Nutrition Masterclass

In this short video, John Pemberton, Head Coach at the Diabetic Muscle and Fitness Online Coaching Academy covers the 10 key nutrition principles for successful body transformation. These include…

1. Calculate energy requirements when gaining mass or shredding fat.

2. Protein intake over the day that hits the optimal zone of 1.4 – 2.2g/kg (0.7 – 1.0g/lb).

3. Protein spread out equally over four to five meals a day for maximum muscle protein synthesis.

4. Meal macronutrient consistency to ensure accurate insulin dosing for type 1 diabetes, and stable after-meal glucose levels for type 2 diabetes.

5. Meal protein sources high in all the essential amino acids needed for optimal muscle growth, especially Leucine at a dose of 3g per meal.

6. Monounsaturated fat is the primary source of dietary fat to ensure the least insulin resistance, and to promote heart health.

7. Oily fish to provide with plenty of Omega-3 fats.

8. High intake of various fruit and vegetables to flood your body with vitamin, minerals, polyphenols and anti-oxidants.

9. Promote a healthy microbiome (your gut) by including plenty of pre-biotic fibre, fermented foods, soluble fibre and other vital nutrients.

10. Enough carbohydrate to fuel gym sessions, but not too much to cause blood glucose issues.

• Very little insulin is needed for the fructose part of the fruit.
• The insulin determined by the insulin to carbohydrate ratio is too much for fruit only, as there is no fat and protein.

EVERYTHING YOU NEED TO KNOW ABOUT EATING FRUIT AND BALANCING YOUR BLOOD SUGARS

Ever wondered why you go hypoglycemic after eating fruit and delivering the insulin needed for the carbohydrate?

Ever wondered why pineapples and bananas need more insulin that apples and cherries?

This used to catch me out ALL THE TIME!

I would have a healthy fruit snack, usually, a couple of apples (30g carb), apply my ratio (1u:15g), deliver the insulin (2 units) and BANG – in 90 minutes I was HYPOGLYCAEMIC!

Has this ever happened to you?

How frustrating is it?

Has it put you off choosing fruit?

If it has, this article is a MUST READ for you.

In less than 5 minutes you will discover the two main reasons why this happens and what to do about it. So focus, get your thinking cap on, land let’s get stuck in.

FRUCTOSE AND GLUCOSE HAVE DIFFERENT EFFECTS ON BLOOD SUGAR

Fructose is metabolized differently to glucose; therefore, its insulin requirements are very different.

Fructose is the main source of carbohydrate found in fruit, especially grapefruit. However, some fruits like pineapple have glucose as their main source of carbohydrate.

How do you know which fruits contain more glucose or fructose?

The easiest way to find out is using the glycaemic index tables.

Very simply:

• The lower the glycaemic index of a fruit, the higher the fructose content.
• The higher the glycaemic index of a fruit, the lower fructose content.

Why is it important to know if the fruit is mainly fructose or glucose?

Fructose gets taken up by the liver ONLY (not the muscles).

This process DOES NOT REQUIRE INSULIN.

In the liver, fructose is converted into glucose for immediate energy use and further stored as glycogen when there isn’t an immediate energy demand. When glycogen stores are full, fructose can be converted into fat by a process called lipogenesis.

RANT: FRUIT SUGAR DOES NOT CAUSE OBESITY

Just because fructose can be converted into fat doesn’t mean fruit WILL MAKE YOU FAT.

You will only gain body fat when you over consume calories and remain inactive for prolonged periods of time.  Keep it simple – DON’T OVEREAT IN THE FIRST PLACE, and enjoy all the health benefits of fruit:

• Vitamins and minerals
• Anti-oxidants
• Fibre
• lovely natural sweet taste

It just riles me when people say fruit makes you fat due to fructose.

This is an incorrect statement often played upon by the media who has at best, have a very limited understanding. I highly recommend reading this article WHY HEALTH NEWS IS ALMOST ALWAYS WRONG!

Overeating makes you fat – respect the principle of energy balance.

Moving on…

Why do you go hypoglycaemic if you deliver insulin for fructose?

After digestion, fructose goes straight to the liver and is taken up without the need for insulin.

Fruits with a low glycaemic index provide very little glucose into the peripheral blood stream. Therefore, the insulin you have just delivered is surplus to your requirements, resulting in a rapid decline in your blood sugar levels.

The best solution for this is to lower your insulin dose when eating fruit on its own.

Besides the fact fructose has a minimal effect on blood glucose levels we need to consider another important factor.

Even though you didn’t know…

The Insulin to carbohydrate ratio actually covers the usual fat and protein of mixed meals.

There has been a raft of evidence over the last four years that have proved this unique insight. The insulin you deliver for a meal, that is determined by counting the carbs, actually also covers the glucose-raising effect of your usual protein and fat amounts (1).

So, what’re the issues when delivering insulin for fruit?

Fruit has no fat and protein.

Therefore, when you eat carbohydrate only, the insulin to carbohydrate ratio is too strong. Too much insulin is delivered and a hypo is very likely. This happens for a lot of just carb only snacks like:

• Cereal bars
• Fruit
• Vegetable sticks

That’s why most people’s insulin to carb ratio for snacks is much less aggressive than meal times.

It’s not because you are less sensitive to insulin at that time. But, due to the fact there is very little fat and protein in those snacks, so less insulin is required.

Sound familiar? Are you are starting to see there is a double whammy?

EATING FRUIT AND MANAGING DIABETES

I have tried a few that have been successful for me and people I coach; they might work for you.

If eating fruit only snacks, a great question to ask is this…

Is it a low GI fruit (high fructose)?

If NO (pineapple, raisins, banana).

Work out the insulin dose and take off 25% because there is no fat and protein.  For example, if I eat a banana (20g) with tablespoon raisins (10g).

Then I apply my ratio (1u:15g) to work out the dose (2units), then deduct 25% (0.5units) and bolus that (1.5units).

If YES, (apples, cherries, oranges).

Work out the insulin dose and take off 50% because the fruit is mainly fructose and there is no fat and protein.

If I eat an apple (15g) and orange (15g). Then I apply my ratio (1u:15g) to work out the dose (2units), then deduct 50% (1.0units) and bolus that (1.0units).

If eating fruit with a meal, then just count it all, as there will be fat and protein in the meal and there are so many other variables.  It’s not worth considering in mixed meals, IMO.

This may be worth giving a try if you have had issues with going hypo after blousing for fruit.

As always, please remember to run this idea past your medical team.

If you want to take your knowledge, skills, and strategies to the next level then you should seriously consider checking out my two courses inside the training lab on how you can perfect your insulin dosing strategy. The two courses are called:

Become a Bolus Wizard.

The Definitive Guide to Insulin Dosing for Carbohydrate, Fat, and Protein.

Be warned, the knowledge and strategies inside these courses will elevate your skills to a level way higher than 99% of diabetes teams. You may end up teaching your diabetes team a thing or two.

References

1. https://www.ncbi.nlm.nih.gov/pubmed/25998293

• 3000 words – 30 min read.

Key Points

• Artificial sweeteners do not increase blood glucose levels.
• The safety of artificial sweeteners compounds in use is supported by numerous international agencies and scientists in the field.
• Artificial sweeteners support fat loss and are a suitable replacement for calorically sweetened beverages/foods.

Artificial Sweeteners and Diabetes: The Ultimate Guide

If you spend any time on social media or reading about nutrition and health online, then you’ve likely seen the hysteria:

• “artificial sweeteners will give you cancer!”
• “aspartame will kill your brain cells!”
• “artificial sweeteners trick your brain into releasing insulin and spiking your blood glucose!”

And these are just gen pop headlines, what about for someone like you – a diabetic?

If there is even a shred of truth in there, what could this mean for both your blood sugar management and long-term health?

Are artificial sweeteners just thrown into the food supply in some conspiracy between governments and the food industry?

Does anyone actually care whether they’re safe or not?

Fortunately, we do: and we’ve cut through the BS to see what the science really says, and to give you the right advice for using artificially sweetened products safely and effectively.

So, leave the “internet guru” nutrition nonsense you’ve heard at the door, and let’s get into this…

Role of Artificial Sweeteners and Global Use in the Food Supply

Non-nutritive sweeteners have become really popular within the food industry as a strategy to help reduce the energy content of popular foods and drinks, in particular from sugar-sweetened beverages, across the population (1).

Note the term ‘non-nutritive’ above: this term covers both synthetically derived artificial sweeteners (AS), like aspartame, and naturally derived non-caloric sweeteners, like stevia. This article will focus on AS, in particular aspartame, acesulfame-K, sucralose, and saccharin, as they are the predominant non-nutritive sweeteners in use (2).

AS have unique and distinct qualities due to their chemical differences, and each individual compound varies in potency of sweetness, sweetness duration, mouth feel, and aftertaste (3). This allows the food industry to be quite flexible with the type of taste it wants from a product, and it’s also likely why some people love Coke and some love Pepsi.

Each AS also possesses unique pharmacokinetic profiles – how it is absorbed, distributed throughout the body, metabolised, and ultimately excreted – that means when we assess the health effects of AS, we give individual consideration to each one (3). So, where appropriate throughout, this article will refer specifically to the particular AS in question, not simply the overall category.

Why use AS?

Simply, AS provide an alternative to sugars commonly used in the food supply – sucrose in Europe or high-fructose corn syrup in the US – allowing the food industry to maintain palatability in a given product, without compromising on the sweetness which gives a product a particular quality (4). They are characterised by contributing little to no calories, while having a sweetness potency of greater intensity than sugar (3).

Concerns over sugar consumption in the population have led to an expansion of the food produce containing AS. Historically, diet carbonated beverages have represented the product category with most common AS use, a fact which corresponds to this category being the most significant contribution of AS consumption at a population level (4).

However, specific product categories – in particular waters and yogurts – have a significant proportion of their market share in artificially sweetened versions (4). And AS use is now extending into low calorie alternatives to ice-cream, jams, syrups, grain products, and bars (4). The global market for AS products is projected to reach 2.2 billion by 2020, reflecting a strong consumer shift toward lower calorie or non-caloric alternatives to common food products (4).

However, despite significant research into these compounds, and ongoing safety monitoring programs by the European Food Standards Agency [EFSA; or the Food and Drug Administration in the US], there remain concerns voiced over the safety and efficacy of AS.

Of particular concern to diabetics is the suggestion that AS in fact stimulate blood glucose and insulin responses. Let’s look at that in more detail.

Effects of Artificial Sweeteners on Blood Glucose and Insulin

The concerns in relation to the potential impacts of AS on diabetes arise from some observational studies which found associations between high intake of AS and Type-2 diabetes (5;6).

However, an explanation for this observation is “reverse causality”. What this means is that people who are at high risk of diagnoses, are overweight and/or obese, and with a poor quality, high-calorie diet, are more likely to consume a lot of AS products (1). Basically, “I’ll have a Diet Coke” says the pre-diabetic who just ordered the KFC family bucket.

Thus, we need to look at controlled interventions assessing the potential impact of AS on relevant parameters of blood glucose regulation and insulin.

How might AS lead to increases in blood glucose and insulin? There are two suggestions offered.

The first is that the intense perception of sweetness alters insulin responses, in anticipation of a glycaemic response.

The second is that sweet-taste receptors in the intestinal lining are activated by AS, which increases glucose uptake from the digestive tract.

The AS sucralose has recently caused some eyebrow-raising in research. Prior to the EFSA, the Scientific Committee on Food [SCF] of the European Union undertook a review of sucralose. One trial included was a 6-month study in Type-2 diabetics which found that HbA1c was elevated above baseline in subjects administered 667mg sucralose daily (7).

However, there were no observed impacts on insulin or blood glucose levels, and thus the increase in HbA1c is difficult to reconcile as it occurred in the absence of impacts on other parameters of blood glucose regulation (7). In addition, the dose used in the trial significantly

exceeded even the highest levels of population consumption, and the SCF concluded that any potential effect would be minimal to the point of being clinically insignificant (7).

A recent trial in subjects with morbid obesity yet normal insulin sensitivity – which was assessed by HOMA-IR – found that pre-loading subjects with 48mg sucralose [a realistic dose] 10-minutes before an oral glucose tolerance test with 75g glucose led to a greater insulin response and peak plasma glucose levels (8).

However, both glucose and insulin responses were both within normal range for an OGTT, and the actual difference between the control group and sucralose group was nominal, again suggesting no material clinical significance to the finding (9).

The couple of trials suggesting some glycaemic interaction notwithstanding, multiple studies have assessed sucralose and glycaemic responses and this AS is generally considered to have no impact on carbohydrate metabolism (10). In particular, a trial that assessed the effects of 1,000mg sucralose – an enormous dose – on glucose homeostasis in both Type-1 and Type-2 diabetics found no effect on blood glucose levels in either group (11).

It’s important be aware of the fact that any of the positive findings in studies on different AS suggesting an impact on glucose metabolism may be a reflection of the trial design, not necessarily a clinically relevant finding. For example, the use of a placebo – like water –  to compare to AS may lead to misleading findings when AS are designed to substitute for sugar, so a comparison with a caloric sweetener would arguably be a more appropriate design (1).

The reason for this is that, if we assume for one second that AS do in fact stimulate glucose uptake, this would occur in the presence of low concentrations of glucose in the gut (12). Conversely, a caloric sweetener would obviously result in greater glucose absorption from the digestive tract (12).

Given the specific purpose of AS is to substitute for the effects of sugar, not a benign placebo like water, this would arguably present a truer comparison of glycaemic effects. It could provide an explanation for the fact that in trials finding an impact of AS on glycaemic and insulin responses, the differences between intervention and placebo – often water – are in fact nominal, to the point of clinical insignificance (7;13).

In relation to sucralose specifically, it should be noted that the two trials cited above excepted, the majority of studies have found no effect on blood glucose levels (9).

A recent systematic review including 28 trials looking at the effects of different AS – including aspartame, saccharin, sucralose, and acesulfame-K – on glucose metabolism confirmed this overall position: the majority of trials have found no effect, while certain trials have concluded AS do impact on glucose metabolism (9).

The wide variability in characteristics of subjects, the particular AS used, the placebo issue, and the outcomes assessed, limits comparisons between studies (9). So, we need to take a closer look at the second issue identified above, that the underlying mechanism is the activation by AS of glucose transporters in the gut, in turn stimulating glucose uptake and insulin responses.

In particular, it has been suggested that AS activate glucagon-like peptide-1 [GLP-1], which itself stimulates insulin release and mediates glucose uptake from transporters in the gut (12;14). In a systematic review which included 11 studies that measured GLP-1, 1 study found a decrease in GLP-1 from aspartame while 2 found increases (9). What is interesting, however, is that neither measurable parameters of satiety nor subjective measures of appetite have been found to be influenced: this is interesting because increases in GLP-1 typically reduce appetite and delay gastric emptying (12;14).

This calls into question the clinical significance of the findings in a handful of studies of increased GLP-1 concentrations.

Trial design may again be an issue in the studies finding positive effects of AS on GLP-1. For example, a controlled trial in healthy subjects using a diet soda containing a combination of 46mg sucralose and 26mg acesulfame-K found an increase in GLP-1 in response to an oral glucose tolerance test after diet beverage administration, compared to water (15).

However, in the first instance the use of an oral glucose tolerance test is an issue, as glucose itself would activate GLP-1 and thus the increased GLP-1 levels in the diet beverage group may reflect the influence of other factors. In particular, the trial failed to control for other compounds in the diet beverage – citric acid, potassium citrate, phosphoric acid, potassium benzoate, and colourings – that could have influenced the results (15).

A subsequent trial addressed this limitation by administering only the AS themselves, and neither 52mg sucralose, 200mg acesulfame-K, or a combination of 46mg sucralose and 26mg acesulfame-K [the dose used in the aforementioned trial] were found to have any effect on insulin concentrations, blood glucose, or GLP-1, in healthy subjects (16).

In assessing the cumulative body of evidence assessing the impact of AS on GLP-1, 2 trials have found increased GLP-1 but it is important to note that these findings have occurred in the absence of any other impacts on insulin or blood glucose (17).

Also bear in mind that in one of the studies, the impact on GLP-1 from sucralose ingestion was only observed in healthy controls, not in subjects with T2DM (17).

Other interventions (16;18), and a systematic review including 11 studies that measured GLP-1 (12), taken together indicate that the majority of human trials have found no impact of AS on intestinal sweet-taste receptors and glucose uptake. As yet, no biological basis has been established to explain the findings of the limited number of studies showing such effect in humans (12).

Another factor that calls into question the studies finding positive associations is the relationship between GLP-1 and insulin, as increased GLP-1 stimulates insulin secretion and activation of sweet-taste receptors signals for insulin release (12;14). One of the studies which reported an increase in GLP-1 levels also found no effect on insulin (17).

Multiple studies in Type-2 diabetics have failed to find any impact on insulin (12;19;20;21). More particularly, trials that compare AS to a caloric sweetener, like sucrose [table sugar] have found an effect only from the sugar (12;17;22).

In a systematic review of studies assessing the impact of AS on glucose metabolism, of the included 14 studies which measured insulin, none found a negative impact of AS (9).

A significant criticism of this area of research has been that some authors have overreached on data from in vitro and animal model studies to make speculative assumptions on the effects of AS on sweet-taste receptors, insulin, and glucose homeostasis (12).

The majority of the research finding particular effects amounts to identification of potential mechanisms in vitro or in animal models, and there is limited human data supporting these findings. Indeed, the evidence for any direct effect of AS on glycaemic control is limited (1).

The weight of evidence suggests AS do not adversely impact on blood glucose regulation.

Artificial Sweeteners: Myths and Truths

And this is where we come to the real hysteria about AS, the kind you see on some naturopath’s blog, in particular that AS are carcinogenic, and neurotoxic.

Let’s deal with these briefly in turn.

Before we even get into those, I think it’s helpful to explain that these compounds are not simply unleashed on the population as some Orwellian experiment. There is ongoing toxicology monitoring for all of the AS in use, and a regulatory framework in which they are approved for use.

Because they have potential for high consumption in the population, AS are designated a high concern level: this means that there are specific directions for the design of toxicology studies to be carried out (3;8). Animal toxicology studies are designed to elicit a response and assess toxicity thresholds, but also for the potential for lower doses to impact on reproduction, development, cancer, genetic mutations, and the immune system (3).

Based on these toxicology studies, a threshold known as the ‘No Observable Adverse Effect Level’ [the NOAEL] is set, and this is the lowest dose at which any toxic effects were found in the animal studies (23). The Acceptable Daily Intake [ADI] is then set by dividing the NOAEL by an “uncertainty factor” of 100. This ultimately results in a highly conservative assessment of safety thresholds, factoring in anticipated concentrations of a given AS in food and beverages, compared to population levels of intake of those foods and drinks (23).

For some context, the NOAEL for the AS aspartame is set at 4g per kilogram of bodyweight per day, based on long-term toxicology studies (8;23). By dividing that by the uncertainty factor, the ADI was set at 40mg/kg, and actual average intake of aspartame is 4mg/kg (24;25).

To reach the ADI, a 60kg adult would have to consume 4L of beverages sweetened with the maximum amounts of aspartame permitted by regulation (23).

And in reality this cannot even happen, because recall that the permitted thresholds are set based on data on population consumption, thus no one food or drink contains the maximum level of any AS. Even the subsets of the population consuming the highest levels of aspartame consume 10mg/kg, i.e., the very highest levels of consumption observed in the population are still consuming only 30% of the ADI (24;25).

The European Union has ongoing toxicology monitoring programs, and in 2009 mandated that every AS in use be subject to full revaluation of toxicology and technical data (26). There is often a cynical view of AS expressed by some in relation to the efficacy of such programs, and the safety of AS.

I would highlight that to date, the EU’s toxicology monitoring has resulted in over 1,300 compounds being banned from use in personal care and cosmetic products, based on even preliminary evidence of toxicity (26).

An unbiased assessment of the regulatory framework in which AS are assessed and approved for use would see a well-regulated and ongoing consideration of safety, which acknowledges that there is always a degree of uncertainty where animal studies inform long-term human risk.

It’s important to understand the toxicology assessment framework in order to put to bed most of the myths generated about effects on the brain or cancer. All studies showing neurotoxic potential are in such animal studies.

As an example of where Internet-hysteria is generated, a recent study examined the neurotoxic potential of aspartame in rats using doses of 500mg/kg to 1,000mg/kg (27).

This experimental dose is 2,400% times greater than the ADI for aspartame, and thus of zero relevance to both typical population levels of consumption and established safety thresholds.

The same can be said for carcinogenicity. No significant relationship has been observed between aspartame at various experimental doses and tumour occurrence in meta-analysis of animal toxicology studies (28), which is consistent with observational evidence in humans (23).

Acesulfame-K was reviewed by the EU in 2009 and concluded to be safe, even for use in pregnancy and infancy, and in particular that concerns over carcinogenicity were unsubstantiated (29;30).

Sucralose is considered to have a strong safety profile, and a review of toxicology studies found no evidence of carcinogenicity either in long-term animal models or in studies in humans (31). Saccharin is also non-carcinogenic in human studies (32;33).

Ultimately, when it comes to the safety of AS across important health outcomes – from neurology to cancer – the safety of the various AS compounds in use is supported by numerous international agencies and scientists in the field (2).

Possible Considerations for People with Diabetics

The first and most relevant question is: are AS going to negatively impact on your blood glucose regulation?

And can AS beverages and foods be used in the context of blood glucose management safely in lieu of calorically sweetened products?

The answer to the former, based on the majority of human research, is no: use of AS beverages or foods will not negatively impact on insulin or blood glucose regulation.

The answer to the latter, is yes: substituting calorically sweetened beverages/foods for non-calorically AS sweetened can be a useful means of maintaining adherence and palatability in diabetics, a position supported by the National Academy of Nutrition and Dietetics (34).

The considerations, therefore, are more contextual. AS products should not displace overall diet quality:

they are simply “less unhealthy” versions of their calorically-sweetened cousins and cannot be said to be contributing to improved health as much as providing a sweet alternative.

However, that is the context in which you should feel comfortable in using them. Put this way: sugar-sweetened drinks are strongly associated with diabetes risk and profoundly impact on blood sugar levels. We are all human, and we want to be able to have some highly palatable, sweet foods. For you as a diabetic, the most important variable is staying on top of blood sugar management. So, if some AS products allow you to consume some sweet stuff, without negatively impacting on your blood glucose, then that is a positive – and the purpose for which they should be incorporated into your life.

Also, be mindful to avoid the pitfall of increasing calorie intake from other sources on the assumption that consuming AS products creates some leeway in this respect: if you’re looking to improve body composition, energy balance still matters!

And finally, consider the caffeine content of artificially sweetened drinks, particularly energy drinks, as caffeine can increase blood glucose levels and reduce insulin sensitivity (35;36).

Let’s put this all into a hierarchy of needs and quality, from drinks that can materially add to or improve your health, to one’s that won’t:

1. Water: obviously vital, and still the No.1 hydration agent.
2. Tea’s and coffee: careful not to exceed 400mg caffeine (or 200mg if pregnant). Tea’s and coffee were once believed to be dehydrating: that’s broscience. They can contribute to hydration.
3. AS beverages: be wary of caffeine content and keep to an absolute maximum of 1-2L per day (because higher levels inevitably mean displacing water and other health-promoting non-caloric products like green tea or coffee.
4. Sugar-sweetened beverages: ideally ZERO. They contribute nothing, and you can get your sweet hit from the AS version of your favourite product, i.e., the purpose for AS are used! So, use them.

So, there’s some truth on AS. Use them instead of sugar, not diet quality. And don’t believe the scaremongering: it doesn’t stand up to scrutiny.

References

1. Gardner, C. (2014). Non-nutritive sweeteners. Current Opinion in Lipidology, 25(1), pp.80-84.
2. Lohner, S., Toews, I. and Meerpohl, J. (2017). Health outcomes of non-nutritive sweeteners: analysis of the research landscape. Nutrition Journal, 16(1).
3. Roberts, A. (2016). The safety and regulatory process for low calorie sweeteners in the United States. Physiology & Behavior, 164, pp.439-444.
4. Sylvetsky, A. and Rother, K. (2016). Trends in the consumption of low-calorie sweeteners. Physiology & Behavior, 164, pp.446-450.
5. Nettleton, J., Lutsey, P., Wang, Y., Lima, J., Michos, E. and Jacobs, D. (2009). Diet Soda Intake and Risk of Incident Metabolic Syndrome and Type 2 Diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care, 32(4), pp.688-694.
6. Hu, F. and Malik, V. (2010). Sugar-sweetened beverages and risk of obesity and type 2 diabetes: Epidemiologic evidence. Physiology & Behavior, 100(1), pp.47-54.
7. Scientific Committee on Food of the European Commission. Opinion of the Scientific Committee on Food on sucralose. SCF/CS/ADDS/EDUL/190 Final 12/9/2000.
8. Pepino, M., Tiemann, C., Patterson, B., Wice, B. and Klein, S. (2013). Sucralose Affects Glycemic and Hormonal Responses to an Oral Glucose Load. Diabetes Care, 36(9), pp.2530-2535.
9. Romo-Romo, A., Aguilar-Salinas, C., Brito-Córdova, G., Gómez Díaz, R., Valentín, D. and Almeda-Valdes, P. (2016). Effects of the Non-Nutritive Sweeteners on Glucose Metabolism and Appetite Regulating Hormones: Systematic Review of Observational Prospective Studies and Clinical Trials. PLoS One, 11(8), p.e0161264.
10. Brown, R. and Rother, K. (2012). Non-Nutritive Sweeteners and their Role in the Gastrointestinal Tract. The Journal of Clinical Endocrinology & Metabolism, 97(8), pp.2597-2605.
11. Mezitis, N., Maggio, C., Koch, P., Quddoos, A., Allison, D. and Pi-Sunyer, F. (1996). Glycemic Effect of a Single High Oral Dose of the Novel Sweetener Sucralose in Patients With Diabetes. Diabetes Care, 19(9), pp.1004-1005.
12. Renwick, A. and Molinary, S. (2010). Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release. British Journal of Nutrition, 104(10), pp.1415-1420.
13. Grotz, V. and Jokinen, J. (2014). Comment on Pepino et al. Sucralose Affects Glycemic and Hormonal Responses to an Oral Glucose Load. Diabetes Care 2013;36:2530–2535. Diabetes Care, 37(6), pp.e148-e148.
14. Grieve, D., Cassidy, R. and Green, B. (2009). Emerging cardiovascular actions of the incretin hormone glucagon-like peptide-1: potential therapeutic benefits beyond glycaemic control?. British Journal of Pharmacology, 157(8), pp.1340-1351.
15. Brown, R., Walter, M. and Rother, K. (2009). Ingestion of Diet Soda Before a Glucose Load Augments Glucagon-Like Peptide-1 Secretion. Diabetes Care, 32(12), pp.2184-2186.
16. Steinert, R., Frey, F., Töpfer, A., Drewe, J. and Beglinger, C. (2011). Effects of carbohydrate sugars and artificial sweeteners on appetite and the secretion of gastrointestinal satiety peptides. British Journal of Nutrition, 105(09), pp.1320-1328.
17. Temizkan, S., Deyneli, O., Yasar, M., Arpa, M., Gunes, M., Yazici, D., Sirikci, O., Haklar, G., Imeryuz, N. and Yavuz, D. (2014). Sucralose enhances GLP-1 release and lowers blood glucose in the presence of carbohydrate in healthy subjects but not in patients with type 2 diabetes. European Journal of Clinical Nutrition, 69(2), pp.162-166.
18. Ma, J., Chang, J., Checklin, H., Young, R., Jones, K., Horowitz, M. and Rayner, C. (2010). Effect of the artificial sweetener, sucralose, on small intestinal glucose absorption in healthy human subjects. British Journal of Nutrition, 104(06), pp.803-806.
19. Grotz, V., Henry, R., McGill, J., Prince, M., Shamoon, H., Trout, J. and Pi-Sunyer, F. (2003). Lack of effect of sucralose on glucose homeostasis in subjects with type 2 diabetes. Journal of the American Dietetic Association, 103(12), pp.1607-1612.
20. Nauck, M., Niedereichholz, U., Ettler, R., Holst, J., Ørskov, C., Ritzel, R. and Schmiegel, W. (1997). Glucagon-like peptide 1 inhibition of gastric emptying  outweighs its insulinotropic effects in healthy humans. American Journal of Physiology-Endocrinology and Metabolism, 273(5), pp.E981-E988.
21. Horwitz, D., McLane, M. and Kobe, P. (1988). Response to Single Dose of Aspartame or Saccharin by NIDDM Patients. Diabetes Care, 11(3), pp.230-234.
22. Abdallah, L., Chabert, M. and Louis-Sylvestre, J. (1997). Cephalic phase responses to sweet taste. The American Journal of Clinical Nutrition, 65(3), pp.737-743.
23. Marinovich, M., Galli, C., Bosetti, C., Gallus, S. and La Vecchia, C. (2013). Aspartame, low-calorie sweeteners and disease: Regulatory safety and epidemiological issues. Food and Chemical Toxicology, 60, pp.109-115.
24. Mortensen, A. (2006). Sweeteners permitted in the European Union: safety aspects. Food & Nutrition Research, 50(3).
25. Magnuson, B., Burdock, G., Doull, J., Kroes, R., Marsh, G., Pariza, M., Spencer, P., Waddell, W., Walker, R. and Williams, G. (2007). Aspartame: A Safety Evaluation Based on Current Use Levels, Regulations, and Toxicological and Epidemiological Studies. Critical Reviews in Toxicology, 37(8), pp.629-727.
26. REGULATION (EC) No 1333/2008 OF THE EUROPEAN PARLIAMENT AND OF THE COUNCIL of 16 December 2008 on food additives.
27. Abhilash, M., Sauganth Paul, M., Varghese, M. and Nair, R. (2012). Long-term consumption of aspartame and brain antioxidant defense status. Drug and Chemical Toxicology, 36(2), pp.135-140.
28. Mallikarjun, S. and Sieburth, R. (2013). Aspartame and Risk of Cancer: A Meta-analytic Review. Archives of Environmental & Occupational Health, 70(3), pp.133-141.
29. Regulation (EC) No 1223/2009 of the European Parliament and of the Council of 30 November 2009 on cosmetic products.
30. Statement of EFSA on the scientific evaluation of two studies related to the safety of artificial sweeteners. (2011). EFSA Journal, 9(2), p.2089.
31. Berry, C., Brusick, D., Cohen, S., Hardisty, J., Grotz, V. and Williams, G. (2016). Sucralose Non-Carcinogenicity: A Review of the Scientific and Regulatory Rationale. Nutrition and Cancer, 68(8), pp.1247-1261.
32. Shankar, P., Ahuja, S. and Sriram, K. (2013). Non-nutritive sweeteners: Review and update. Nutrition, 29(11-12), pp.1293-1299.
33. Gallus, S., Scotti, L., Negri, E., Talamini, R., Franceschi, S., Montella, M., Giacosa, A., Dal Maso, L. and La Vecchia, C. (2006). Artificial sweeteners and cancer risk in a network of case-control studies. Annals of Oncology, 18(1), pp.40-44.
34. Fitch, C. and Keim, K. (2012). Position of the Academy of Nutrition and Dietetics: Use of Nutritive and Nonnutritive Sweeteners. Journal of the Academy of Nutrition and Dietetics, 112(5), pp.739-758.
35. Greer, F., Hudson, R., Ross, R. and Graham, T. (2001). Caffeine Ingestion Decreases Glucose Disposal During a Hyperinsulinemic-Euglycemic Clamp in Sedentary Humans. Diabetes, 50(10), pp.2349-2354.
36. Keijzers, G., De Galan, B., Tack, C. and Smits, P. (2002). Caffeine Can Decrease Insulin Sensitivity in Humans. Diabetes Care, 25(2), pp.364-369.

HOW TO STOP BINGE EATING & GAINING UNWANTED BODY FAT

Binge eating can be a problem for many people, but with diabetes in the mix as well, it can cause havoc with glucose levels, insulin dosing, not to mention weight gain. It often leaves people feeling out of control, frustrated and depressed.

Binge eating can occur in a number of ways: for some, there might be a really strong urge to eat things you perceive as “bad” for you; for others, it might start with one small “bad” food, which then quickly spirals out of control.

Binge eating is defined by the consumption of large amounts of food over a relatively short period of time – but, of course, this is subjective. What constitutes a binge for one person, might be a perfectly normal small snack for someone else. There’s also a big difference between the occasional over-eating episode, and full-blown binge eating disorder. Essentially, if binge-eating is impacting your weight, mood or diabetes control, it’s probably worth doing something about it.

Identifying Triggers

Log what happens before, during, and after a binge. If you can figure out what is causing you to overeat, you can manage it more effectively.

There are a number of common triggers, these include:

• Physiological Triggers: Hypoglycemia, food restriction, cravings, starvation.
• Behavioural Triggers: Environment, routine and habits.
• Emotional Triggers: Stress, anxiety, low mood, conflict, loneliness.

It may take a while before you can identify the cause of your binge eating. There might even be a number of different triggers responsible.

When a binge occurs ask yourself the following questions in as much detail as possible. Take a note as soon as it occurs – somewhere easily accessible like your phone, computer or in a notebook is ideal.

1. What is the Antecedent (trigger)? Where were you? What were you doing? Who did you last speak to? What emotions were you feeling? When did you last eat?
2. What is the Behaviour? What happened? What did you eat? How did it start? How did it stop?
3. What was the Consequence? How did you feel afterwards? What did you do? Did it help?

Try to record this, as soon as you can, so that it’s as accurate as possible, and then see if there are any obvious patterns.

Why Can’t I stop it?

One of things about binge eating that most people struggle with is the internal battle of really wanting it to stop, but not being able to control it. At the end of the day, the binge eating serves a purpose. If it is in response to physiological triggers (hypoglycemia, starvation and food restriction), it gets the body calories and fuel that it thinks it needs. If it’s a response to emotional factors, food tends to make us feel better (at least in the short term).

Changing What You Do

Often, people end up in cycles of binge eating and it becomes a habit. I regularly hear clients and patients say “why can’t I just stop?”. The idea that we don’t have control over their behaviour is frustrating and often bewildering, but we are all human, and habits and patterns of behaviour save us energy by giving us a shortcut. You probably get ready in the morning in the same way each day – why? It means your brain doesn’t have to think about it every time and it can use that energy for something else. It’s pretty clever really, but as a result, it takes more effort to change that pattern and fight against going the easy way. Imagine you’re stood at the edge of a field of really high grass, and there is one perfectly worn path straight through the middle. Are you going to walk up that path, or try to awkwardly trample a different route? Your brain will take you up the well-worn path. Your job is to trample a new one, again and again, until that one becomes the obvious route and the other one becomes overgrown.

For example, I always end up eating stuff I shouldn’t when I go food shopping on the way home from work. Inevitability, I am marginally hungry and a bit stressed from a busy work day, so I want something to make me feel better. I can often make poor food choices, and end up mindlessly overeating chocolate on the drive home without really noticing it. Consequently, I feel awful about it, my blood glucose levels go high, I then get annoyed that I’ve ruined my control.

So, how have I managed this behaviourally?

Firstly, I don’t go food shopping after work anymore. This is a MASSIVE inconvenience. However, it stops me overeating, so in my eyes – it’s worth it. I have also set myself a personal rule not to eat in the car. I ensure I have something healthy to eat when I finish work, even if I’m not hungry. I also never shop for food when I am hungry! All these small behavioural changes interrupt my pattern of eating on the way home, and stop me overeating at what is (for me) the most vulnerable time.

There are loads of ways you could change your behaviour to interrupt these patterns, regardless of where you are or what you are doing. Bill O’Hanlon uses a good example in his book, Do One Thing Different (1999), where he describes a woman who would put on her favourite pair of shoes before starting to binge eat. This might seem ridiculous, but it’s all about breaking the pattern and shifting your attention in these moments rather than just going to autopilot and following the usual pattern.

Another trick is to do something that you absolutely cannot do if you are eating, for example, it’s pretty hard to sing whilst eating (and it would be a bit gross.) Other ideas could be to paint your nails (I’m pretty much incapacitated when my nails are wet, and I certainly won’t be ruining them by shoving my hand in a bag of crisps), playing a musical instrument, brushing your teeth, chewing gum, calling a friend, etc. Find a strategy that works for you. Check out Phil’s article for more ideas about managing your environment.

Emotional Eating

The first issue of emotional eating is recognising that it is emotional eating, but doing a few ABC examples above should help you recognise it. Here are a few ideas to help you overcome emotional eating:

1. Be mindful of what you are eating. Don’t multitask when you’re eating – turn off the TV, don’t eat when you’re driving, turn off the computer, put down your phone. Sit down to eat, eat on a plate – even if it’s a small snack. If you think you are going to binge, at least do it mindfully. Say to yourself (aloud, if appropriate) “I am choosing to eat this piece of cake”; make it a decision and take responsibility for that decision.  You’re more likely to feel in control of your eating, and therefore able to stop when you want to.
2. Address the stress! Eating might make you feel better temporarily, but if you look at what is causing the difficult emotion in the first place, you’re likely to be far better off in the long run. Have a read of this article for more information on stress management.
3. Acknowledge the emotion that you are feeling. Before reaching for the biscuits, ask yourself what is actually going on, and sit with it. This is easier said than done – loads of people struggle with tolerating negative or difficult emotions, and eating can be a great distraction for this. But, if after you’ve eaten you then have a load more negative emotions about your emotional eating or rising glucose levels, you’re going to be stuck in a tricky cycle. Take yourself off somewhere you feel safe, and actually let yourself feel whatever your feeling. This can be really hard if you are someone who usually squashes or avoids their emotions, so practice with less intensive situations. For example, if someone annoys you at work, go home and think about it. Write out what you’re thinking, feeling and where you feel it in your body…then let it go.
4. Be nice to yourself in other ways. Emotional eating can go both ways; having a great day could lead to “I deserve chocolate for doing so well” just as easily as “I deserve chocolate because I feel so bad”. Unfortunately, many children and adults have grown up being both rewarded and consoled with food (“you were so good at the dentist, you can have ice cream!”) and this can be a tough habit to break. Explore other things, that make you feel better, but which aren’t food-related, as well as identifying things that you can reward yourself with when you deserve it.

Binge eating can be challenging to overcome due to the interaction of its emotional, physiological, behavioural and cognitive aspects, but it can be done. Don’t give up – you will inevitability slip up, just keep going with it. You’re not going to tread a new path on the first attempt.

Key messages:

1. Log your eating and binge patterns. If you don’t know what’s going on, it’s going to be difficult to know what to do about it.
2. Do something different and build a new path.
3. Address your stress! That piece of cake isn’t going to cure your stress, questioning your thoughts and emotions might.
4. Practice mindful eating, and take responsibility for the food choices you make.
5. Reward your progress (but not with food!).
6. Don’t give up!

***This article is intended to give you insight and tips into why binge eating can occur and to provide some basic strategies to manage it. If your eating is out of control, having a significant impact on your health, or you are using compensatory strategies to manage your overeating (self-induced vomiting, laxatives, excessive exercise) please speak to your GP as soon as possible. Diabetes and eating disorders are a very dangerous combination which need to be managed carefully by healthcare professionals. ***

• 800 words – 5 min read.

Key Points

• Food labels are useful but they do have flaws.
• Guideline Daily Allowances do not take into account muscle mass, exercise and diabetes.
• Food manufactures tactfully use unrealistic portion sizes to portray the lowest calorie values possible. This entices health-conscious consumers to buy.
• Many health claims found on the front of food packaging are over exaggerated.

The Biggest Misconceptions of Food Labelling

The aim of food labelling is to inform consumers on what they are eating. Nutritional information on a food label should guide food choice. This is extremely important for people with diabetes and individuals with body composition goals. However, food labels are becoming increasingly more confusing with their layouts, colour codes, percentages of daily amounts and health claims.

Food Labelling Standards

It is a mandatory practice for all pre-packed foods to have food labels located on the back of their packaging. This information is generally available as: 

• Per Serving
• Per Portion
• Per 100g

Food labelling that appears on the front of the packaging is voluntary unless a health claim has been made, such as ‘low in fat’, ‘no added sugar’ or ‘high in protein.’ Nowadays, around 80% of food manufacturers display some form of front-pack nutrition labelling in an attempt to win consumer trust.

The most popular formats are:

1. Traffic Light System – Colours are used to indicate the levels of energy and macro nutrition. As you can see in the picture below High = red, medium = yellow/amber or, low = green.

2. Guideline Daily Amounts (GDA) – The current Guideline Daily Amounts (GDA) nutrition scoring system is in the process of being replaced by Reference Intake (RI). The GDA is a guide to how much of a certain nutrient you should eat per day, and therefore on packaging, a nutrient is shown as a percentage of the GDA/RI. See picture below.

Problems with Food Labels

There are a number of problems with nutrition labels that need to be highlighted.

• For starters, the GDA is based on average members of the population and their assumed nutritional needs.

What’s average?

The last time I checked, average people didn’t lift or have diabetes.

GDA does not take into account the increased nutrient demands of exercise, muscle mass and high blood glucose levels.

• Certain food manufacturers may deliberately exclude the GDA or Traffic Light System on their product as it could deter consumers from purchasing it.

This is common practice with unhealthy food products like chocolate, desserts and fast food.

• Food manufacturers often trick people into thinking their food has more nutritional value than others by using non-GDA labels such as “High in Omega 3” or, “High in Fibre”, without stating the actual grams or the GDA percentage.

• Use of unregulated health claims like “Reduced Fat” and “Reduced Sugar”.

In order for a food to state the above, it must have 25% less sugar/fat than the standard version of the same food.

• The portion size and associated nutrients are undersized and not reflective of a true portion size.

Food manufacturers rely on consumer behaviour of glancing at the packaging and confirming specific nutritional information like the calorie and fat content.

With this in mind, food manufactures tactfully display the nutritional information of an unrealistic sized portion of the specific food. In other words, letting you see what you want to see.

It’s easy to be fooled and think certain foods like pizza and confectionary are low in calories until you read the small print. Some great examples of tactful food labelling include: 2 squares of this chocolate bar include, ½ of this pizza includes etc.

• Food labels are never 100% exact ^1, 2

Don’t think the nutrition labels you read today are an exact representation of the food you are about to eat. Food labels represent average nutritional content.

There are many factors that influence the nutritional composition of individual foods. For example, the time of year it’s grown, the soil, the tree, the diet of the animal, mechanical equipment mixing, ratios of ingredient mix etc.

• Foods containing high amounts of ‘healthy fats’ like omega 3 and certain micronutrients could be coded as red using the Traffic Light System, when in fact they may provide more nutritional benefit than a food coded green – e.g. salmon vs white rice.

Take Home Points

Food labelling is a useful tool to gain basic nutritional information on a food source. The information on the back of the pack can be more informative and less confusing than the front-of-pack labelling.
If you do use food labels to select foods, check the portion size first. If it sounds too good to be true – it probably is.

Check out this example of a Kinder Bueno – the nutrition label on the front is for one bar NOT TWO. Information like this is easy to overlook.

Bear in mind that your nutrition needs to be individualized. Relying on GDA is useless, unless you match the exact profile of ‘average’. When building your diet you should consider your level of activity, exercise, muscle mass and diabetes management.

Don’t fall prey to the health claims on the front of food packaging. The rules and legislation surrounding these claims are not strict. Most claims are a play on words, misleading and over exaggerated.

It pays to be educated. Many people misinterpret the nutrition info on a food label, for example, what is the difference between sugars, in the form of fructose, typically found in fruit, vs. straight glucose found in most processed food; or, saturated and unsaturated fat?

Written by Phil Graham

Founder of Diabetic Muscle and Fitness

Sports Nutritionist, Strength Coach, and Fitness Educator

Type 1 Diabetic for 12 years

References  

1. Jumpertz R et al. Food label accuracy of common snack foods. Obesity (Silver Spring). 2013 Jan;21(1):164-9
2. Urban L et al. The accuracy of stated energy contents of reduced-energy, commercially prepared foods. J Am Diet Assoc. 2010 Jan;110(1):116-23.

How To Adapt Your Nutrition To Everyday Life

One of the biggest problems with people’s fat loss and muscle-building goals is a lack of consistency with their diet.

If you aren’t consistent with your eating you won’t get the results you’re after. No matter how advanced your training or supplement regime is.

In order to be consistent, you need to be flexible and know how to adjust your nutrition ‘off the cuff’ especially when it comes to different life events.

Many individuals are inflexible due to the misconceived notion that they have to eat the same way for the rest of their life, in order to maintain their results.

Ever heard the saying, ‘ more than one way to skin a cat.’?

The same is true for nutrition. There is more than one way to eat for muscle-building and fat loss with diabetes. Life events such as going on holiday, having a baby, going through a period of stress all play a big role in determining how you eat.

This video dispels the common belief that you must eat one way, and one way only to get in shape. Prepare to have your eyes opened.

Train Smart

Phil Graham

Founder of Diabetic Muscle and Fitness

Sports Nutritionist, Strength Coach, and Fitness Educator

Type 1 Diabetic for 12 years

• 4800 words, 35-45 minute read.

Key Points

• Once all the bases are covered, you may get a small benefit of supplemental Whey Protein if you struggle to hit 1.5-2.0g/kg (0.7-1.0g/lb) of quality protein from real foods.
• Before considering Whey protein, ensure you have covered all the bases of the Diabetic Muscle and Fitness NUTRITION PYRAMID and TRAINING PYRAMID.
• Remember Supplements are the least important component. Focus on REAL FOOD first to hit your protein requirements.
• Real food provides a host of nutrients and nutritional factors that benefit your overall health.
• When nutrient timing is important such as training twice a day, whey protein has some nutritional properties that can help with oxidative stress, non-alcoholic fatty liver disease, and possibly body composition.
• Whey protein requires more insulin to be metabolized, due to the high Leucine content – You need to know how to manage this for both type 1 and type 2 diabetes.
• Don’t be tricked by marketing, know the difference between Whey Concentrate, Isolate and Hydrolysate. Find out how to choose wisely and save your money.

Does whey protein live up to the hype for people with diabetes?

Can I take whey protein safely if I have Diabetes? What about my kidneys?

Am I wasting my money on another marketing scam?

My healthcare professional says I do not need protein supplements, do they really know, or are they playing it safe?

All my gym buddies take whey and swear by it, but they don’t have diabetes, will it work for me?

These are questions I hear all the time in my clinical Diabetes practice, mainly by men and women who are starting the gym and want to build a great physique. They want to maximise their gym efforts by supplementing with whey protein, but they are concerned with safety, the effects on blood glucose level, and their finances. Sound familiar?

There are some amazing articles online that have every last detail of whey protein.

But I am guessing you do not want every last detail, right?

If you want the most potent information, in an easy to understand format, that is specific to diabetes? This article is perfect for you.

Not only that, it details the best practical strategies, straight from the pioneering Diabetic Muscle and Fitness Community. These strategies are guaranteed to put you in control of your blood glucose levels and get the most out of whey protein.

Oh, one more thing, I guess you want a diabetes-specific guide for how to choose the right whey? Don’t worry that is covered too.

Ready? Let’s go.

Before we get into the specifics, let’s get some perspective.

Where do you think whey protein fits into the diabetes pyramid of muscle building?

What about other supplements like Creatine, L-Leucine, Magnesium, Fish oil?

What other nutrition factors like calories, carbs, fats and the timing of your meals?

If you were to believe the marketing hype, you would think protein supplements are the essential ingredients for building muscle and getting in great shape. This couldn’t be further from the truth, especially if you have diabetes.

Let’s get real shall we?

The Diabetic Muscle and Fitness Nutrition Pyramid lays out all the key diet-related factors in order of their importance. Let’s review each of them and get context on where whey protein lies and how it can be incorporated into a successful muscle building regime for men and women with diabetes.

Personal Value For Health and Fitness

Your personal values for health and fitness are the foundation for your results. You need to be driven to eat in a certain way. That means respecting key principles, all of which are outlined in order of importance in the pyramid above.

The same goes for your training and lifestyle. If you don’t value getting in shape and improving your health you’ll not put the effort into your training and living correctly to get the results you need.

If you can envision a goal, become emotionally attached to it, and identify exactly what you need to do, you’ll have no problem being consistent with your daily actions.

Over time, these actions mount up and will get the results you desire.

There are many people who take a notion of getting in shape, buy a tub of whey protein and expect miracles to happen overnight.

Many of you who have tried this, will know too well, that a great body doesn’t come that easy. It takes time.

See, if your head and goals aren’t in the right place it doesn’t matter what protein you buy. You won’t get results.

Diabetes Management (Blood Glucose Control)

The research is crystal clear. If you have a high HbA1c, or if you have consistent high glucose levels before or during training, you will cripple your muscle building efforts (1)

Bottom line – Get your diabetes well controlled before considering whey protein. Period.

Dietary Adherence 

If your nutrition doesn’t suit your personal needs you won’t stick to it, whether it includes whey protein or not. Simple. Make sure to check out the execution plans on how to build a diet that’s enjoyable, sustainable and gets results.

Energy Balance

Depending on whether your goal is fat loss or mass gain, you need to be consistently consuming the correct number of calories.

If leaning out is your goal, you need a daily 10-20% calorie deficit.

Whereas if you are trying to gain mass, you need a daily 5-10% calorie surplus.

“What about the effect of carbs, protein and fat?”

Yes, they have a big impact, but don’t be misled, energy intake is king, no matter what the gurus say. You just have to review the metabolic ward studies (2) by Kevin Hall to confirm how important calories are with respect to fat gain and fat loss.

How many calories do you need to hit consistently? Go and get your personalized prescription from the Diabetes Muscle and Fitness calculator (check the resources section).

Macronutrients

When it comes to macronutrients, the research demonstrates time and again that, ‘Consuming an optimal level of protein for your phase of training is the force multiplier for physique development.

Most of the marketed benefits of whey protein are due to one simple thing: achieving an optimal level of protein for your phase of training.

Those benefits include:

• Improved fat loss
• Increase in lean muscle mass
• Improved power output
• Reduced Grehlin (hunger hormone)

Be sure to check you are hitting the optimal level of protein intake. The well researched Diabetic Muscle and Fitness Guide recommendations are:

• Leaning or dieting: 1.7 – 2.0g/kg (0.8 – 0.9g/lb) of lean body mass
• Bulking or gaining: 1.4 – 1.7g/kg (0.6-0.8g/lb) of lean body mass

The Diabetes Muscle and Fitness calculator in the resources section can simplify this for you.

Science always trumps what a diet guru proclaims.

Nutrient Timing

Nutrient timing is important if you live with diabetes.  Consuming carbohydrates to prevent hypos or delaying a meal to prevent hyperglycaemia is essential. However, when it comes to the timing of your protein and protein supplement intake, many supplement companies would have you believe it is essential to consume your protein post workout. This isn’t necessarily true. What is more important is how much protein you consume across the day rather than at just one sitting.

The only key time that protein intake really matters is after fasted weight training first thing in the morning. This is a time when amino acid needs are highest.

Micronutrients, Fiber, and Water

Ensure your food choices cover all the vitamin and minerals essential for optimal growth. This is equally important for long-term health.

You already know how to do this, right?

Simple, a real food diet with lots of green leafy vegetables, whole grains, quality meats of different cuts, and minimally processed food.

Basically, respect three billion years of human evolution. Eat what the earth provides, not what man makes and packages!

Supplements

Last but not least are supplements.

The name gives it away ‘supplement’. Whey protein and every other health supplement on the planet was designed to supplement your diet. They are of least importance when it comes to building your diet. You must have every other variable in place before you look into what whey protein to buy.

Surprisingly, most people worry about what whey protein is the best rather than looking at the essential stuff like personal values for health and fitness, calorie intake and essential fatty acid intake.

On top of these nutrition factors, there are other important variables you need to consider,

• Progressive Overload
• Sleep
• Stress Managment

Progressive Overload

Your body is a stimulus-response machine. When you increase and vary your strength training stimulus (load, volume, training techniques) using a well-crafted training plan, guess what? Your body will adapt and grow new muscle mass to deal with the stress better next time round.

How will you know if you are progressing?

What gets measured, gets managed.

Want the fast track?

Get yourself a personalized training plan, and get accountable to a training partner, PT, or online coach. Preferably someone who knows diabetes inside out!

Sleep

Do you live by the motto:

“Life’s too short, why waste it sleeping?”

You will certainly get something, a short life. Sleep is the ultimate recovery tool. If you are not getting 7-9 hours QUALITY sleep per night, you can forget about building a great physique.  This is especially massive for people with diabetes because sleep deprivation causes insulin resistance.

Allostatic load (Stress)

A fancy way of saying manage the stress on your whole system. If you are working sixty hours a week, you have a newborn baby, and you are in mortgage trouble, do not expect to pack on muscle.

Your body needs time to rest and recover. Minimise your stress and buffer it with relaxation practices and social events. Barbecue anyone?

How many times have you jumped down the rabbit hole and spent madly on the next breakthrough supplement?

Many times?

Me too!

Before you do it again, ask yourself these questions:

• Is my diabetes control on point?
• Do I have an HbA1c of 6.5% (48mmol/mol) or less, with less than five hypos a week?
• Have I got killer consistency with energy intake?
• Do I get 7-9 hours quality sleep each night?
• Am I hitting my protein needs?
• Are my food choices real or fake?
• How stressed am I?

Ok, now you have the fundamentals in place. Let’s see what whey protein has to offer people with Diabetes.

What is whey protein? How is it manufactured? And, What has Miss Muffet got to do with all of this?

Whey is the water-soluble protein in dairy, its fat-soluble sibling is casein. Whey and casein are separated by adding renin (digestive enzyme), leaving the curds and whey, cue Little Miss Muffet!

Whey is technically the group of milk protein polypeptides (lots of amino acids bonded together) left in the liquid portion after renin has done its job. Whey protein is then separated from casein by ion-exchange. Finally, it is dried to leave the protein powder you see on the shelf.

Here comes the detail…

Ready?

Whey is unique in that it is complete with a high level of all the essential amino acids (EAA). It also contains a high content of branch chain amino acids (BCAAs). It has the closest amino acid make up to skeletal muscle, much closer than any animal protein. This gives whey the potential of driving muscle protein synthesis, as it provides all the building blocks, in the right amounts.

Does this potential get realized? Keep reading and you will find out.

Whey has a unique set of bioactive polypeptides. Polypeptides are lots of amino acids joined together in different structures that have different effects in the body. I am only going to discuss the most important polypeptides for Diabetes, to keep us focused:

• ß-Lactoglobulin: This 127 amino acid polypeptide is 25% branch chain amino acids (BCAA). The high L-Leucine content from the BCAAs is the main reason why whey requires more insulin than standard animal protein. How do you manage this with type 1 and type 2 diabetes? This will become clear as you read on.

• Alpha-Lactalbumin: This 123 amino acid sequence is high in L-Cysteine, an amino acid that is vital for cellular antioxidant capacity. Could this protect you against oxidative stress and the muscle inflammation that slows growth? We will explore this shortly. But first, let’s get clear on oxidative stress and antioxidants.

What is oxidative stress, and how do antioxidants work?

Although your body needs oxygen to survive, it is oxygen that can lead to oxidative stress in the body. As you breathe oxygen to produce energy, there are by-products created called FREE RADICALS.

If these FREE RADICALS are not neutralized, they cause damage to cell membranes, proteins and genes, by a process called oxidative stress.

Imagine you start a little fire to keep warm whilst camping in the dry bushland. You need the fire for your survival, but you would surely put the fire out before you went to bed, right?

Of course, you would. The water you extinguish the fire with is that same principle of how antioxidants work. Antioxidants are forever neutralizing free radicals before they can cause oxidative stress.

Now imagine one night you left the fire flickering and fell asleep, what’s the risk? Complete bushfire! Probably not, it would not go up that night, but if you do this often enough, eventually a massive bushfire is guaranteed!

Those bushfires in the body are caused by persistent oxidative stress with little antioxidant neutralization. If this goes on uncontrolled for years, the risk of cancer, heart disease, and Alzheimer’s increases massively. As for building muscle, very little progress!

You might be thinking, the solution is easy, just throw back some vitamin C and a load of other antioxidant pills, right? 100% not right!

The most powerful antioxidants are already present in the body. One of the most potent being Glutathione. Glutathione is responsible for 24/7 protection in all your cells, by neutralizing free radicals.

Therefore it is more important to supply an abundance of building blocks needed to re-generate Glutathione. That’s where L-Cysteine come in. This amino acid is the rate-limiting factor for the regeneration of Glutathione.

As whey is very high in L-Cysteine, it may have potential in preventing oxidative stress. Worth investigating, don’t you agree?

• Immunoglobulins: These small sulfur-rich polypeptides are very high in L-Cysteine (our friend again).

• Glycomacropeptides: These polypeptides have been shown to impact Cholecystokinin, a digestive system hormone that suppresses appetite.

Ok, that’s the heavy science over, let’s have a look at what you see on the shelf.

Once separated from casein, whey undergoes a variety of purification processes, leaving it in one of three forms:

Whey Protein Concentrate – Contains 30-80% protein depending on the manufacturer. This is the cheapest because it contains a small amount of fat and lactose. If you want the best bang for your buck, and you are not concerned with a little fat and lactose, this is perfect for you. Look for whey concentrate that is 70-80% protein by weight. This will ensure you get a good protein content, and not a mass gaining blend full of fast-acting carbohydrate.

Per 100g it should be:

• 70-80g of protein
• Total carbohydrate less than 10g
• Total fat less than 10g
• As few additives and ingredients as possible
• Cost between £12-20 per 100g

Below is a comparison of some of the popular whey protein concentrates, in protein content order. Notice a few things as you look at them.

• The names can be deceiving, 100% Whey!
• Cost range from £12 – £20.
• Differences in fat and protein content

Also remember a typical serving is 25-50g, so the fat and carb content are a quarter to half of what is shown in the table.

Questions to consider when selecting whey concentrate with Diabetes:

• How much impact will 3-6g carbohydrate have on my blood glucose level?

• How does an extra 4-8g of fat impact on my overall daily calorie intake?

• Do I have an unfavourable reaction to milk proteins or lactose?

• Do I want flavourings added or not?

Source: http://compareproteins.co.uk/

Bottom line: If you ensure the protein at least 70g per 100g weight, you are not going to get a huge amount of fat and protein per serving.

Whey Protein Isolate – is the result of further purification, to remove almost all the fat and lactose. Look for whey isolates that have more than 80% protein by weight. To ensure getting a good whey isolate, and not a glucose busting mass mix, it should be per 100g:

• 80g or more protein
• Total carbohydrate less than 5g
• Total fat less than 6g
• As few additives and ingredients as possible
• Cost between £17 – £35 per 100g

Below is a comparison table of some of the popular whey protein isolates. They are in order of protein content. The real questions you need to ask yourself are:

• What’s the benefit of a 97g vs. 90g vs. 80g whey isolate?

• Is a difference in carb and fat content per 25-50g serving of 0.25-2.0g a deal breaker?

• Do I want flavoured or unflavored?

• Do I have issues with a tiny amount of lactose or milk proteins?

Source: http://compareproteins.co.uk/

Bottom line: Don’t be dragged into the hype that 97% pure protein is massively better than 90%! If you have lactose intolerance then you may need the 97% stuff, otherwise, save your hard earned cash!

Whey protein hydrolysate– is the most purified form, following partial hydrolysis of large polypeptides into di-peptides and free amino acids. This does lead to some loss of the sulfur-rich amino acids, such as L-Cysteine, and makes it taste very bitter. This form is ideal for people who have allergies to milk proteins or digestive issues, such as infants and people with Chron’s disease. Adults with intact digestive systems tolerate whey concentrate and isolate very well. Their pockets tolerate it even better! If you have digestive issues, a good whey hydrolysate should be per 100g:

• 90g or more protein
• Total carbohydrate less than 1g
• Total fat less than 2g
• As few additives and ingredients as possible
• Cost £25-50 per 100g 

Bottom line: 99% of adults have the digestive capability to process whey concentrate and isolate. So only go for whey hydrolysate if you have a specific digestive issue, or have not managed well with isolate.

How do you know if you are buying a quality product that has been rigorously tested?

This is a great question.  Regulations on supplement manufacturers vary from country to country. Enforcement of them over the internet is virtually non-existent.

My suggestion is to head over to Labdoor.com, they independently test and score whey protein, among many other supplements. You can filter your criteria by cost, quality, and several other useful metrics.

If you want to compare brands and costs, go to http://compareproteins.co.uk/. You can filter your search by protein content, and almost any variable you can think of!

Now you have the equivalent of a food tech degree in whey protein, let’s see what the research says about whey protein! More importantly, let’s look at whey protein through the lens of a person with diabetes.

Whey Protein Effect on Muscle Protein Synthesis and Insulin Requirements

Whey protein spikes amino acid levels in the blood within 40-60minutes. Most importantly, it spikes L-Leucine. Research (3) shows this spike in L-Leucine is accompanied by an increased insulin production in non-diabetics. This leads to an elevation in protein synthesis by 30%, when compared to casein and animal protein in the first three hours, although net gain in muscle growth is equal over seven hours, for all these proteins.

What does this all mean for diabetes?

There are a few important take-homes:

• If you are training twice a day, whey protein may well offer an advantage in overall muscle protein synthesis. If training just once per day, just focus on getting your daily g/kg/day of protein. If whey is convenient and helps you meet your daily intake, smash it down!

• If you choose whey protein with Type 1 Diabetes, you are going to need more insulin than expected due to a spike in L-Leucine. If you don’t, you will miss that 30% increase in muscle protein synthesis, and have a high glucose level!

• There is a course at Diabetic Muscle and Fitness all about insulin dosing at meal times, Becoming a Bolus Wizard. There is a module on covering protein with insulin, and a calculator that makes it simple.

• If you choose whey protein with Type 2 diabetes, the effect on your blood glucose level could go either way. If you still have adequate beta-cell function in your pancreas, the L-Leucine spike will trigger a surge of insulin. This has been shown (4) to reduce after-eating glucose levels by 20%. However, if your beta-cell function is exhausted, you may require extra insulin if you are injecting.

Bottom line: Whey protein will require more insulin than expected to cover the L-Leucine spike. If you do not give the extra, you miss out on the muscle!

Whey protein: Does it induce strength gains and body composition change?

Ever seen a claim such as:

“Whey protein, scientifically proven to increase muscle mass whilst shredding fat!”

Often this headline is followed up with a write-up such as:

“People who took a specialized whey fraction (Prolibra™, high in leucine, bioactive peptides and milk calcium) “lost significantly more body fat and showed a greater preservation of lean muscle compared to subjects consuming the control beverage.” (5)

The above is true, but when you dig into the study, you find the protein intake in both groups was only 0.76-0.81g/kg/day!

I know what you are thinking, the baseline protein intake is not optimal! Well spotted, it’s only half of what it should be!

One study (6) of interest recruited thirteen recreational Australian bodybuilders. Using a blinded randomised control trial (the gold standard), they supplemented both groups with an ADDITIONAL 1.5g/kg/day of either whey or casein protein. The bodybuilders followed a ten-week resistance training program whilst supplementing. This took their daily protein intake to 2.1g/kg/day during the study. Now that’s more like it!

Interestingly the whey group increased lean body mass by 5kg (11lb) in ten weeks, whereas the casein group only by 0.8kg (1.8lb). The whey group shed 1.5kg (3.3lb) of fat, which was more than the 0.2kg (0.4lb) in the casein group. To cap it off the whey group improved their 1 rep max across barbell bench press, squat, and cable pull-down.

This sounds AMAZING, but proceed with caution:

• There were originally nineteen subjects, six dropped out, leaving only seven bodybuilders in the whey group, and six in the casein group. Is this representative of you?

• The whey group’s starting weight was 4.5kg higher, with the same amount of body fat. Could the whey group have been the more athletic, and therefore respond better to training?

• The whey group reported consuming 250kcal/day more than the casein group. This would certainly have an anabolic effect, wouldn’t it?

• Finally, are you willing to consume 1.5g/kg/day of protein powder? Both groups only consumed a measly 0.6g/kg/day from dietary protein. To maximise dietary quality, it should be at least 1.2g/kg/day from quality animal sources. Then supplement with a much smaller amount of whey.

My conclusion would be: Try to meet your daily protein requirement from quality dietary protein sources, such as beef, chicken, eggs, and fish. If you cannot meet your requirement by dietary sources, then supplemental whey is a great option. But it should not be a total replacement.

This may be especially true for people with type 1 diabetes who may get consistent L-Leucine blood glucose spikes. If I followed this study I would be chugging 150g of whey per day, powder overload, and vigorous blood glucose testing.

Whey Protein – does it have an antioxidant effect?

Diabetes is unique in that it poses an extra oxidative stress challenge to the body. Constant fluctuations in blood glucose reduce cellular antioxidant levels (Glutathione, out fire hydrant), which in turn increases oxidative stress, and leads to inflammation of the tissues (7). Whey protein is rich in L-Cysteine, the rate-limiting building block for glutathione. Glutathione is one of the most potent antioxidants in the body, therefore having an optimal level is even more important for a person with diabetes.

Animal studies (8) have shown the addition of whey protein reduces inflammation, elevates glutathione stores, lowers HbA1c and reduces insulin resistance. I hear you, you are not animal, what about human research?

Human research is lacking in terms of mechanistic proof of the antioxidant effect. But, at the very least, there some human trials showing cardioprotective effects for people with type 2 diabetes when supplemented with whey protein (9).

Whey Protein: Does it cure Non-alcoholic Fatty Liver Disease (NAFLD)?

NAFLD is very common in people with type 2 diabetes, and a serious health risk. One study (10) showed up to 75% of insulin-naive type 2s had the clinical markers of NAFLD. It was suggested insulin resistance is the main culprit. The same study showed the type 1 diabetes population had no increased risk, shining the spotlight on insulin resistance as a main contributing factor.

A study (11) supplementing NAFLD subjects with 20g whey protein per day over 12 weeks showed an improvement in liver function, elevated liver glutathione levels,  reduction in liver fat mass, and improvement in body composition. The benefit is thought to be due to the increase in L-Cysteine from the Whey protein.

If you have type 2 diabetes and are training, it may be worth supplementing with whey to meet your protein needs for muscle growth. But only if you are taking out other calorie sources.

Whey Protein: Does it cause kidney damage?

 Are your kidneys not in poor health?

Do you have chronic kidney disease stage 3 or higher?

If you answer yes to either of these two, check with your healthcare professional before adding extra protein to your diet. It may make it worse.

If you answered no to both, then a higher protein intake does not pose an issue (12) for your kidneys. If unsure, always check with your healthcare provider.

Whey Protein: When’s the best time to take it?

Are you meeting your daily protein intake for your phase of training?

If you are, there is little benefit to be gained by adding extra whey protein. You will be wasting your money by downing multiple shakes before and after training.

However,

Are you are planning on training twice a day, training fasted first thing, or are you not meeting your daily protein needs?

If yes, then having 20g whey protein before (13), and certainly in the one hour after, will ensure adequate amino acid supply, especially the L-Leucine spike to drive muscle protein synthesis.

Let’s whey all this up

What are the most important factors for building muscle and a great looking physique with diabetes? The Diabetic muscle and fitness nutrition pyramid outlines the important nutrition factors that MUST be in place before considering supplements.

On top of these nutrition factors, there are other important variables you need to consider,

• Progressive Overload
• Sleep
• Stress Managment

When you have these checked off, then consider whey protein.

Let’s summarize the potential benefits for different types of diabetes.

People with Type 1 Diabetes who may benefit from supplemental whey protein.

1. Those with sub-optimal dietary protein intake <1.2/kg/day.
2. Those who train twice per day.
3. Those who struggle to meet protein requirements through real food due to time.
4. Those who are leaning down and need to hit 2.0g/kg/day.

People with Type 2 Diabetes who may benefit from supplemental whey protein.

1. Those with sub-optimal dietary protein intake <1.2/kg/day.
2. Those who train twice per day.
3. Those who struggle to meet protein requirements through real food due to time.
4. Those who are leaning down and need to hit 2.0g/kg.
5. Those who have NAFLD if substituted for other calorie sources.

Key things to pay special attention to

1. Whey will require more insulin than expected due to L-Leucine content – very important for people with type 1 diabetes, and people with type 2 diabetes that have exhausted beta-cell pancreatic function.

2. If you have chronic kidney disease stage 3 or above, it is not advisable to have extra protein. Check with your healthcare professional.

What to consider when choosing a Whey Protein?

1. Do I have lactose intolerance or milk protein allergy?

• If yes, go for a 97% whey isolate or hydrolysate.
• If no, then go for a whey concentrate or isolate.

2. Does it matter if per serving, the carb and fat content is 3-6g?

• If yes, choose a whey isolate >90%
• If not, choose a 70-80% whey concentrate

3. Is cost a major consideration?

• If yes, choose a 70-80% whey concentrate
• If no, choose a whey isolate >90%

There is a host of other considerations depending on the type of person you are:

1. Grass-fed animals vs. not grass fed.
2. Added sweeteners vs. no added sweeteners.
3. Flavourings vs. no added flavourings.

For these, it is over to you to check the labels!

I hope this has helped.

Stay strong

John  Pemberton

Registered Dietitian

PG Dip: Nutrition and Dietetics

Bsc: Sport, Health, Exercise and Nutrition

Type 1D 10 years and counting

References

1. Galassetti, P. & Riddell, M.C (2013) Exercise and type 1 diabetes (T1DM). Compr Physiol. Jul;3(3):1309-36. doi: 10.1002/cphy.c110040.
2. Hall, K.D. et al., (2016) Energy expenditure and body composition changes after an isocaloric ketogenic diet in overweight and obese men. doi: 10.3945/ ajcn.116.133561
3.  Reitelseder, S. et al (2011) Whey and casein labelled with L-[1-13C]leucine and muscle protein synthesis: effect of resistance exercise and protein ingestion. Am J Physiol Endocrinol Metab. 2011 Jan;300(1):E231-42. doi: 10.1152/ajpendo.00513.2010.
4.  Frid, A.H. et al (2005) Effect of whey on blood glucose and insulin responses to composite breakfast and lunch meals in type 2 diabetic subjects.  Am J Clin Nutr. 2005 Jul;82(1):69-75.
5. Frestedt, J.L (2008) A whey-protein supplement increases fat loss and spares lean muscle in obese subjects: a randomized human clinical study Nutr Metab (Lond). 2008; 5: 8. doi: 10.1186/1743-7075-5-8
6. Cribb et al (2006) The effect of whey isolate and resistance training on strength, body composition, and plasma glutamine. Int J Sport Nutr Exerc Metab. 2006 Oct;16(5):494-509.
7. Asmat, U. (2015) Diabetes mellitus and oxidative stress—A concise review. Saudi Pharmaceutical Journal Volume 24, Issue 5, September 2016, Pages 547-553
8. https://doi.org/10.1016/j.jsps.2015.03.013
9.  Jain, S.K. (2009) L-cysteine supplementation lowers blood glucose, glycated haemoglobin, CRP, MCP-1, and oxidative stress and inhibits NF-kappaB activation in the livers of Zucker diabetic rats. Free Radic Biol Med. 2009 Jun 15;46(12):1633-8. doi: 10.1016/j.freeradbiomed.2009.03.014.
10. Ballard, K.D. et al (2013) Acute effects of ingestion of a novel whey-derived extract on vascular endothelial function in overweight, middle-aged men and women. Br J Nutr. 2013 Mar 14;109(5):882-93. doi: 10.1017/S0007114512002061.
11. Cusi, K. (2017) Non-alcoholic fatty liver disease (NAFLD) prevalence and its metabolic associations in patients with type 1 diabetes and type 2 diabetes. Diabetes Obes Metab. 2017 Apr 17. doi: 10.1111/dom.12973.
12. Chitapanarux, T. et al (2009) Open-labeled pilot study of cysteine-rich whey protein isolate supplementation for nonalcoholic steatohepatitis patients. J Gastroenterol Hepatol. 2009 Jun;24(6):1045-50. doi: 10.1111/j.1440-1746.2009.05865.x
13. Friedman, A. N. (2004) High-protein diets: potential effects on the kidney in renal health and disease. Am J Kidney Dis.2004 Dec;44(6):950-62
14. Tipton, K.D. (2001) Timing of amino acid-carbohydrate ingestion alters anabolic response of muscle to resistance exercise. Am J Physiol Endocrinol Metab. 2001 Aug;281(2):E197-206.

• 1200 words – 9 min read.

Key Points

• Dietary fat can increase blood glucose levels when consumed on its own. However,
• When dietary fat is consumed alongside carbohydrates and protein – the effect on blood glucose is more significant.
• Consume the bulk of your dietary fat from monounsaturated food sources and the least from highly processed food sources.
• Dietary cholesterol is not a nutrient of concern – stop panicking and eat foods that contain cholesterol in peace.
• Fat is incredibly easy to eat, especially when combined with carbohydrate, protein and salt.
• Be mindful that dietary fat can drive you into an energy surplus quicker than any other macronutrient.

In this article, I want to dispell the common fear most people have about the fat content of their foods and highlight the more important aspects people need to consider when chasing the goal of better health, body compsotion, sports performance and highly effective diabetes management.

Good and Bad Fats – Let’s Begin.

Before we get to the interesting stuff, I want to give a quick rundown on the different types of dietary fat.

Why?

Because not all fats are created equal.

Although the terms ‘Good / Bad’ Fats are quite subjective, it is generally agreed amongst scientists that the terms apply to the effects a certain type of fat has on cholesterol in the blood, more specifically, lipoproteins (the carriers of cholesterol).

Enter cholesterol a small waxy substance that serves many important roles within the body, including being an important component of every cell membrane in the body and playing a major role in tissue repair.

High-density lipoprotein (HDL) and Low-density lipoprotein (LDL) are the two main classifications of plasma lipoprotein particles and are dubbed “good” and “bad” cholesterol.

Respectively: LDL-Cholesterol is labelled as ‘bad’ due to its potential atherogenic properties.

When a blood vessel is damaged, LDL-Cholesterol is called upon to repair it. Depending on the extent of the damage, fatty deposits can appear on the walls of the blood vessels (known as plaque). These plaques (or atheromas) are known as atherosclerosis and cause the arteries to harden and narrow, restricting the blood flow and oxygen supply to vital organs.

However, just because LDL-Cholesterol is correlated to the formation of plaque and furrowing of the arteries does not mean it caused the damage in the first place.

Damage to blood vessels is increased by a number of risk factors, including:

• Obesity (metabolic syndrome and T2)
• Poor glycaemic control
• Genetic predisposition
• Excessive intake of man-made trans-fat
• Smoking
• Oxidative stress
• Low-grade inflammation ( other illness etc.)
• Chronic stress

Generally speaking, the distinction between ‘good’ and ‘bad’ cholesterol is valid, making further distinctions beyond the scope of this article.

Cholesterol – Correlation Doesn’t Equal Causation.

 

A Short Primer on The Effect of Different Dietary Fats

Dietary fats, technically speaking, triglycerides, are made up of one molecule of glycerol (a sugar) and three fatty acids.

I don’t want to go into a whole biochemistry lesson on the structure of fatty acids in this article; however, it is important to know that the effects of fatty acids on health and metabolism depend primarily on their structure.

Picture of a Triglyceride Molecule

Triglycerides can differ in length, from short to medium to long chain (depending on the number of carbons present), and by the number of double bonds. There are four main subtypes of dietary fat/triglycerides.

Trans Fats

Man-made trans-fatty acids AKA partially hydrogenated vegetable oils, occur mainly in margarine and junk food to give them long shelf lives.

The consumption of industrially produced, partially hydrogenated vegetable oils (trans fat) is associated with an increased risk of cardiovascular disease, infertility, endometriosis, gallstones, Alzheimer’s disease, diabetes and some cancers.

Thankfully, many fast-food and supermarket chains have either considerably reduced, or eliminated the use of these types of fats in their food.

The intake of trans fat is relatively low in the UK and northern Europe. It tends to be consumed in greater quantities in other countries, particularly the United States. Be mindful of this when travelling.

The 2015-2020 Dietary Guidelines for Americans recommends trans fat should be avoided.

There is nothing good to come out of eating man-made trans fats. They are one of the only sources of fat that should be avoided.

Saturated Fats

The type of fat most will be familiar with.

Saturated fat is solid at room temperature, has no double bonds and occurs predominantly in animal foods, such as meat, eggs,  dairy products and certain plant products like coconut oil.

The hysteria surrounding saturated fat has worn off since the 1980s as it then became sugar’s turn to take a bashing.

Check this article out after The Truth: Is Sugar Addictive?

Saturated fats are not essential to have in the diet. Our bodies can create saturated fat from excess carbohydrate and protein.

The 2015-2020 Dietary Guidelines for Americans recommends people limit saturated fat to less than 10% of calories a day.

Though there are many types of saturated fats, they tend to increase both HDL (good) and LDL (bad) cholesterol. As the ratio of HDL to LDL is more important than the quantity of each, they are pretty neutral with respect to health in most instances.

That said, at low doses saturated fats are acceptable in our diets and not atherogenic (promoting the formation of plaque in the arteries). However, if you consume the bulk of your fat intake from saturated fats, particularly palmitic acid (commonly found in butter), you may dramatically increase your risk of developing atherosclerosis.

So, if your fat intake largely consists of cream, butter, lard and other saturated goodness – you might be as well to start incorporating the following sources of fat, as of today…

Monounsaturated Fats

Monounsaturated fats are liquid at room temperature, have a single double bond and occur predominantly in foods like olive oil, nuts, and seeds.

In terms of health, monounsaturated fats are neutral to beneficial, as they tend to reduce levels of LDL in the blood.

As such, monounsaturated fats should make up the bulk of your fat intake.

Saturated fats can also be replaced by monounsaturated fatty acids, which are considered health-neutral, provided they are consumed within an individual’s energy needs and consumed as part of a diet that provides all the necessary essential nutrients. This is often considered to be a Mediterranean diet.

Polyunsaturated Fats

Polyunsaturated fats are also liquid at room temperature and have multiple double bonds.

The two primary classes of these fats are the essential omega-3 and omega-6 fatty acids.

The body cannot produce omega-3 and omega-6 fatty acids. For this reason, they are known as essential fats or EFAs.

Omega-3 helps to reduce inflammation; omega-6 promotes inflammation, which at times is healthy and essential for human growth, development and repair.

While both of these fats are essential…

Chronically high levels of Omega-6, at the expense of Omega-3,  have been shown to promote inflammation and contribute to modern diseases, such as heart disease, obesity and diabetes.

Omega-6 is hard to avoid considering everything is cooked in some form of vegetable oil –  the most popular source of omega-6 fatty acids.

Most people could benefit from increasing their omega 3 intakes, particularly from animal sources – which tend to be higher quality over plant-based sources.

• Strive to eat eight or more ounces (226g) a week from a variety of oily seafood.
• The American Heart Association recommends 1g daily. If the goal of supplementation is to reduce soreness, a 6g dose, spread over the course of a day, will be effective.

Plant sources such as flaxseed, chia, hempseed, canola oil, walnuts and certain vegetable oils contain significant amounts of the plant-based omega-3 fatty acid A-linolenic acid (ALA) and stearidonic acid (SDA).

Animal sources, particularly fish/krill oil and oily fish contain the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)

Researchers now believe that the majority of health benefits we get from dietary omega-3 fats come from EPA/DHA, particularly DHA. They carry just about any positive health effect you can think of.

Does Fat Content Really Matter?

Fat content is important.

However, we rarely eat dietary fat on its own.

When was the last time you chugged down a bottle of olive oil or ate a pound of lard pre-workout?

Never?

Thought so.

We consume 99% of our dietary fat alongside other nutrients – other foods.

Pure fat sources like olive oil and butter are traditionally consumed with bread, salad and other nibbles.

Cooking oils are the foundation of pretty much every dish on the planet.

The only exceptions to this – is when we eat pure dietary fat, such as…

• Supplementing with fats like cod liver or flaxseed oil.
• Falling prey to crazy pseudoscience nonsense like bulletproof coffee or the whole ‘coconut oil is good for me’ craze.

Food choice matters most, not the fat content.

Even your favourite peanut butter (a source of fat) or a certain variety of nuts contain their fair share of carbs and protein.

The concept Food choice matters most, not the fat content is supported by the relatively new recommendations on dietary fat set by the U.S. Department of Health and Human Services Dietary Guidelines Advisory Committee, which states…

There is no longer a recommended upper limit for total fat intake. 

There really is no scientific basis for placing a limit on fat intake, with the exception of avoiding man-made trans fats.

In fact, fearing fat can encourage poor dietary choices.

For example, restricting dietary fat may hinder an individual from consuming foods rich in healthy fats, like salmon, mackerel and avocados which pack significantly more nutritional value than popular dietary foods like rice cakes or artificially processed dressings, deli meats, confectionery and ready meals with ‘fat-free claims.’

No more freaking out about the total fat content of your food. Shift your focus to food choice.

Rather than worrying about the type of fat you are eating, consider asking yourself more important questions like.

• What quantity and other types of nutrients am I eating alongside the dietary fat in my meal?
• Does my meal/food portion sit within or outside my calorie targets for my particular body composition goals?
• Will this fill me up? or leave me hungry and wanting more calories?
• How will my blood glucose levels respond to the fat content in this food/meal?
• Are there any additional nutrients that accompany the fat source, e.g Protein, Carbs, Vitamins and Minerals?

Failing to ask these questions will likely lead to body composition issues and problems with managing blood glucose levels.

Look beyond the fat!

Take Home

• Dietary fat promotes the secretion of insulin in people without diabetes.
• For those living with diabetes, dietary fat has the potential to increase blood glucose levels. Dose and frequency specific.
• Dietary fat has the most insignificant impact on blood glucose levels when compared to carbohydrate and protein alone.
• Consume the majority of your dietary fat from monounsaturated sources, with the rest split between saturated and polyunsaturated fats.
• Consume as little man-made trans fatty acids as possible.
• Though the quantity and types of fat that you consume on a daily basis are certainly a key factor in optimising health, it is important to realize that other dietary and lifestyle factors are far more important.

References

Written by Phil Graham

Founder of Diabetic Muscle and Fitness

Sports Nutritionist, Strength Coach, and Fitness Educator

Type 1 Diabetic for 12 years

2100 words, 25-minute read.

Key Points

• Dietary protein isn’t as harmful as smoking.
• Consuming too many calories from protein and processed meats without enough exercise is an issue.
• IGF-1 plays a role in the ageing process and mortality.
• IGF-1 is an anabolic agent that causes cell growth, including cancerous cells.
• High-protein diets can be effective in improving key markers of cardiovascular risk in people with diabetes and should be considered part of an effective nutritional strategy for managing diabetes.
• Most shock stories on health, diet and fitness are written by journalists with little to no knowledge (or experience) of human physiology, nutrition or exercise physiology.

Is eating red meat and cheese really as bad as smoking?

You may or may not have heard the recent study that made the headlines, with the news that ““Eating large amounts of meat, cheese may be as deadly as smoking.”

That’s a pretty serious claim that would give many bodybuilders, weightlifters and fitness addicts the meat sweats.

Linking popular foods like meat and cheese to smoking is pure and utter sensationalism. The sole aim of a title like this is to grab your attention and encourage you to buy a newspaper or view the news.

They need to make their money and get views from somewhere.

The study in question is genuine, but only if you disregard the ridiculous claim that eating meat is as harmful as smoking.

Let’s take a quick look at the study goals, design, and general findings.

Epidemiological and rodent intervention studies set out to assess the role of dietary protein intake on IGF-1 levels, cancer risk and overall mortality in the 65 and younger (but not older) population.

You can read more about the study here.

What is IGF-1?

IGF-1 is a primary mediator of the effects of growth hormone (GH). Growth hormone is made in the anterior pituitary gland, is released into the bloodstream, and then stimulates the liver to produce IGF-1.

Why research it?

It has been suggested that IGF1 levels influence physiological changes related to ageing and development of age-related diseases such as cancer and cardiovascular disease (CVD) ^1,2,3

Two Studies Were Involved.

An epidemiological and mouse study.

An epidemiological study observes a specific population for a period of time and tries to determine a particular outcome in relation to set factors.

In this case, the effect of long-term dietary protein intake on IGF-1, cancer risk, and mortality.

A mouse study to support the findings of the epidemiological study. Humans and mice share many common genetic features and by examining the physiology, anatomy, and metabolism of a mouse, scientists can gain a valuable insight into how humans function.⁴

Needless to say, the findings from both types of research cannot be used to state “X causes Y”. On the other hand, any time cancer or tumour growth is mentioned in the mouse study, it solely applies to the mice in question and cannot be applied to the human study findings.

Observational studies like this are useful incentives for further research.

The Human Epidemiological Study

Pre-existing survey data was taken from The 3^rd National Health and Nutrition Examination Survey (NHANES).

This particular survey research is conducted by the National Centre for Health Statistics (NCHS) to assess the health and nutritional status of adults and children in the United States, and to track changes over time.

The 3^rd NHANES survey assessed 6381 adults over the age of 50 years old.

The baseline protein intake data showed that, on average, protein made up 16% of the cohort’s caloric intake and 69% was derived from animal-based protein (meat, fish, eggs etc.)  This data was used to subdivide the population size into three distinct sample groups.

• High Protein intakes >20%
• Moderate Protein – Between 10-20%
• Low Protein intakes <10%

The data for these three groups of people were observed over the next 18 years to ascertain if disease or mortality rate differed between those consuming different amounts of protein.

What did they find?

• A positive link between moderate and high protein intakes and diabetes-related mortality, compared to the lowest protein intake.

• No relation between higher protein intake with all-cause mortality, cancer-related mortality, or cardiovascular mortality overall.

• A small increase in risk was seen when looking only at people between the ages of 50-65 years old.

• This risk was reversed for people above the age of 65 years old, where dietary protein seemed to have a protective effect against all forms of mortality (excluding diabetes-related).

In conjunction with these findings, IGF-1 levels were investigated from a smaller population size of 2,253 individuals. They found that,

• IGF-1 levels increased in correlation to meat intake, predicted overall mortality seen in the 50-65 cohort as well as the 66+ cohort.

• The protective effects of protein intake in the elderly (66+) persisted when IGF-1 levels were lower.

• Higher levels of IGF-1 were not linked to protective effects, although they weren’t correlated with increased mortality either.

• This part of the study was only conducted in people over the age of 50 years old only.

• Animal and/or plant protein intakes were accounted for.

• Once protein intake had been assessed, other dietary variables like general calorie and macronutrient intakes were accounted for.

• Additional controls included sex, age, ethnicity, education, disease status, smoking status, dietary changes, and previously attempted weight loss.

Given all the epidemiological evidence additional research was conducted using mice to confirm causation.

The Rodent Study

• A population of mice was implanted. Mice were fed a high (18%) or low (4-7%) protein diet for 7 days prior to being implanted with B16 melanoma cells, a murine tumour cell line used for research as a model for human skin cancers.

• It was observed that the majority of mice in both the high (100%) and low (90%) protein groups bore tumours.

• However, the size of the tumours in the low protein group was 78% smaller relative to the size in the high protein group.

• The high protein mouse group had higher levels of IGF-1 whereas there were higher levels of IGF-1 inhibitor protein (IGFBP-1) in the low protein group.

• The study was repeated in mice deficient in growth hormone(GH), to replicate the lower GH output of older adults.

• Tumour growth was lower in the high-protein group (10-20% of what was seen previously in normal mice given the same dose of protein).

• The study was replicated using breast cancer cells rather than B16 melanoma. The results were similar.

• The study was also repeated to compare the effects of higher quality animal protein (casein) to plant (soy) protein. This did not change the results much, as serum IGF parameters were similar.

• It was noted that the expected negative effects of high protein intakes turned positive in older mice.

So, what do the studies tell us?

• IGF-1 plays a role in the ageing process and mortality.
• IGF-1 is an anabolic agent that causes cell growth, including cancerous cells.
• IGF-1 levels can be influenced by overall protein intake
• Higher protein means more IGF-1.
• Higher protein intakes may be protective in individuals over 65 years old (unless they had diabetes)
• Protein is not as harmful as smoking.

Take These Findings with A Pinch of Salt.

There are many questions that this kind of research doesn’t address, and another reason why they cannot prove causation.

1. What about the noted health benefits of exercise? Can exercise have a protective effect? What about those who strength train and have increased protein demands?
2. What about the source of protein? The study only observed animal vs plant sources and didn’t address the nutritional quality between minimally processed fresh cuts of meat compared to highly processed meats like salami, and fast food burger patties.
3. What about people younger than 50 years old? Do the findings still apply? Are they at more or less risk?
4. What about different sources of fruits and vegetables? Surely, if rotated they would have provided a broader spectrum of health-promoting nutrients? These were not counted, just carbs and fats.
5. What did the low protein group eat to compensate? Could the macronutrient used to replace protein have a protective effect or not.
6. What about levels of stress, and sleep? These are very important lifestyle factors that play a role in health.

Does this mean protein is bad for people with diabetes?

NO.

First of all, the number of people with diabetes involved in the study was extremely small and would have had an inflated effect on their findings.

The authors even highlight this:

“We underline that our hazard ratios and confidence intervals may be inflated due to our sample size and the extremely low incidence of diabetes mortality in the low protein group. Overall, there were only 21 diabetes deaths among persons without diabetes at baseline, only 1 of which was from the low protein group”

Consequently, we need to look at the bigger picture and overall body of evidence outside one study before jumping to conclusions.

First of all, let’s look at the facts:

• Higher protein intakes increase the workload on the kidneys.
• People with diabetes are at increased risk of kidney disease (nephropathy) especially if their diabetes is poorly managed.

Is it wise for people living with diabetes to consume more protein?

In poorly controlled individuals with signs of kidney trouble, maybe not.

On the contrary, what about the person with well-controlled diabetes who exercises regularly?

Protein intake in T1D

There is substantial evidence to suggest high protein diets do not harm a set of healthy kidneys in people without diabetes.

Although people living with T1D may have healthy kidney function, they are at increased risk of kidney complications, which may caution against high intakes of protein.

If the individual strength trains, this may permit a higher protein intake.

Research investigating protein intake in people living with T1D with healthy kidney function is limited and definitely warrants further research.

Protein intake in T2D

The Systematic review and meta-analysis of different dietary approaches to the management of type 2 diabetes provides strong evidence to support the consumption of protein in people with diabetes.

The review suggests that a high-protein diet is effective in improving various markers of cardiovascular risk in people with diabetes and should be considered in the overall strategy of diabetes management.

In both populations, protein has been proven to improve glycemic control and help control appetite, both of which are important in preventing obesity and diabetes-related complications.

Take Home

Dietary protein has been linked to mortality in these two studies. However, the research is limited to people over 50 years old, doesn’t account for exercise and other important factors such as the source of meat (processed vs non-processed).

The studies support IGF-1’s role as an anabolic agent responsible for cell growth, no matter the type of cell.

For those who exercise regularly, increased levels of IGF-1 will assist with muscle growth and recovery. On the other hand, increased levels of IGF-1 in sedentary overweight/obese individuals consuming a poor diet may be problematic.

As a journalist, with very limited knowledge/experience in evidence-based nutrition and health data, it’s easy to take things out of context and make misleading sensationalist claims.

A more accurate title for the findings of this study would have been “People between the ages of 50-65 years of age who are overweight, and have a history of poor diet and lifestyle habits are at increased risk of cancer.”

Oh and as for ‘cheese’  – given that it’s a major source of dietary fat with limited protein I’m still confused how it got thrown into the headline. This would be a different article altogether.

Written by Phil Graham

Founder of Diabetic Muscle and Fitness

Sports Nutritionist, Strength Coach, and Fitness Educator

Type 1 Diabetic for 12 years

When it comes to Nutrition & Health, the media ONLY report on topics that can be sensationalized, and with no apparent concern about the accuracy of such pieces.

The details and complexities of interpreting research findings can be time-consuming and hard, but very worthwhile.

Don’t fall for click bait health and nutrition headlines.

References

1. Janssen JA & Lamberts SW. IGF-I and longevity. Hormone Research 62 2004104–109.
2. Renehan AG, Zwahlen M, Minder C, O’Dwyer ST, Shalet SM & Egger M. Insulin-like growth factor (IGF)-I, IGF binding protein-3, and cancer risk: systematic review and meta-regression analysis. Lancet 2004 ;363:1346–1353.
3. Kaplan RC, Strickler HD, Rohan TE, Muzumdar R & Brown DL. Insulin-like growth factors and coronary heart disease. Cardiology in Review 2005 ;13:35–39
4. Why use the mouse in research? www.yourgenome.org/facts/why-use-the-mouse-in-research

• 3000 words, 30-minute read.

Key Points

• Alcohol contains 7 kcals per gram.
• If you want to keep on track with your diet, you will need to plan your alcohol consumption. This involves cutting back on calories throughout the day so that they can be used for alcohol consumption.
• A great tool for learning the calorie and alcohol content of your drink is the website and app http://www.getdrunknotfat.com/
• Alternate between periods of alcohol and glasses of ice cold water during a night out to keep on top of your hydration.
• Be mindful of dietary choices and food environment when drunk.
• You don’t have to live like a monk. Getting drunk once in a while in good company can make you happy, improve your social life and help with dietary adherence in the long run.

First things first.

This article does not encourage you to go out and get drunk. Getting drunk is not healthy and will increase your likelihood of injuring yourself, pissing people off, running your blood glucose levels all over the place, and possibly dying sooner than expected.

In saying that, we’ve all been there. Whether it’s a family do, get-together with an old friend or a full-blown night on the town when many of us enjoy a drink (or two).

In this article, I want to address how you can drink alcohol without ruining your diet, causing unwanted fat gain, and still manage your diabetes safely.

Go Out, or Stay in and ‘Be Good.’?

Judging by the fact you’re reading this article you’ve probably asked yourself that question many times before.

You’ve maybe started a diet or training regime and can’t quite get your head around what to do when one of the following circumstances occurs,

• Your best friend is back for the weekend and wants to hook up for a drink?
• You have a family wedding where everyone will be drinking?
• Your best mates are looking to go out and get loose?

But, you’re stuck at home pulling your hair out pondering about what to do, stuck between “being healthy” and suffering that feeling of FOMO (fear of missing out)

Should I go for one or two drinks?

You could, but you’re worried about breaking your diet. Plus 1-2 drinks is never a true story.

Should I just let loose?

You could, but you’ll feel guilty because you’re going off the plan.

Netflix and chill?

Maybe the safest option, but the most boring? Maybe…

Here’s the thing.

There is no reason you can’t adhere to your diet whilst still having a night out and enjoying yourself.

If you’ve read my book or watched any of the execution plans on how to build your own diet, you’ll know by now that a successful diet for fat loss and muscle gain is grounded on principles, not a fixed hard plan.

Principles give flexibility, with flexibility comes enjoyment and, most importantly, adherence – the most important building block of any diet.

When it comes to including alcohol in your diet and continuing to make good progress in the gym, there are a number of factors you need to consider.

1. Total caloric intake of alcohol consumed.
2. Managing blood glucose levels when drinking.
3. How often you feel the need to drink.
4. Dietary choices while drinking.

Let’s talk through each of them with respect to enjoying alcohol as part of a healthy lifestyle.

Total caloric intake of alcohol consumed.

Ideally choose alcoholic drinks that contain very few calories in the form of carbohydrates, protein, and fat.

Do you know the calorie and alcohol content of your usual tipple?

A great tool for doing this is the website and app http://www.getdrunknotfat.com/

Get Drunk Not Fat is a site that lists and ranks alcohol based on the amount of included alcohol % versus calorie content. The tool is supported by beer, wine, and liquor manufacturers to bring you the most accurate calorie and carbohydrate information. Knowing the carbohydrate content of your drinks is vital information to understand the impact it will have on your glucose level. Use this tool the next time you plan your drinking escapades.

Spirits and diet mixers score best over higher calorie options like beer, creamed liquor, and wines.

If you want to keep on track with your diet, you will need to plan your alcohol consumption. This involves cutting back on calories throughout the day so that they can be used for alcohol consumption.

For example, let’s consider a man who is planning a night out with mates, where he drink 8 units of alcohol (classed as a binge), whose total daily macronutrient targets are:

• 200 Protein,
• 100g Fat
• 250g Carbohydrate
• Totalling = 2700 kcals.

A simple way of going about things would be to cut back his fat intake by 50 grams and protein by 40g, leaving 450kcal (50g x 9kcal/g) from fat and 160 kcal (40g x 4kcal/g) from protein to go towards alcohol. Respectively, that’s 610kcals left in the bank for his night out. 610 / 7kcals/g alcohol = 87g Alcohol to play with.

Of course, this is only an example, you could cut more calories and drink more alcohol if you wanted. Do bear in mind the more calories you cut in favour of alcohol, the greater risk you run of falling short on key nutrients. Don’t do this.

Carbs are left untouched as a preventative measure for hypoglycaemia during drinking.

Protein requirements are already above his essential needs, so there is wiggle room to cut. 

What do we get for 85g Alcohol (610 kcals)?

When it comes to working this out, I like to go with straight spirits and diet soft drinks since they are zero calorie

Most spirits contain around 40% alcohol. If we multiply an average spirit shot of 25ml by 40%, each 25ml shot provides 10g of alcohol. Each gram of alcohol contains 7kcal. So 70kcals per shot.

So giving up 50g fat and 40g protein (610 kcals) gives us approximately 8.5 shots (85g alcohol).

Combine this with diet mixers and you’re good to go.

However, alcohol has a higher thermic effect of feeding (costs more energy to process), you’re usually more active on a night out (boogie) and the fact that you won’t be drinking every night of the week – the calorie intake from alcohol doesn’t do as much damage as people think.

If you don’t like spirits…

Whilst using the alcohol exchange system above is a better way of getting drunk for fewer calories, if you really don’t like spirits, then using the website/app above will allow you to search for your favourite beer or wine and work out its calories. So instead of doing the carb-alcohol swap, you’d just be filling in the calories you’ve saved with your favourite alcoholic drink.

Managing blood glucose levels when drinking.

This is often one of the most challenging aspects of diabetes management because you have a lot of variables to contend with. Have you ever been bemused by what happens to your glucose level, and its lack of consistency when drinking alcohol? Is it any wonder when you consider:

• Do you keep to spirits, or do you mix drinks?
• Did the bartender give me a diet or full sugar mixer?
• What drink did my friend just buy me?
• Have I had five or seven drinks now?
• Am I going to a dance club?

The main impact of alcoholic drinks on your blood glucose level is mainly determined by two factors.

Do your drinks contain carbohydrate?

How much are you going to drink?

Do your drinks contain carbohydrate?

If you choose non-carbohydrate drinks, such as spirits and diet mixers and dry wine, your big risk is hypoglycaemia. Why? When you drink alcohol, your liver goes into overtime detoxifying the alcohol and forgets to pump out its usual supply of glucose. If you do not reduce your background insulin or have small amounts of additional carbohydrate, say the occasional full sugar mixer, you will most likely go hypo.

If you choose carbohydrate based drinks, such as beer, lager, ale, cider, cocktails – it is common to consume from 50-100g of carbohydrate after just five drinks. You better believe you will have a glucose level through the roof. The DAFNE program teaches to give half the usual insulin for the carbohydrate in alcoholic drinks to prevent massive hyperglycaemia; but then to reduce background insulin overnight to prevent the hypo.

How many units of alcohol will you drink?

A good rule of thumb is that your liver takes one hour to detoxify one unit of alcohol. So for people with diabetes, that means one hour of hypo risk. If you are only having one medium glass of wine that is two units of alcohol, your risk is very small. However, if you get carried away and end up on a bender with shots, you can easily consume 20+ units. This means your risk of hypo lasts until the next evening.

Have you ever gone hypo after eating breakfast and giving your usual insulin following a big night? Well, that’s because your liver has not resumed its usual service of pumping out glucose.

I personally recommend eating a proportion of your daily calories in and around your drinking activities so you at least have some carbohydrate and nutrients to help keep your blood glucose levels stable.

To keep it simple and safe, you may be best served going for non-carbohydrate based drinks, because you only have to prevent going hypo, and you keep your calorie count down. Also take note of how many units of alcohol your drink, because that’s the number of hours you are at hypo risk for.

Even though alcohol is a liquid, it is a diuretic and promotes fluid loss. Your chances of dehydration will increase the more alcohol you consume.

You also need to be mindful of other factors that will accelerate the onset of dehydration.

These include,

• Pre-drinking hydration status. What have you drunk prior to your first sip? If you haven’t drunk much all day you may be at increased risk of dehydration.

• The hotter the climate the greater risk of dehydration. Think holiday time.

• The proximity of your alcohol fuelled activities to your last training session.

• Use of certain medications that promote fluid loss (diuretics etc.)

Alternate between periods of alcohol and glasses of ice cold water during a night out to keep on top of your hydration. Also, remember to rehydrate with at least 1-2 litres of ice cold water when you get back in the door after your night out.

How often you feel the need to drink?

The strategies outlined in this article are for casual drinking sessions.

If you feel the need to go out and get drunk every single night of the week, you run the risk of developing various alcohol-related health issues and nutrient deficiencies that will jeopardize your quality of life and efforts in the gym.

Dietary choices while drinking

Dietary choices while drinking are probably one of the biggest factors you need to be aware of , since, while counting your calories and planning your drinking intake can be a great way to keep on track with your diet, circumstances can change (quickly) when your ‘half cut’ (Irish for drunk) and intoxicated.

Sensory awareness drops and everything seems to taste good. The problem is, after 12 pm most of your food options boil down to pizza, kebabs, Mc Flurries and a 24-hour garage.

This opens up the possibility of doing a lot of damage to your fat loss efforts and diabetes management. It also renders all that time and effort you spent planning your alcohol intake, a complete waste of time

This is why I advocate drinking alongside a mixed macronutrient meal at the start of a drinking ‘session’ rather than hitting the spirits on an empty stomach. People with more experience of drinking with diabetes, who know their body inside out, may wish to opt for a lower carb meal to prevent bloating. However, I do feel it is important to have carbohydrate on board if you plan to get drunk.

If you do feel the need to eat after you stumble out of a nightclub, then some great worldwide available calorie controlled ‘take away’ options include,

• A 6” Subway sandwich, stacked with chicken breast and a tonne of veg + light salad dressing if you feel like it.

• Grilled tikka or paprika chicken kebab on its own or wrapped in naan bread with salad. Pretty much all kebab houses across the world will cook this for you when asked.

• Pack of rice cakes and some pre-cooked chicken or ham with an apple. Every 24-hour convenience shop will sell this kind of stuff. Only 2-5 rice cakes mind you.

If you do screw up and end up eating double your bodyweight in pizza, don’t panic you can always trim off the excess calories over the next few days or compensate with extra physical activity.

On a blood glucose management note, you may have to reduce your usual insulin dose for this late night feast if you have had a lot of alcohol. Remember, your liver is not back to pumping out glucose until the last drop of alcohol has been detoxified.

Take Home

Getting drunk once in a while can complement your muscle building and fat loss progress – not from the empty nutrition alcohol provides, but from having the flexibility to socialize and enjoy yourself from time to time. This does great things for the mind and long-term dietary adherence.

When you’re given an inch, don’t take a mile. Getting drunk every once in a while is not every other night of the week or every single weekend. Keep your heavier drinking sessions to once every month or more.

Being drunk all the time has no place in any healthy lifestyle, least of all in a person with diabetes who trains hard to be in great shape.

Written by Phil Graham

Founder of Diabetic Muscle and Fitness

Sports Nutritionist, Strength Coach, and Fitness Educator

Type 1 Diabetic for 12 years

• 1000 words, 8-10 minute read.

Key Points

• Organic food is not all it’s made out to be. It certainly won’t help prevent or control diabetes better than non-organic alternatives.
• People automatically assume organic food commodities are healthier and lower in calories than non-organic alternatives.
• People are willing to pay more for organic food – with no clear understanding of organic food production laws or loopholes.

When you have diabetes eating a healthy diet is always top of your mind.

Why?

Because you hear YOU MUST in the media, you see IT’S ESSENTIAL on the internet, and YOU ARE TOLD SO every time you go to see your healthcare team.

But do you know what healthy choices are?

Where should you be prioritising you money?

What about Organic food? That’s healthy, right?

When you go to the supermarket, do you always reach for the Organic options?

When discussing food choices with friends, are fighting the corner of the organic options?

Some questions you may want to consider are:

• What’s the evidence for organic vs. non-organic?
• What’s the price differential?
• Are my beliefs based on fact, or clever marketing?

As you read this article you may find yourself challenging your beliefs about Organic food, and by the end, you may even be thanking me for saving you a pretty penny.

Let’s get down to business.

Over the past decade or so food marketers, restaurants and supplements companies have capitalised on the growing trend of health and fitness. This has led to a massive consumer trend in purchasing ‘organic food’. In many cases, the sale of organic food is growing faster than conventional foods.

It’s not difficult to find the ‘Organic’ versions of your favourite food pretty much everywhere you go, usually at double the price.

A so-called ‘health halo’ has been attached to organic food.

Consumers are more concerned about food production methods than ever before. This includes hormones, pesticides, additives, antibiotics and all the other modern-day food technology methods used to boost food production and shelf life.

The health halo effect of organic food has lead many consumers to believe organic food is superior, both taste wise and nutritionally.

But, is there any truth to this?

Interesting Research by Lee and colleagues in 2013 cornered 115 members of the public in a regular supermarket and asked them to evaluate three paired food samples,

• Two types of cookies, crisps and yoghurt.
• One of each food was labelled ‘regular’ and the other ‘organic’, though both were organic.

What were the findings?

Despite there being little data to support the majority of organic claims being nutritionally superior to conventional foods, (which I will cover in another article), the researchers found the food labelled as ‘organic’ was perceived to be lower in calories than foods without the organic label. It also yielded better nutritional evaluations (e.g., tastes lower in fat, higher in fiber) than foods without the organic label.

Participants were also willing to pay more for foods labelled as organic.

What is the reason for this? 

The report concluded that the health halo effect is primarily driven by automatic processing, based on individual heuristics.

In other words, people choose organic food without thinking or knowing too much about it. Automatically they assume it will be a healthier and more nutritious food choice compared to its non-organic alternatives.

Are you paying over the odds?

Lack of education on the ‘lack of evidence’ behind organic food is leading more and more people to spend unnecessary amounts of cash on their diet. As a result, this may jeopardize certain individuals willingness to start, never mind follow, a healthy eating lifestyle.

If you’re going to pay double the price for your food, you should expect double the return on your investment, if not more. There is no evidence whatsoever to support organic food will provide this, especially when it comes to organic commodities like cookies, yoghurts and crisps.

The next time you visit the supermarket don’t automatically assume a food with an organic food label is healthier for you than a non-organic version. Buying a food with an organic food label is buying on blind faith especially from a commercial supermarket. There are so many loopholes in respect to organic food production that I’ll cover them another time. Safe to say, it’s often hard to know what you’re getting unless you visit a farm or produce the food yourself.

Rather than splashing the cash on organic food commodities like bars, crisps, yoghurts and snacks, just buy the non-organic foodstuff. There really is no difference, just price bracket. The money you save can go into more important stuff like quality meat, fish and eggs, fruit, vegetables, gym membership, key supplements, diabetes healthcare supplies and everyday normal living costs.

TAKE HOMES

Instead of worrying about whether or not your next yoghurt is organic, focus on more important stuff like where was the food was produced and how was it handled up until reaching the shelves of your local food store.

Always ensure every food product you buy is clean, in date and undamaged.

Instead of worrying about where the ‘organic food label’ is, ask yourself these five more important questions,

What is the use by date? (this is more important than the ‘best before’ date)

• Does the food look off?
• Does the food smell off?
• Is the packaging damaged?
• Has it accidentally thawed?
• Have I cooked and prepared it properly?

Provided all these answers are positive, you can rest assured your food is suitable for human consumption and won’t make you ill.

Exceptions

There are exceptions to buying organic food.

1. If you want to support your local farmer or food producer.
2. If the organic food product is free from a particular nutrient you may be intolerant or allergic to (and the non-organic version contains it).
3. If eating organic simply sits better with you, and you can afford it. Keep eating it.

Written by Phil Graham

Founder of Diabetic Muscle and Fitness

Sports Nutritionist, Strength Coach, and Fitness Educator

Type 1 Diabetic for 12 years

References

1. Smith-Spangler C et al. Are organic foods safer or healthier than conventional alternatives?: a systematic review.Ann Intern Med. 2012 Sep 4;157(5):348-66. doi: 10.7326/0003-4819-157-5-201209040-00007. Ann Intern Med. 2012 Sep 4;157(5):348-66.
2. You taste what you see: Do organic labels bias taste perceptions?. Food Quality and Preference Volume 29, Issue 1, July 2013, Pages 33-39

• 1873 words, 20-minute read.

Key Points

• Blaming today’s obesity problem on sugar is narrow-minded.
• Hyper-palatable foods and food environment are much bigger culprits in the obesity puzzle.
• There is a no compelling evidence to suggest sugar is addictive in humans.

Sugar has got itself a bad reputation and is considered by many to be the main reason for today’s obesity problem. In fact, the notion that sugar is an addictive substance is becoming increasingly popular.

A google search of the words ‘Sugar + addiction’ returns over 10 million results. If you ask the average layperson on the street about sugar, they’ll tell you it’s unhealthy, addictive and will make you fat.

Even the UK government has published draft legislation for a tax on sugar-sweetened drinks, which is set to begin from April 2018. Health campaigners have broadly welcomed the initiative. There will be two bands – one for soft drinks with more than 5g of sugar per 100ml and a higher one for drinks with more than 8g per 100ml.¹

Ministers hope it will help tackle the nation’s obesity problem.

Is sugar addiction really the culprit?

Firstly, let’s define the words sugar and addiction.

Sugar is the generic name for sweet, soluble carbohydrates, many of which are used in food.

Addiction is a brain disorder characterized by compulsive engagement in rewarding stimuli, despite adverse consequences. The stimulus can vary from a range of activities including gambling, sex, shopping, drinking alcohol, smoking and food.

The link between sugar addiction and obesity is a growing matter.

As the number of people living with obesity continues to climb, the idea that overconsumption of food is a result of an underlying ‘food addiction’ is becoming gradually more popular.

Understanding Food Addiction.

The term ‘food addiction’ was first used by the physician, allergist, and researcher Theron Randolph from the United States² to describe the addictive-like consumption of various foods, such as corn, milk, eggs, and potatoes back in 1956. However, the food industry has had massive advances in food technology and product development since this research first evolved; in particular, the increased production of highly processed, hyper-palatable (tasty) junk food, is nowadays considered much more addictive³ that good old-fashioned corn, milk and eggs.

Why research food addiction?

The problems related to obesity have resulted in it being a major public health burden worldwide, in industrialised societies, due to its colossal social and economic impact⁴. Despite the important developments in the study of obesity, incidence rates continue to rise, suggesting other factors must be involved in the development of this disease.

Health researchers hope that studying obesity under the umbrella of addiction will highlight key areas of focus for prevention, treatment, and public health policy^5,6.

Interesting new theories like the food addiction (FA) model have evolved to help explain the widespread advancement of obesity over the last 30 years. The FA suggests that excessive consumption of palatable foods may be understood within the same neurobiological framework as drug addiction.

The FA model has been open to much questioning ^7,8 especially the popular view that ‘Sugar is addictive’.

Sugar addiction ‘should be treated as a form of drug abuse’ according to the Independent, another British national newspaper.

Sugar ‘is the new crack cocaine’ according to British national newspaper The Daily Mail.

While there is evidence to suggest sugar and sweetness can induce reward centres in the brain (food, in general, does that), it’s hard to take the above claims seriously.

Fortunately, a recent paper by Westwater and colleagues⁹ published in the European Journal of Nutrition titled ‘Sugar addiction: the state of the science’ sheds some great light on the topic and highlights the evidence for sugar being addictive in humans is far from convincing.

The authors made the following key findings

• The science of sugar addiction at present is not compelling.

• Most of the evidence is limited to the animal neuroscience literature, and it is far from convincing.

• Importantly, several key elements of drug addiction have not been evaluated in sugar addiction models, such as the transition to compulsive drug-taking and dose-dependent effects on addiction liability. There remains a paucity of human evidence in this area, and we did not consider the literature encompassing the behavioural and neural effects of sweet or palatable food consumption as this would be far too indirect to the question of sugar addiction.

• There is limited data on pure sugar consumption as we rarely consume sugar in isolation, and the ecological validity of studies examining pure sugar consumption in humans would be limited.

• Nevertheless, sugar addiction remains a very popular and powerful idea, but as this special issue illustrates, it is by no means alone in this regard when it comes to misconceptions about sugar.

• Even the most perfunctory Internet search reveals how much emotive and explanatory power the term ‘sugar addiction’ has when used in its lay sense for individuals personally, as well as in the context of major public debates such as those over the sugar tax or campaigns such as Action on Sugar in the UK.

• From a health policy perspective, it is unlikely that sugar could be excluded from individuals’ diets given its presence in numerous food items.

• Given the multitude of interacting factors that increase one’s risk for eating disorders and obesity, we argue that support of sugar addiction as a primary causal mechanism of weight gain represents an extremely narrow view that fails to capture the complexity of these conditions, and one that may hamper more coordinated and appropriate responses.

• Furthermore, while there is a pressing need to address these important concerns, we argue that it is dangerous to draw strong conclusions about the validity of sugar addiction based on the current evidence. There are many strong arguments for cutting down the consumption of sugar and reformulating food products accordingly, yet these arguments will all stand or fall according to the scientific case that supports them.

Whilst there’s no real evidence that sugar is addictive in humans, it is fair to say that certain individuals may struggle to control their sugar intake due to food environment, improved availability and access to hyper-palatable, calorie-dense junk food.

Let’s take a closer look at each.

Hyper-palatable junk food

Palatability is the pleasure (i.e. hedonic reward) provided by foods or fluids that is agreeable with our ‘palate’ at a specific time.  The palatability of a food or fluid changes relative to the homeostatic satisfaction of our nutritional, water, or energy needs.

The palatability of a food will increase when you are hungry or have an appetite.

Hunger is an experience when your body needs to refuel. Usually, after fasting or physical activity, you’ll get all kinds of symptoms including stomach rumbles, nausea, low blood sugar and weakness.

Once hunger has been fulfilled, the very foods that seemed palatable at the time, become undesirable. This is especially true for whole foods like meat, fish and vegetables.

However, moments later you order a dessert because you fancied something sweet and cold on your tongue.

The latter is known as appetite.

That being, the ‘desire’ to eat.

Even when full, appetite can cause certain individuals to eat.

This is where hyper-palatable junk food can increase obesity risk.

Hyper-palatable foods are designed in such a way that we get increased feelings of pleasure when consuming them. This is achieved by suffusing the foods with increased levels of fat, sugar, flavours, and food additives.

These foods are low in fibre and protein – the two most filling nutrients, meaning they don’t fill you up and are easily overeaten, resulting in a larger food and calorie intakes ^10,11.

The end result is increased sugar consumption, higher calorie intake and increased chances of fat gain if the excess energy isn’t burnt off.

Hyper-palatable foods are more to blame for today’s obesity problem than sugar alone. The fact of the matter is: sugar is rarely eaten on its own.

Food Environment

Your environment can have a major influence on what you eat.

If you live in a house that’s full of hyper-palatable junk food, you’re more likely to eat it.

If you get asked out regularly on social occasions, are you at a greater risk of exposing yourself to hyper-palatable food options, and, in order to fit in, you eat what’s given to you.

If you are coping and trying to forget about your problems, there a chance you may reward yourself with hyper-palatable foods because they make you feel better.

If you get a sharing dessert, are you more than likely going to eat more and prevent good food going to waste?

Availability/Access of Hyper-palatable

Junk food is a convenient snack. It doesn’t take much effort to peel back a wrapper and devour. It’s available everywhere you go, even on the road. There’s no escaping it.

Busier lifestyles and less time to cook food from scratch = a greater temptation to grab something on the go in order to ‘fill the gap.

If you lack a basic understanding of how different food sources impact appetite, or how excess calories affect body composition, it’s inevitable you’ll overeat these foods and ramp up the sugar grams.

Take Home  – Is Sugar Really Addictive, like everyone says it is?

No, Sugar is not addictive.

It’s unfair and narrow-minded to blame the obesity problem on sugar alone. Generally speaking, as a population we are eating more sugar as a result of improved access and availability to great tasting, highly convenient, calorie-dense junk food.

However, not everyone exposed to hyper-palatable food environments develops obesity.

This gives rise to research that helps identify the biological and/or behavioural motives why people eat highly palatable foods, which could help explain an individual’s susceptibility, or resilience, to obesity. Future research is also required to more extensively study the validity of food addiction in humans.

Written by Phil Graham

Founder of Diabetic Muscle and Fitness

Sports Nutritionist, Strength Coach, and Fitness Educator

Type 1 Diabetic for 12 years

References

1. UK pushes ahead with sugar tax http://www.bbc.co.uk/news/health-38212608
2. Randolph T (1956) The descriptive features of food addiction; addictive eating and drinking. Q J Stud Alcohol 17:198–224
3. Meule A (2015) Back by popular demand: a narrative review on the history of food addiction research. Yale J Biol Med 88:295–302
4. Lopez-Legarrea P, Olivares PR, Almonacid-Fierro A, Gomez-Campos R, Cossio-Bolanos M, Garcia-Rubio J. Association between dietary habits and the presence of overweight/obesity in a sample of 21,385 chilean adolescents. Nutr Hosp. 2015;31(5):2088–2094.
5. Gearhardt A, Roberts M, Ashe M (2013) If sugar is addictive… what does it mean for the law? J Law Med Ethics 41(Suppl 1):46–49. doi:10.1111/jlme.12038
6. Gearhardt AN, Grilo CM, DiLeone RJ et al (2011) Can food be addictive? Public health and policy implications. Addiction 106:1208–1212. doi:10.1111/j.1360-0443.2010.03301.
7. Ziauddeen H, Farooqi I, Fletcher P (2012) Obesity and the brain: how convincing is the addiction model? Nat Rev Neurosci 1:279–286.
8. Ziauddeen H, Fletcher PC (2013) Is food addiction a valid and useful concept? Obes Rev 14:19–28. doi:10.1111/j.1467-789X.2012.01046.
9. Westwater et al. Sugar addiction: the state of the science. Eur J Nutr (2016) 55 (Suppl 2):S55–S69 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5174153/pdf/394_2016_Article_1229.pdf
10. Yeomans MR, Lee MD, Gray RW, French SJ. (2001). Effects of test-meal palatability on compensatory eating following disguised fat and carbohydrate preloads.Int J Obes Relat Metab Disord. 25(8):1215-24. PMID 11477507
11. Robinson TM, Gray RW, Yeomans MR, French SJ. (2005).Test-meal palatability alters the effects of intragastric fat but not carbohydrate preloads on intake and rated appetite in healthy volunteers. Physiol Behav. 84(2):193-203. PMID 15708771