand for insulin contributes to beta-cell ‘exhaustion’ and the development of type 2 diabetes. Until studies are carried out to answer these types of questions, the glycemic index remains a proven dietary tool for predicting the effects of food on health.

GI testing by an accredited laboratory
North America
Dr Alexandra Jenkins
Glycemic Index Laboratories
20 Victoria Street, Suite 300
Toronto, Ontario M5C 298 Canada
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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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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
Contact email (for questions or permission to reproduce stories from this newsletter): info@gisymbol.com for technical problems or faults please contact smb.ginewstech@sydney.edu.au

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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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