I was interested to see a recently published study which links shift work with an increased risk of type 2 diabetes, and this association was particularly strong in men [1]. This study cannot be used to conclude that shift work somehow causes diabetes (only that they are associated). The same is true of studies which have linked short-sleep with an increased risk of diabetes [2].

However, there is some evidence that short sleep has the potential to impair blood sugar control (glycaemic control).

In one study, nine healthy adults were tested to see what effect sleep deprivation has on insulin resistance [3]. On one night, individuals were allowed to sleep for up to 8.5 hours (23.00 – 7.30 hrs). On another night, sleep was only permitted for four hours (01.00 – 05.00 hrs). The actual average sleep times were 7 hours 34 minutes and 3 hours 46 minutes respectively.

The results showed that in the sleep-deprived state there was evidence of insulin resistance. ‘Endogenous’ sugar production (internal production of sugar, say, from the liver) was higher, and clearance of glucose (say, into muscle cells) was lower in the sleep-deprived state.

Now, less than four hours sleep is not much sleep. But then again, increased insulin resistance was seen in individuals after just one night of sleep deprivation. It’s possible that less extreme sleep deprivation or sleep disruption (such as shift work) over longer periods of time also poses hazards regarding diabetes risk.

In one study, the impact of ‘shift work’ on disease markers, including those for diabetes [4]. 26 healthy individuals were allowed to sleep for up to 10 hours a night for 10 nights. Then, they were restricted to no more than 5 hours sleep for 8 nights. In this setting, some individuals took their sleep at night. Others, however, simulated ‘shift work’ by taking their sleep in the day on four of the eight days.

Short sleep led to a reduction in insulin sensitivity (as has been noted in previous studies), as well as an increase in markers of inflammation. Also, in men, reductions in insulin sensitivity and increases in inflammation were about twice a bad when they were sleeping in the ‘shift’ setting, compared to those sleeping normally (at night).

The evidence as it stands supports the idea that both duration and pattern of sleep can have a bearing on risk of type 2 diabetes, and other chronic health issues too.

References:

1. Gan Y, et al. Shift work and diabetes mellitus: a meta-analysis of observational studies Occup Environ Med doi:10.1136/oemed-2014-102150

2. Chaput JP, et al. Sleep duration as a risk factor for the development of type 2 diabetes or impaired glucose tolerance: Analyses of the Quebec Family Study. Sleep Med. 2009;10(8):919-24

3. Donga E, et al. A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects. J Clin Endocrinol Metab. 2010;95(6):2963-8

4. Leproult R, et al.^, Circadian misalignment augments markers of insulin resistance and inflammation, independently of sleep loss. Diabetes. 2014;63(6):1860-9

However, blood sugar control is a spectrum: between what are thought to be ‘healthy’ blood sugar levels and type 2 diabetes exist states which are not extreme enough to be called diabetes, but are associated with enhanced risk of developing this condition.

For example, if the glucose concentration 2 hours after the glucose load is 7.8-11.1 mmol/L (140-200 mg/dL), then a diagnosis of ‘impaired glucose tolerance’ is made. The term ‘Impaired fasting glucose’ is also used to define individuals with fasting blood glucose levels of 6.1-6.9 mmol/L (110-125 mg/dL) (according to the World Health Organization).

Another relatively newly-coined term is ‘pre-diabetes’. This diagnosis is based on a measurement known as the HbA1c which gives an indication of the overall blood sugar (glyaemic) control over the preceding 3 months or so. One of the supposed advangates of this test is that it does not require fasting nor an oral glucose load. According to the American Diabetes Association, a HbA1c of 5.7%-6.4% indicates ‘pre-diabetes’, though some bodies have recommended a slightly higher threshold for this condition. The basic thinking here is that by identifying pre-diabetes, individuals may be helped with interventions including drug therapy.

While this all may seem eminently sensible on the surface, there are a number of problems with this approach. These are explored in quite some detail in a paper published this week in the British Medical Journal co-authored by Professor John Yudkin from University College London and Professor Victor Montori from the Mayo Clinic in the US [1].

The article explains that the relationship between glycaemic control and health risks are a continuum, and where we begin to diagnose pre-diabetes is utterly arbitrary. If we apply the criterion recommended by the ADA, then apparently half the Chinese population (that’s almost half a billion people) have pre-diabetes. The authors question whether we even have the resources to treat vast swathes of the population according to these arbitrary criteria.

Of course a stronger case might be made for those arguing for population treatment if this had been tested. But as the authors point out, there simply is no evidence that earlier intervention based on the ADA’s criteria leads to either improved health or a reduced risk of death.

What we do know if that certain interventions appear to be able to delay the onset of diabetes by about 2-4 years. The real effects in terms of reducing healthcare costs or disease burden, though, are unknown.

And even if genuine benefits exist, let’s not forget that applying a diagnosis of ‘pre-diabetes’ to someone is not without risk. We have risks associated with medication, say, but also there may be issues with self-image, health and life insurance (particularly in the US).

One of the first-line drugs used to treat pre-diabetes is metformin. The authors point out that data suggest that using this drug may reduce the risk of developing type 2 diabetes by about 31 per cent. However, as the authors point out, what this means is that treating pre-diabetes in this way means individuals now have a “100% chance of using metformin with the goal of reducing by 31 per cent their risk of developing a condition that might require them to use metformin.”

This approach with metformin or some other drug may have some sections of the drug industry rubbing their hands with glee, I suppose, but it’s certainly true that overall benefit is not assured, and there is even considerable potential for harm.

The authors are sceptical regarding any supposed benefits, and also warn that we risk deflecting from the real issues with diabetes and pre-diabetes relating, for instance, to diet and exercise. The article ends with three points that doctors should discuss with patients. These are:

• A diagnosis of pre-diabetes does not mean that you will develop diabetes. In fact, of 100 people like you, fewer than 50 are likely to develop diabetes in the next 10 years

• There are ways of reducing your risk of developing diabetes that involve changing your diet and being active. These can result from efforts you make as well as changes in your environment (food supply, workplace conditions, education, and other social determinants of health)

• There are drugs to delay diabetes, but these are the same drugs you will need if you do develop diabetes, and the value of starting them before you have developed diabetes is unknown

The footnotes to the article state that: “The authors are clinical academics with a shared interest in patient centred diabetes care and shared decision making.” And this comes loud and clear in their article, I think. Their focus really does seem to be on taking an objective look at the data and giving patients the very best information on which a truly informed decision can be made.

The article also states that it is: “…part of a series on overdiagnosis looking at the risks and harms to patients of expanding definitions of disease and increasing use of new diagnostic technologies. The underlying message here is that more medicine is not necessarily better (and may in fact be a bad thing). We need more articles like this, and we need more high profile medical journals willing to publish them.

References:

1. Yudkin JS, et al. The epidemic of pre-diabetes: the medicine and the politics. BMJ 2014;349:g4485

In some respects, IGT can be thought of as a potential stepping stone between health and type 2 diabetes: 25 – 75 per cent of people with IGT go on to develop type 2 diabetes within a decade, apparently.

If someone was to give three words of advice for someone with IGT they would undoubtedly be ‘cut the carbs’. Cutting back on sugar and starch in the diet is what I have found works best for improving blood sugar control and perhaps retaining some insulin sensitivity. There are other things that might be considered too (such as physical activity, if this is not currently a feature of someone’s life), but scaling back carbohydrate intake would be my number one piece of advice.

I was therefore interested to read a recent study in which a ‘low carbohydrate diet’ (LCD) was trialled in a group of 72 individuals with IGT [1]. Half were educated about low-carbohydrate eating and encouraged to adopt this diet for a year. The other half of the group was left to its own devices. For a free pdf of this article, click here.

Here is a description of the intervention for the ‘LCD’ group.

The individuals in this group were instructed to aim for a maximum daily intake of carbohydrate of 120 grams (a higher threshold than popular low-carbohydrate diets).

At the end of study, 12 months, the LCD group saw significant improvements in practically every parameter measured by the investigators, including:

• Body weight
• Fasting blood glucose level
• HbA1c (measure of blood sugar control over approximately the last 3 months)
• Fasting insulin level
• Measures of insulin sensitivity
• ‘Healthy’ HDL cholesterol level
• Triglyceride levels

Crucially, about 70 per cent of the group saw a return on blood sugar levels to normal, compared to only about 8 per cent in the control group. Not one person in the LCD group developed diabetes during the study, compared to 5 (14 per cent) in the control group.

The results clearly show that compared to ‘doing nothing’, restricting carbohydrate helps people with IGT. One might argue that perhaps another sort of diet (e.g. a low fat one) would work even better. However, as the authors point out, other studies have found that in those with IGT, low-fat eating leads to a one-year incidence of type 2 diabetes of between 2.0 and 12.5 per cent. This does not compare so favourably the 1-year incidence of 0 per cent found in LCD eaters in this study.

References:

1. Maekawa S, et al. Retrospective study on the efficacy of a low-carbohydrate diet for impaired glucose tolerance. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy 2014:7 195–201

In its statement, Diabetes UK informs us that “while the NHS is spending £10 billion per year on diabetes care, this money is too often being used ineffectively, with the vast majority spent on treating complications that could often have been prevented if the person had received good healthcare in the first place.”

Diabetes UK bases its claims on a report it commissioned, which I have not read, but have no reason to doubt either.

However, when I hear anyone talking the good management of diabetes, my mind very often goes to dietary approaches first. Diabetes is principally a condition of impaired ability to handle glucose in the bloodstream. While the body can liberate glucose into the bloodstream (particularly from the liver), much of the sugar in the bloodstream tends to find its way there from the food we eat. Sugar is an obvious source, but another major potential provider of glucose is starch (because starch is basically made up of chains of glucose molecules).

I can categorically state here that when individuals with diabetes cut back on carbohydrates, they almost always see significant improvement in their blood sugar control. They usually lose weight, and see improvements in markers of disease too. I’m most certainly not the only person to have noticed this. Just yesterday I met a most wonderful general practitioner who has come to the low-carb approach quite late in his career, but has used it to utterly transform the health of his patients. He showed me a variety of graphs from several patients pre- and post-adoption of a lower carbohydrate diet. He relayed a few stunning anecdotes too of people who believe eating a lower-carb diet has given them their health and their lives back.

None of what he told me surprised me, but it did not fail to warm my heart, either.

Beyond me and my GP friend, though, we have the collective experience of literally thousands of individuals with diabetes who have often seen comprehensive improvement in their condition and general health by scaling back the carbohydrate. Many type 2 diabetics them have been able to scale back their medication too, or even dispense with it entirely. Type 1 diabetics will very often report the need for much less insulin.

The generally better blood sugar control these people enjoy will, by rights, lead them to suffer less in the way of diabetic complications. In its statement this week, Diabetes UK highlighted the foot-related complications that diabetics can suffer, one potential end-result of which isamputation.

I do not doubt Diabetes UK’s desire for diabetic care to be better, and I also do not doubt the ability of lower-carb diets to help diabetics control their blood sugar better and improve their general health. So, excuse me for being a little aghast at the dietary advice given to diabetics here. Here’s a screenshot of Diabetes UK’s dietary advice for diabetics regarding starch in the diet:

Yes, that’s right, according to Diabetics UK, a third of a diabetic’s diet should be made up of foods that are essentially concentrated glucose (many of which, by the way, are known to be highly disruptive to blood sugar). Note that the charity recommends diabetics eat up to fourteen portions of starchy foods each day.

I won’t mince my words and state here that I believe these recommendations are utterly mad. My experience tells me they will generally just entrench diabetics in their condition and the need for medical care. Compared to a lower-carbohydrate diet, the regime advocated by Diabetes UK stands to worsen blood sugar control and increase the need for medication and risk of complications. If Diabetes UK is serious about helping diabetics, I suggest it starts by ceasing to recommend a diet that, in my view, is utterly unsuitable for diabetics.

The authors suggest that a possible explanation for the latter finding is ‘reverse causality’. Essentially, the idea here is that as people get sick, they then reduce their coffee consumption. In other words, illness leads to reduced coffee consumption, not the other way round. However, even then the analysis was performed to adjust for this (by excluding those with other illnesses), the results were pretty much the same.

The authors also found that the benefits associated with coffee consumption only existed for caffeine coffee (not decaffeinated). However, as they explain, decaffeinated consumption was generally low and the numbers of relevant people in the study may not have been enough to pick up any effect.

Other evidence ha founds a link between caffeinated coffee and reduced risk of type 2 diabetes (but no such link for decaffeinated coffee) [2].

Before we get too far ahead of ourselves, I feel it’s worth reminding ourselves here that these studies (so-called ‘epidemiological’ studies) cannot be used to conclude that drinking caffeinated coffee reduces the risk of type 2 diabetes (only that there is an association).

However, we do have some ‘clinical’ evidence that suggests that coffee may indeed be protective. In a study published in the American Journal of Clinical Nutrition, the effect of coffee-drinking on a variety of biochemical markers of disease was assessed [3].

A group of coffee drinkers were asked to abstain from drinking coffee for a month. The following month they were asked to drink four cups of coffee a day (a total of 600 mls of coffee a day). The month following this they were instructed to drink 8 cups of coffee a day.

Compared to drinking no coffee, drinking 8 cups a day was associated with significantly reduced levels of inflammatory markers (interleukin-18 and 8-isoprostane), as well as significantly raised levels of adiponectin. This hormone is secreted by fat cells, and has been shown to have generally beneficial effects on the body’s physiology including an ability to help the functioning of the hormone insulin. Broadly, these effects from drinking coffee would be expected to translate intorelative protection from type 2 diabetes.

While the evidence is not definitive, there is I think significant evidence that supports the idea that drinking coffee may help to reducerisk of succumbing to type 2 diabetes. There is some type 2 diabetes in my family, and I do drink coffee. I imagine I’ll continue to drink it (and enjoy it) for some time yet.

References:

1. Bhupathiraju SN, et al. Changes in coffee intake and subsequent risk of type 2 diabetes:
three large cohorts of US men and women. Diabetologia DOI 10.1007/s00125-014-3235-7

2. Floegel A, et al. Coffee consumption and risk of chronic disease in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Germany study. Am J Clin Nutr 2012;95:901-908

3. Kempf K, et al. Effects of coffee consumption on subclinical inflammation and other risk factors for type 2 diabetes: a clinical trial. Am J Clin Nutr 2010;91:950-957

While we do not want blood sugar levels to be too low, we do not want them too high, either. Abnormally elevated blood sugar levels is a hallmark feature of diabetes. One of the risks here is that glucose can bind to and damage tissues through the process ‘glycation’, and this can lead to a variety of complications for diabetics including nerve, kidney, blood vessel and eye damage.

One of the ways doctors can assess broad blood sugar control is through a test known as the ‘HbA1c’ (also known as the ‘A1c’, or ‘glycated haemoglobin’ or ‘glycosylated haemoglobin’). This test measures the amount of the protein haemoglobin in the red blood cells that is bound up with glucose. Basically, higher levels of HbA1c signal poorer blood sugar control.

In this week’s study, the relationship between brain structure and function and HbA1c levels was assessed in a group of non-diabetics. Higher HbA1c scores were found to be associated with smaller regions in the brain known as the ‘hippocampus’ (a part of the brain involved in memory). Those with higher HbA1c levels performed generally worse in tests of memory and learning.

In recent years, there has been growing interest in the relationship between blood sugar control and Alzheimer’s disease. Some researchers have suggested that at least some cases of this condition are due to what is being terms ‘type 3 diabetes’ – essentially, a mix of insufficient insulin (a feature of type 1 diabetes) with poorly functioning insulin (a common feature of type 2 diabetes).

Raised blood glucose levels might perhaps damage the brain through several mechanisms. Glycation is one. Also, though, raised blood sugar is inflammatory in nature, and inflammation in a potential underlying factor in deteriorating brain function over time.

Another mechanism that may be relevant here concerns cholesterol. Cholesterol is highly concentrated in the brain, where it performs several functions. It’s critical, for instance, to the function of the synapse (the ‘gap’ where one cell can communicate with another), and also has a role as an electrical insulator and as a structural ‘scaffold’ in the brain. Cholesterol is also a functional component of all cell membranes in the brain [2]. Higher levels of glycation (through higher blood sugar levels) can impair cholesterol uptake into the brain, potentially starving this organ of a component critical for its proper functioning.

What is perhaps interesting about this week’s study is that the relationship between improved blood sugar control and better brain function was found in non-diabetics. This throws up the possibility that scaling back on blood sugar disruptive carbohydrates such as those rich in sugar and starch could well be a good tactic for those of us wishing to preserve their mental functioning as they age, whether we have diabetes or not.

References:

1. Kerti L, et al. Higher glucose levels associated with lower memory and reduced hippocampal microstructure. Neurology, 23 October 2013

2. Seneff A, et al. Nutrition and Alzheimer’s disease: The detrimental role of a high carbohydrate diet Eur J Int Med 2011;22:134-140

However, while this may make sense, the reality is that studies do not generally link nut-eating with weight gain. In fact, some studies suggest that nuts may actually help weight control [1].

There are several potential explanations for this, including the fact that nuts will not tend to cause much upsurge in blood levels of sugar and subsequently insulin – a key fat storage hormone.

Moreover, another potential factor at play here concerns the effect of nuts on appetite and hunger. The relevance of this relates to the fact that some foods are more satisfying than others. The more satisfying a food is, the less we will tend to eat of it, and the less we may eat of other foods too.

There is some evidence that the sating effects of food can be related to characteristics such as its tendency to disrupt blood sugar levels (less disruptive foods being more sating) and its protein content (higher protein foods being generally more sating too). Nuts are relatively protein rich, and are not destabilising for blood sugar levels either. In theory at least, nuts should there do a decent job of satisfying the appetite.

Earlier this month saw the publication of a study in which individuals were asked to eat nuts each day in addition to their usual diet [2]. Individuals were asked to consume 43 grams of almonds (about 250 calories-worth) in one of four ways:

1. with breakfast
2. with lunch
3. as a mid-morning snack
4. as a mid-afternoon snack

Other individuals did not add nuts to their diet and were used as a comparison group (control).

Technically speaking, the groups eating the nuts should have eaten a total of about 7,000 additional calories over the course of the study, which might have translated into about an additional two pounds (about 1 kilogram) of body fat. Yet, those eating nuts were no heavier than those who did not eat them. This appeared to be due to the fact that the nut-eaters just automatically ate less of other foods.

One of the other measures used to assess subjects in this study was the ‘oral glucose tolerance test’ – a measure of blood sugar control. This test improved in those eating nuts compared to those not eating them. In fact, there is quite a lot of evidence which suggests that nut-eating may improve blood sugar control and perhaps help protect against the development of type 2 diabetes.

My experience that the appetite-sating effects of nuts can be highly valuable when this food is used as a snack between lunch and the evening meal. For many individuals, this is often too long a period of time to avoid getting very hungry. This can cause a tendency to overeat in the evening (and usually not very healthy foods at that). My experience tells me that hunger can drive increased consumption of alcohol.

And even before the eating and drinking begins, hunger and perhaps low blood sugar can cause some people to find themselves on a bit of a short fuse and quite impatient. Many individuals recognise that should they come home very hungry, they can somehow be a not very nice version of themselves, which can be annoying and distressing for those around them (such as their partner or child).

I’ve found repeatedly and consistently that when individuals manage their appetite and do not, say, come home in the evening very hungry, they eat and drink more healthily, and find their mood and tolerance are often vastly improved too.

References:

1. García-Lorda P, et al. Nut consumption, body weight and insulin resistance. European Journal of Clinical Nutrition. 2003;57 Suppl 1:S8-11

2. Tan SY, et al. Appetitive, dietary and health effects of almonds consumed with meals or as snacks: a randomized, controlled trial. European Journal of Clinical Nutrition advance online publication 2 October 2013

Another key underlying biochemical feature of PCOS is raised levels of insulin, usually related to ‘insulin resistance’ (impaired functioning of insulin). There is some thought that insulin acts on the ovaries to stimulate testosterone production.

One nutritional approach to PCOS is to take dietary steps to reduce insulin levels. This, in effect, means reducing in the diet carbohydrates that liberate significant quantities of glucose into the bloodstream (and therefore stimulate significant surges in insulin). At its heart, this is a ‘low-carb’ diet made up ostensibly of meat, fish, eggs, nuts, seeds, non-starchy vegetables and a little fruit such as berries. Not only does this sort of diet seem to help improve some of the biochemical imbalances typically found in PCOS, it often leads to weight loss too.

However, not all women with PCOS are overweight, but may nevertheless have features such as insulin resistance, raised testosterone and ovulation issues. I was very interested to read about a recent study in women with PCOS but normal body weight in whom two different diets were trialled [1]. In this study, it was not the ‘macronutrient’ make-up of the diet that was being tested (e.g. low fat v low carb), but the phasing of food intake.

In this study, 60 women were randomised to eat the same diet in one of two ways:

1.    a 980 calorie breakfast, a 640 calorie lunch and a 190 calorie dinner

2.    a 190 calorie breakfast, a 640 calorie lunch and a 980 calorie dinner

The trial lasted 90 days.

Neither group lost weight, but there were significant differences in several other measurements, all of them favouring the first regime (big breakfast, small dinner).

Some of these beneficial changes included:

• a 54 per cent reduction in levels of insulin
• a 50 per cent reduction in levels of free (active) testosterone
• an improvement in the frequency of ovulation

I think these results are impressive, and deserve attention. As I stated above, I believe the best diet, overall, for women with PCOS is one which is relatively low in carbohydrate. What this new study suggests is that the phasing of food intake can be important too, and there is evidence that benefits may be had from having a ‘breakfast like a king, lunch like a prince, and dinner like a pauper.’

References:

1. Jakubowicz D, et al. Effects of caloric intake timing on insulin resistance and hyperandrogenism in lean women with polycystic ovary syndrome. Clinical Science 2013;125(9):423

In an email I asked Dr Ruxton to refer specifically to the part of the review which supports he claim, and she provided me with this:

One [sic] page 19 of the 2011 Cochrane review, it is stated that: “dietary saturated fat reduction (through reduction and/or modification of dietary fat) may be protective of cardiovascular events overall, reducing them by 14%”

The implications for practice on page 29 also states that: “Dietary change to reduce saturated fat and partly replace it with unsaturated fats appears to reduce the incidence of cardiovascular events”

However, ‘cardiovascular events’ covers a multitude of conditions and events, not all of which are heart-related (e.g. stroke and circulatory problems in the legs known as ‘peripheral vascular disease’). To not understand the difference between ‘heart disease’ and ‘cardiovascular events’ either shows a fundamental lack of understanding or intellectual dishonesty (as I suggest to Dr Ruxton in an email to her which I reproduce in full below). There were also things about the ‘positive’ evidence which casts considerable doubt on whether any change in dietary fat was responsible for whatever benefits were seen (see below).

I also point out this critical fact: when the reviewers looked at heart-disease related outcomes (heart attack), there was no reduced risk associated with lower-fat or modified fat diets.

All these findings are the same across both 2011 and 2012 versions of the review.

Here’s my email response in full:

In her response to me, Dr Ruxton accused me of being “rather pedantic.”

Really?! Is it pedantic to point out that the claim she made was in no way at all supported by the review she cites? Is it ‘pedantic’ to point out the evidence which specifically contradicts her claim?

But, Dr Ruxton explains all when she tells me that:

While the Cochrane review used the terminology of ‘cardiovascular events’, the consumer tends to understand ‘heart disease’ better and this is why I chose this term for my press quote.

But as we know and as Dr Ruxton should know, ‘cardioavascular events’ and ‘heart disease’ are not the same thing at all.

And Dr Ruxton has nothing to say at all on the fact that when impact on risk of heart attack was assessed, no benefits were found at all.

Dr Ruxton also tells me that:

The view that reducing saturated fats and replacing them with unsaturated fats lowers heart disease risk is not at all controversial and is supported by public health bodies including NHS Choices…

and supplied this link http://www.nhs.uk/Livewell/Goodfood/Pages/Fat.aspx and this extract:

Notice that nowhere in these extracts is the claim made that replacing saturated fat with a ‘healthier’ fat reduces the risk of heart disease. And quite right too, seeing as there is essentially no evidence to support that idea.

In her response to the original piece, Dr Ruxton tells us that:

I can see that John and many of those who have commented on this forum do not believe the evidence suggesting that saturated fats represent a risk to cardiovascular health. You are, of course, entitled to your opinion, as am I.

Actually, I am not sure any of us are entitled to our opinions, when we have abundant evidence to look to. We know that reducing saturated fat or replacing it with other fats does not reduce the risk of heart attack, stroke, risk of death from cardiovascular disease or overall risk of death (all findings from the review Dr Ruxton herself quotes). And this is what really matters.

In my experience, individuals who do not believe that saturated fat poses hazards for health hold that view because they have read and assimilated the research and found nothing to incriminate saturated fat in terms of its influence on health.

Not only do we have the evidence being discussed here, but we also have several recent reviews of the epidemiological evidence that simply fail to link saturated fat and heart disease [2,3,4].

Anyone can make an honest mistake, of course, but I think Dr Ruxton compounds her error by refusing to accept the facts even when they were put in front of her face.

In her response to the previous post, she describes herself as an ‘independent dietitian’. Personally, I believe that use of the word ‘independent’ here is stretching it a bit, seeing as the Fat Information Service (and, I assume, Dr Ruxton) is bankrolled by Unilever.

To my mind, either Dr Ruxton does not have the ability to interpret the review she cites or has misinterpreted it and misled us. Only she will know the truth. The rest of us will just have to decide for ourselves.

References:

1. Hooper L, et al. (2011). Reduced or modified dietary fat for preventing cardiovascular disease. The Cochrane Library

2. Mente A, et al. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med 2009;169(7):659–69

3. Siri-Tarino, PW, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, Am J Clin Nutr 2010;91(3):535–46

4. Skeaff CM, et al. Dietary fat and coronary heart disease: summary of evidence from prospective and randomised controlled trials. Annals of Nutrition and Metabolism 2009;55:173–201

UPDATE: As of some time on 24 July 2013 clicking on the link to where Dr Ruxton makes her unsubstantiated claims on the Fat Information Service website returns this page:

Diabetics are generally advised to moderate their weight and take regular exercise. A huge study has tested the effectiveness of this advice in terms of its ability to reduce the risk of heart attacks and strokes, and the results were published this week [1]. See here for the full text of the article.

Before we look at the results, let’s look at how the study was set up.

5,145 overweight and obese type 2 diabetic were randomised to receive counselling and support regarding diet and exercise (the ‘treatment’ group), or regular diabetes education and counselling. Those in the treatment group were asked to exercise at moderate intensity for at least 175 minutes each week. With regard to diet, they were to aim at an intake of 1,200-1,800 calories a day, and that the diet should contain (as a percentage of calories) less than 30 per cent fat and at least 15 per cent protein.

Individuals were followed for up to 13½ years, but the average follow up was 9½ years. At the end of the study, the average weight loss was about 6 kg in the treatment group and about 3.5 kg in the control group. The main aim of this study, remember, was to assess the effect on risk of heart attack and stroke. Unfortunately, no benefits were seen here at all compared to the control group.

Here are the changes in weight and waist circumference seen in the treatment (blue) and control (red) groups over the course of the study.

Take a look at this next graph, which charts levels of ‘glycated haemoglobin’ (also known as ‘HbA1c’). This measure gives us an indication of overall blood sugar control over the preceding 3 months or so.

After an initial fall, HbA1c levels gradually climb again and end up essentially where they started.

While a 6 kg weight loss looks good on the scales, if this didn’t come from fat (and perhaps came more from muscle) and if blood sugar control did not improve then perhaps we should not be too surprised that the intervention did not work to reduce the risk of heart attacks and strokes.

What might explain these duff results?

Lots of things, potentially, but one thing that sticks out to me is the dietary intervention deployed here. Essentially, what we have here is a reduced calorie, low-fat diet.

The issue with such a diet is that it will, almost inevitably, cause individuals to put more emphasis on carbohydrate rich foods. In fact, as a general rule, diabetics are often advised to base their diet on carbohydrate including starchy carbohydrates. But it’s a plain and simple fact that starch is essentially made up of glucose molecules, and many starchy foods are, weight for weight, about as disruptive to blood sugar levels as table sugar (sucrose).

This  is not the sort of diet, obviously, that is likely to work well for improved blood sugar control (or weight loss, I think). I don’t rate the chances of such a diet to stave off diabetic complications, either.

At one point, the authors question whether the weight loss achieved in the treatment group was enough to yield benefit. They go on to add, though: “However, our trial was planned to test the effects of an intensive lifestyle intervention, and the weight loss achieved in the intervention group is representative of the best that has been achieved with current lifestyle approaches.”

I feel we’re being sold short here. My experience in practice is that low-fat diets (such as the one recommended here) do indeed give modest or insignificant weight loss results, but those lower in carbohydrate (and less restricted in fat) very often lead to substantial weight loss and significantly improved blood sugar control in type 2 diabetics.

I scoured the paper to see if at any point it occurred to the authors that the prescribed diet might actually be the explanation for the poor results found in this study. I was disappointed, though: not only was this idea not mooted, there was not even one single reference to carbohydrate in the whole study. There’s not a single reference to sugar or starch, either.

Diabetes is essentially a problem of carbohydrate intolerance. This huge, multimillion dollar study assessed the impact of lifestyle interventions including diet on diabetics. Quite how the write-up of this study managed to omit any reference to carbohydrate at all is anyone’s guess. But there you have it.

References:

1. The Look AHEAD Research Group. Cardiovascular Effects of Intensive Lifestyle Intervention in Type 2 Diabetes. NEJM epub 24 June 2013

In his latest column, Dr Spence turns his attention to the management of diabetes. This is a subject that is close to my heart, because I know only too well that this is a condition that so often responds well to the appropriate diet (in my opinion, that’s one low in carbohydrate). Yet, it is often the case that the dietary advice given to diabetics is woeful: diabetics are often encouraged to emphasise carbohydrate over fat, which almost inevitably ensures problems with blood sugar control and reliance on medication.

Dr Spence’s frustration is not centred on the dietary management of diabetes, but the pharmaceutical approaches to it. Specifically, he questions the wisdom of doctors increasingly using an increasing array of medications to lower blood sugar, when there is essentially no evidence that this actually translates into clinical benefits such as a reduced risk of heart disease or death.

Dr Spence goes on to write:

Worse, there is evidence that these new drugs cause harm. Rosiglitazone has already been withdrawn; pioglitazone has been linked to bladder cancer; and exenatide and sitagliptin double the risk of acute pancreatitis. All this is an example of the scientific illusion that is so called evidence based medicine, where research is just mechanically reclaimed statistics pulped into junk educational nuggets—mere marketing by another name.

Here’s what Dr Spence describes as the ‘drug industry’s business plan for diabetes…’

He ends with the following indictment:

The complicity of doctors and lack of dissent against the drug model of diabetes care is bad medicine.

It’s rare to read such candour in a medical journal, and I think Dr Spence is to be commended for, I think, saying it like it is. Personally, I think diabetics have been seriously let down by the medical profession. There is some light at the end of the tunnel, though: increasing numbers of diabetics are discovering for themselves just how effective low-carbohydrate eating usually is for controlling blood sugar and improving health markers.

Back in October, I wrote about a diabetic who had transformed his health through diet, but was admonished by his doctor when it was revealed that a ‘low-carb’ diet is what appeared to make the difference. This did not deter the diabetic though. And this is what I’m finding increasingly: individuals are less and less deferring to their doctor and more and more inclined to turn their back on what they see as out-of-date, unscientific and non-evidence-based advice.

I think we need more doctors like Dr Spence. Some may see him as a pesky whistleblower. I think the reality is that without doctors like him, the medical profession is just going to see a continuing erosion of its credibility.

References:

1. Spence D. Bad medicine: the way we manage diabetes. BMJ 2013;346:f2695

And by way of example, just this week saw the publication of a study in which obese individuals were treated with vitamin D with good effect. The study subjects were adolescents (average age 14) with an average body mass index of about 40 (obese). They were treated with 4,000 IU (international units) of vitamin D or placebo for 6 months. Vitamin D levels in the study subjects started at about 19 ng/ml (47 nmol/l) and doubled in those taking vitamin D (no significant change in those taking placebo).

A number of parameters were measured, and here’s a brief summary of the findings:

• Vitamin D did not affect body mass index
• Vitamin D did not affect blood markers of inflammation
• Vitamin D did lead to a lower level of fasting insulin levels
• Vitamin D did lead to better functioning insulin (insulin ‘sensitivity’ was improved)

The finding that vitamin D did not affect body mass index is consistent with the recent research which suggests obesity is a potential cause of vitamin D deficiency, but not so much the other way round.

The finding that vitamin D improved insulin sensitivity is encouraging, though. In general terms, the better insulin works, the better blood sugar control is, and the lower the risk of someone developing type 2 diabetes. Proper functioning insulin basically facilitates the uptake of nutrients from the bloodstream into the body’s cells, which can improve physical and mental energy and reduce hunger.

This is only one study, but other evidence exists which shows vitamin D has the capacity to enhance insulin functioning. In one study, 4,000 IU of vitamin D given for 6 months improved insulin sensitivity in a group of insulin resistant and vitamin D-deficient women [2].

References:

1. Belenchia AM, et al. Correcting vitamin D insufficiency improves insulin sensitivity in obese adolescents: a randomized controlled trial. AJCN. First published ahead of print February 13, 2013

2. von Hurst PR, et al. Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient – a randomised, placebo-controlled trial. Br J Nutr. 2010;103(4):549-55

I was therefore interested to read today about a study in which mindful eating was trialled in a group of individuals with type 2 diabetes [1]. You can read about the study here. Basically, though, individuals were instructed in the art and practice of mindful eating through group sessions spanning a 3-month period. This instruction involved encouraging people to tune into their body before eating and taking a few moments to assess their level of hunger. They were also encouraged to make conscious choices about how much they would eat, as well as stopping eating once they were full.

Results in this group were compared with those in individuals who were not instructed in mindful eating, but instead were given standard nutrition advice as dispensed during conventional diabetes education programmes.

Both interventions led to improvements in weight (the standard and mindful approaches led to losses of about 3 and 1.5 kg respectively). More impressive, though, was the reduction in a marker of blood sugar control known as HbA1c (which measures overall blood sugar control over the last 3 months or so). This fell by about 0.7 and 0.8 per cent in the standard and mindful group respectively. This is the sort of reduction (improvement) one expects to see through the addition of a diabetes medication.

My experience in practice tells me that quite a lot of self-confessed over-eaters are victims of habit and conditioning. If you feel this may be true for you, here’s a few things that might help:

1. Get in tune with your hunger signals
Spend just a few seconds, several times each day, asking yourself just how hungry you really are. Rate your hunger on a scale of 0–10. Just doing this will help you get back in touch with the signals your body uses to tell you how genuinely hungry you are.

2. Avoid eating ‘by the clock’
Some individuals get themselves into the habit of ‘eating by the clock’, for example having lunch because it’s ‘lunch time’ whether hungry or not. If you are aware that you do this resolve, wherever practical, to delay eating until genuine hunger is present.

3. Avoid ‘clearing your plate’
One potential driver of unnecessary eating that is the belief that we need to finish everything on our plate. A common cause of this is messages received in childhood about the importance of not wasting food, particularly in light of the plight of starving children in the Third World. Yet, in reality, the eating of more than you need to in no way helps starving children (or anyone else). Being mindful of this can be all that it takes to rid yourself of a ‘clear the plate’ mentality.

4. Use smaller crockery
A meal that’s big enough to truly satisfy may still look insignificant or ‘lost’ on a large plate or in a big bowl. Using crockery that is appropriate for smaller-sized but properly satisfying meals can reduce the tendency to pile food unnecessarily high.

5. Avoid ‘eating for later’
Some individuals eat with a goal of avoiding hunger before the next meal. However, this can encourage overeating when the time between meals is long (e.g. between lunch and dinner). Aim to eat enough at each meal to be comfortably full. Remember it’s perfectly fine to eat a healthy snack (e.g. nuts) to tide you over to the next meal should you get peckish.

References:

1. Miller CK, et al. Comparative Effectiveness of a Mindful Eating Intervention to a Diabetes Self-Management Intervention among Adults with Type 2 Diabetes: A Pilot Study. Journal of the Academy of Nutrition and Dietetics. 2012;112(11):1835

After reading Nora’s book, he followed most of her advice and then slowly extricated himself from the wheat and grain-dominated foods that he “was supposed to eat to obtain energy and remain healthy.” He started eating animal fats for the first time in years and gave up alcohol. Here’s his email to me:

I had my 6 monthly diabetes check-up last Wednesday. The diabetes consultant was really happy with all of my figures on cholesterol, triglycerides, blood pressure, weight (I’ve lost another 4 kg since February without really trying), kidney and liver function are excellent – in fact he was really impressed and asked me what I was doing to get these improvements.

Simple, I said, I’ve stopped eating wheat in all its forms and grains in general, I avoid rice and all potato products. I eat animal fat and the only oil that I use is extra virgin olive oil. Breakfast is typically a one-egg omelette and with a small amount of bacon, smoked salmon or Parma ham. I have spinach or other leafy greens and tomatoes. Lunch is often not taken as I do not feel hungry until 6.00 pm when I have my evening meal. Another small portion of meat and plenty of veggies. The only fruit that I have are a few blueberries, wild strawberries (when they are available) and raspberries – and I mean a few.

I sleep better than ever, don’t feel tired and have lost weight. I really ought to exercise though, that is the only flaw in my regime.

“No, you MUST eat some carbohydrates” he said.

“I do, I told you, I eat plenty of vegetables.” I said.

“No, no, starchy carbohydrates, you NEED them”

“Why do I NEED them?”

“For energy, your body needs carbohydrates for energy” came his concerned reply.

“How do you think that I’ve managed to survive since you last saw me then? And, you told me how pleased you were with all of my readings – doesn’t that suggest that I’m doing fine without refined, starchy carbohydrates?”

He had no reply other than to repeat to me that I MUST eat carbohydrates for energy.

I urged him to read Primal Body, Primal Mind by Nora T Gedgaudas and made him write it down. I could see that he wasn’t convinced. So, I told him that the bullshit that he’d been taught by the food industry-research funded nonsense that the Government taught him is causing all of the major health problems that he has to deal with every day.

I also said that I throw a fat-fuelled log onto the fire in the morning rather than the carbohydrate kindling throughout the day to keep me provided with energy and avoid the feeling of hunger. Again, nothing seemed to penetrate that simple head of his; it was full of the guff that he’d been taught not to question.

I decided to post this story because it represents to me many facets of a growing theme in the interactions patients have with their health and healthcare professionals. This is the sort of scenario I’m talking about (I’m using diabetes as an example, but the themes can apply to lots of conditions):

1. someone gets diagnosed with diabetes and takes conventional advice to eat a high-carbohydrate, low fat diet.

2. the diabetic finds it difficult to control blood sugar levels effectively, even with sometimes multiple medications.

3. the diabetic starts reading information on the internet and in books which explains why a high-carbohydrate diet is (generally) a disaster for diabetics and what works better (a diet richer in fat and adequate protein).

4. the diabetic decides to take matters into their own hands, changes their diet, and their blood sugar control and general health improve through the roof.

5. when their doctor finds out that their patient is eating a ‘fad’, ‘low-carb’ or ‘Atkins’ diet, they either elect not to engage with this, or positively dissuade the diabetic from taking this approach.

In this particular case, the doctor shows a mind-numbing ignorance about basic physiology (assuming he’s been quoted correctly): No-one needs to eat starchy carbohydrate (or any carbohydrate) for energy. For a start, fat is a suitable fuel for the body. Plus, sugar can be made from other dietary elements (e.g. protein) in the liver.

I fear that we doctors are going to have to ‘get with the programme’ by ensuring we are better educated about the impact of nutrition on health. And another thing we could do better, I think, is not to dismiss our patients who have been motivated enough to educate and help themselves, and in so doing have experienced significant improvements in their health and wellbeing. Isn’t it by listening to patients that we doctors get to know what works and what doesn’t? And won’t this information and experience be invaluable to us when we come to advise other patients?

The age of the internet means patients can quite easily know much more about their health and health management than their doctors. Rather than dismiss what they have discovered, I suggest we doctors embrace these experiences and learn from them. That is, of course, if we care about our patients getting the best advice and support possible.

Baroness Young has been on somewhat of a media blitz recently, raising awareness of the ‘need’ for diabetics to have their cholesterol levels managed, including with drugs. Here’s a typical story on the BBC website, which includes this quote from the Baroness:

It will often be appropriate to prescribe medication such as statins, but it is no good doing this without explaining the importance of taking the medication regularly and the potentially devastating consequences of not doing so.

Baroness Young’s charity is not known for the evidence-based nature of its information and advice, and I decided to see if her urging diabetics to manage their cholesterol properly is scientifically supported.

I came across a pertinent review of this subject published earlier this year [1]. The authors of this review assessed studies in which cholesterol-lowering drugs were used in individuals with diabetes. They excluded studies which had been terminated early for no good reason (early stopping of studies is known to exaggerate the benefits and reduce the apparent harms of a treatment), and well as studies in which the participants were not properly ‘randomized’ (which effectively means that the underlying characteristics of those on the medication and placebo were not equivalent, which in turn can give misleading results).

Four trials were left: three in which a statin was the drug being tested [2-4] and one which tested the effects of a fibrate (another type of cholesterol-lowering drug) [5].

Here’s a brief summary of the results of each of these studies.

Study [2]: A reduction in risk of major cardiovascular events (e.g. heart attack or stroke) of 37 per cent but no reduced risk of death overall.

Study [3]: No reduced risk of a ‘composite endpoint’ encompassing a variety of outcomes including death from heart attack or stroke, non-fatal heart attack and stroke, and coronary artery bypass surgery. No reduced risk of death overall.

Study [4]: No reduced risk of a composite endpoint made up of cardiovascular death as well as non-fatal heart attacks and strokes. No reduced risk of death overall.

Study [5]: No reduced risk of fatal and non-fatal heart attacks. No reduced risk of death overall.

The authors of the review conclude:

This review does not support the use of cholesterol-lowering drugs (such as statin and fibrate) to reduce mortality and cardiovascular complications in type 2 diabetics.

The authors suggest that the guidelines regarding cholesterol management in diabetics have been corrupted somewhat by the conflicts of interest some advisors have by remarking:

Official guidelines should be re-examined and reformulated by experts independent from the pharmaceutical industry.

 

Sound like a good idea to me. And it reminded me that Diabetes UK has conflicts of interest of its own in the form of corporate sponsors in the form of drug and food companies. See here for a full list.

References:

1. de Lorgeril M, et al. Is the use of cholesterol-lowering drugs for the prevention of cardiovascular complications in type 2 diabetics evidence-based? A systematic review. Rev Recent Clin Trials 2012;7(2):150-7

2. Colhoun HM, et al; CARDS investigators. Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS): multicentre randomised placebo-controlled trial. Lancet. 2004;364(9435):685-96

3. Knopp RH, et al. Efficacy and safety of atorvastatin in the prevention of cardiovascular end points in subjects with type 2 diabetes: the Atorvastatin Study for Prevention of Coronary Heart Disease Endpoints in non-insulin-dependent diabetes mellitus (ASPEN). Diabetes Care. 2006;29(7):1478-85

4. Wanner C, et al, for the German Diabetes and Dialysis Study Group. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med 2005; 353:238-248

5. Keech A, et al; FIELD study investigators. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet. 2005 Nov 26;366(9500):1849-61