Resistance training benefits diabetics (and others too)

Resistance training benefits diabetics (and others too)
by Dr. Briffa

Diabetes is a condition characterised by raised levels of sugar in the blood stream. It comes in two main forms: type 1 and type 2. Type 2 is by far the most common, and is generally related to ‘insulin resistance’ – a failure of the body to respond adequately to the blood sugar-lowering effects of insulin. While some argue for a low-fat diet for diabetics, I generally don’t. Low-carbohydrate diets are the ones that, according to the science and in keeping with common sense, usually lead to improved blood sugar control and a reduction in or complete dispensing of diabetic medication.

Activity and exercise can help blood sugar control too. Traditionally, diabetics have been encouraged to partake in ‘aerobic’ exercises such as walking, running, cycling and swimming. ‘Resistance’ exercise (e.g. weight training) is usually not promoted much for diabetics. In a recent study though, the effects of a mix of aerobic and resistance training was tested in a group of type 2 diabetics. The results, published in the Archives of Internal Medicine, were very encouraging indeed [1].

In this study, more than 600 type 2 diabetics were randomised to either exercise counselling and supervised exercise twice a week, or exercise counselling alone. The exercise sessions lasted 75 minutes each. The study lasted a year. You can download a pdf of the full article here.

Both groups became significantly more active during the course of the study, though the group undergoing supervised exercise took more format exercise than the ‘control’ group. This appeared to translate in to enhanced improvements in fitness, strength and flexibility.

Compared to the ‘control’ group (those who got exercise counselling alone), the exercise group saw significant improvements in several health markers including HbA1c levels (a measure of blood sugar control over the preceding 2-3 months), blood pressure, waist circumference, insulin sensitivity and inflammation. Essentially, taken together, these findings add up to evidence of improved health and fitness, better diabetic control and reduced risk of cardiovascular disease.

An accompanying editorial reviews the evidence regarding the effects of activity and exercise in diabetics. In particular, it makes the point that there is evidence that a combination of aerobic and resistance exercise trumps either of these forms of exercise performed alone.

One of the key pieces of evidence here is the so-called ‘DARE’ (The Diabetes Aerobic and Resistance Exercise) trial [2]. In this trial type 2 diabetics were randomised to aerobic exercise, resistance exercise or both forms of exercise, three times a week, for 22 weeks. In terms of HbA1c levels the group doing both forms of exercise did better. However, this group was also, essentially doing twice as much exercise as the other two groups. As a result, it’s difficult to discern from this evidence whether the additional benefits were down to a combination or the two forms of exercise or just increased exercise ‘volume’.

What we do have, however, is a review from last year which shows that in diabetes, resistance training can benefit blood sugar control and insulin sensitivity [3]. Whether it’s somehow ‘better’ than aerobic exercise is not clear.

My sense is that, in reality, the effect of performing both forms of exercise is going to be better for individuals than one form of exercise performed in isolation. Even if resistance exercise did not turn out to be particularly effective for diabetes management and disease risk reduction, it does increase strength. And this has huge advantages for people, in that it reduced the risk of things like falls and fractures, while at the same time helping people lead active, independent lives.

References:

1. Balducci S, et al. Effect of an Intensive Exercise Intervention Strategy on Modifiable Cardiovascular Risk Factors in Subjects With Type 2 Diabetes Mellitus: A Randomized Controlled Trial: The Italian Diabetes and Exercise Study (IDES). Archives of Internal Medicine. 2010;170(20):1794-1803

2. Sigal RJ, et al. Effects of Aerobic Training, Resistance Training, or Both on Glycemic Control in Type 2 Diabetes: A Randomized Trial. Annals of Internal Medicine. 2007;147(6):357-369

3. Gordon BA, et al. Resistance training improves metabolic health in type 2 diabetes: a systematic review. Diabetes Res Clin Pract. 2009;83(2):157-175

Flu vaccination is largely ineffective, despite what your Government may have you believe

Flu vaccination is largely ineffective, despite what your Government may have you believe

A couple of weeks ago I had my lovely elderly parents around for lunch. The subject of flu vaccination came up. My father is dead against this practice, and views flu as a largely self-limiting illness that rarely leads to significant complication (he’s right). My mother, on the other hand, has dutifully attended her doctor’s surgery for the last few years for her flu ‘shot’. Vaccination is, by her own admission, always followed by a persistent cough. This may be coincidence of course, or perhaps a ‘nocebo’ response (like a placebo response, only negative).

Anyway, I ended up suggesting she might rethink her views on the vaccination, especially in light of evidence which suggests that it does not particularly help the elderly (as it’s so often said to do). See here and here for more on this. The upshot is my mum skipped her flu shot this year.

Another reason why I’m not particularly enthusiastic about flu vaccination is that the ‘evidence base’ for it appears pretty flimsy. Last year, the British Medical Journal published a review of the literature which I wrote about here. Read this blog post and/or the original BMJ article and you may come to the conclusion that flu vaccination policy is based on misreporting and misrepresentation of the actual evidence.

I started to think about this topic again on receipt of an email yesterday from an US-based doctor who alerted me to this document. It is written by Dr Eric Kasowski, a doctor the US Center for Disease Control’s (CDC’s) Influenza Division. It urges healthcare workers to get their flu shots. Oddly, for something aimed at health professionals, it cites no studies. I don’t want to be overly suspicious, but this is usually not a good sign.

While we health professionals like to think of ourselves as independently-minded people, the fact is we are as subject to ‘group-think’ as anyone else, in my opinion. Do doctors really have time to go back to the original research, read it and assess it? Not usually. Normally, we doctors will accept what our Government’s tell us quite uncritically.

By way of example, let me relate an experience from a month or so ago. I was listening to the radio and the subject of flu vaccination was being discussed. The issue of the evidence for this practice came up. The doctor in the radio studio giving comment was not only unable to cite any evidence, he also stated that there MUST be evidence, otherwise our Government would not be advising that we have these shots. I’d like to say that such naivety was a rare thing in medicine, but my experience tells me that it is not.

Anyway, after talking with my parents I thought I’d take a look for any more recent evidence relevant to flu vaccination, and came across a review published earlier this year by the Cochrane Collaboration (a collective of international doctors and scientists supposedly dedicated to objective assessments of treatments by proper review of the evidence) [1]. The authors of this review highlight the fact that industry-funded studies were more likely to report positive findings and be published in prestigious journals and be cited more frequently. Here’s the exact wording of the warning:

WARNING:
This review includes 15 out of 36 trials funded by industry (four had no funding declaration). An earlier systematic review of 274 influenza vaccine studies published up to 2007 found industry funded studies were published in more prestigious journals and cited more than other studies independently from methodological quality and size. Studies funded from public sources were significantly less likely to report conclusions favorable to the vaccines. The review showed that reliable evidence on influenza vaccines is thin but there is evidence of widespread manipulation of conclusions and spurious notoriety of the studies. The content and conclusions of this review should be interpreted in light of this finding.

One of the problems with flu vaccination is that it tends not to work at all well if the strains of flu in the vaccine do not match the strains of flu in the environment. Even when the match is perfect, 1 per cent of flu vaccinated individuals ends up with a infection, compared to 4 per cent of unvaccinated individuals. However, in partial matching of vaccine/infecting strains (which is usually how things are), these figures are 1 per cent and 2 per cent respectively. In other words, the true reduction in flu risk in the population is a mere 1 per cent.

Here’s some more findings from this study:

Influenzea vaccines have a modest effect in reducing influenza symptoms and working days lost

There is no evidence that they affect complications, such as pneumonia, or transmission.

Here’s a plain language summary of the study in the authors’ own words:

Over 200 viruses cause influenza and influenza-like illness which produce the same symptoms (fever, headache, aches and pains, cough and runny noses). Without laboratory tests, doctors cannot tell the two illnesses apart. Both last for days and rarely lead to death or serious illness. At best, vaccines might be effective against only influenza A and B, which represent about 10% of all circulating viruses. Each year, the World Health Organization recommends which viral strains should be included in vaccinations for the forthcoming season.

Authors of this review assessed all trials that compared vaccinated people with unvaccinated people. The combined results of these trials showed that under ideal conditions (vaccine completely matching circulating viral configuration) 33 healthy adults need to be vaccinated to avoid one set of influenza symptoms. In average conditions (partially matching vaccine) 100 people need to be vaccinated to avoid one set of influenza symptoms. Vaccine use did not affect the number of people hospitalised or working days lost but caused one case of Guillian-Barré syndrome (a major neurological condition leading to paralysis) for every one million vaccinations. Fifteen of the 36 trials were funded by vaccine companies and four had no funding declaration. Our results may be an optimistic estimate because company-sponsored influenza vaccines trials tend to produce results favorable to their products and some of the evidence comes from trials carried out in ideal viral circulation and matching conditions and because the harms evidence base is limited.

When Governments and the doctors and scientists paid by them urge us to do things but do not cite appropriate evidence (as is the case with the recent missive from Dr Kosowski) I say beware. These folks may put a case that makes their case seem like a no-brainer. In reality, though, what is often going on here is that their hoping that individuals will not look at the evidence base, engage their brains and think for themselves.

References:

1. Jefferson T, et al. Vaccines for preventing influenza in healthy adults (Review). Cochrane Database Syst Rev. 2010 Jul 7;(7):CD001269.

Higher-protein, lower-carbohydrate diets win in the war on weight

The big diet news of the week surely has to be the publication of a study in the New England Journal of Medicine comparing the effect of different types of diet on weight regain [1]. In this study, 938 ‘obese’ (average body mass index – 34) adults (average age – 41) were put on an 800 calorie-a-day diet. Participants lost an average of about 11 kg (24 lbs) on this quite unsustainable regime.

However, the truly interesting part of this study concerned what happened next. Each of the study participants was randomised to eat one of five diets. These were:

1.     a relatively high-protein, low-glycaemic index (GI) diet

2.     a relatively high-protein, high-GI diet

3.     a relatively low-protein, low-GI diet

4.     a relatively low-protein, high-GI diet

5.     a ‘control’ diet

For each of the diet, individuals could eat as much as they like.  This phase of the study lasted 6months.

Here’s a summary of what they found:

In terms of weight regain: individuals who ate the high-protein, low-GI diet did the best, and those who ate the low-protein, high-GI diet did the worst.

The message? If you want to manage your weight without starving yourself, a relatively protein-rich diet is a good starting point, and so is one that avoids blood sugar disruptive (high-GI) foods.

I am gratified to say that this study has had a lot of press. And that’s a good thing, because it has led to people thinking less about calorific intakes, and much more about the macronutrient content of the diet as a means to healthy weight management.

I don’t want to be a killjoy, but I’d also like to add that the results of this study were quite predictable on the basis that previous research has found higher protein intakes are more satisfying, while diets of high-GI tend to be less satisfying, even for a given number of calories.

This helps to explain why individuals who adopt lower-carbohydrate approaches (generally low-GI and usually quite-rich in protein) find they’re less hungry, and eat less as a result. Never mind that – having worked with literally thousands of real people over 20 years I have become convinced that this way of eating really does, overall, trump others (e.g. low-calorie, low-fat) in terms of sustainable weight loss. And this is why it forms the basis of the advice I offered in my latest book.

I have seen countless individuals get on and off ‘diets’ and therefore suffer cycles of weight loss and weight gain. What is it that causes individuals to default back to their original diet? Lots of things, but one factor that almost always plays a part is hunger. It’s a plain and simple fact that unless forced, individuals tend not to tolerate hunger at all well in the long term. And that’s particularly the case where food is often tempting, visible and readily available.

One of the keys to successful weight loss and then maintenance of that loss is not to allow oneself to get too hungry. You see, once someone gets very hungry, it becomes difficult to eat healthily. Hunger tends to cause individuals to want to eat, say, starchy carbohydrates (like bread) that can be fat-forming through their effect on hormones (principally insulin), and are not particularly satisfying anyway.

Not being very hungry makes it generally easy for individuals to eat nutritious, satisfying foods that assist weight loss through moderation of the hormone insulin. Read the reviews of Waist Disposal and you’ll see a common theme is hugely significant weight loss without hunger or portion control. It is this fundamental feature of any regime that makes it truly sustainable. Here’s an example in the form of a review from 12^th November:

This isn’t a diet it’s a lifestyle!!,

Nine years ago I bought a dress which was the perfect dress. There was just one thing wrong with it — it didn’t fit! But I always said that I would get into it one day and that day came last week thanks to the Waist Disposal regime and I’m thrilled. This is the easiest diet I have ever been on — I don’t feel hungry, I know exactly what I can eat and it works. And there’s no guilt so if I find myself at a dinner party or an event where it would impolite to be picky it’s not the end of the world if I have the odd potato or piece of bread cause I know it’s not going to be a permanent situation. So thank you John — I just wish you had written this book sooner!!

A couple of weeks ago I had an email from someone who has lost more than 50 kg (yes,kilograms, not pounds) over several months eating more-or-less as advised in Waist Disposal. I replied offering my congratulations but adding that that I hoped he was not starving himself and doing things sustainably. His reply was that he thought he was probably eating more than before.

I have a bit of refrain when advising individuals about weight loss which is designed to be an antidote to the calorie principle-driven advice that is commonly invoked (and rarely works). It is this: “In the long term, the less hungry you are, the more weight you’ll lose.”

Regular meals and the odd healthy snack is a good starting point here. But, in terms of what to eat, I’d go with what science and experience tells us works: a diet relatively rich in protein and low in carb.

After a few weeks on such a diet I might have occasion to ask an individual this question: “Can you imagine eating like this for the rest of your life?” Almost always, the answer is an unhesitant ‘yes’. This response is, in my opinion, a pretty sure sign that sustained healthy eating is not going to be problem for this individual in the long term.

References:

1. Meinert Larsen T, et al. Diets with High or Low Protein Content and Glycemic Index for Weight-Loss Maintenance. N Engl J Med 2010; 363:2102-2113

Fish oil for stress induced obesity?

Fish oil for stress induced obesity? 
A Research Review by Benjamin Brown ND

Stress can lower metabolism and cause the pounds to pack on. A new report suggests that fish oil may change this picture.

 

To see whether supplemental fish oil has an effect on resting metabolic rate (RMR), body composition and cortisol production, a group of healthy men and women were randomly assigned to one of two groups: Placebo (Safflower Oil, 4 grams a day); or Fish Oil (4 grams a day supplying 1,600 mg/d eicosapentaenoic acid (EPA) and 800 mg/d docosahexaenoic acid (DHA)) and tested before and after 4 weeks.

At the end of 4 weeks the fish oil group had a significant increase in fat free mass (indicating increased muscle), a significant reduction in fat mass, and a tendency for a decrease in body fat percentage compared to placebo. Interestingly there was a tendency towards lower salivary cortisol in the fish oil group and a significant correlation between change in cortisol and change in fat free mass.

Comment: 
This study found a significant effect of fish oil on body composition and salivary cortisol after just 4 weeks. During the period the study group maintained their usual lifestyle and dietary behaviours. This is not the first study to suggest fish oil may favourably affect body composition however the discovery that improvements correlated with reductions in the stress hormone cortisol is a novel and interesting one.

--   Norma Bridge, Dip ION FdSc   Essentia Nutrition  +44 (0)7791 890 541 www.essentianutrition.co.uk  Member of the British Association for Applied Nutrition & Nutritional Therapy (BANT) Nutritional Therapy Council Registered Practitioner (NTC) Complementary and Natural Healthcare Council Registered Practitioner (CNHC) Clinical Studies Tutor, Dip NT - Premier International www.premierglobal.co.uk 

Still no good evidence that eggs cause heart disease (despite what some may say)

Still no good evidence that eggs cause heart disease (despite what some may say)

Eggs are one food that have had wildly different press from the nutritional community over the years. Back in the 1950s, here in the UK, we were encouraged to ‘go to work on an egg’

All that changed, though, when we got all cholesterol-conscious and fat-phobic back in the 70s and 80s. Recently, there was a chance of eggs being rehabilitated, mainly on the basis that egg eating did little to raise cholesterol levels, so was unlikely to raise heart disease risk. But this week saw the publication of a study which give a damning verdict on eggs [1]. Three doctors based in Canada warn, in this review, that “patients at risk of cardiovascular disease should limit their intake of cholesterol,” and that “Stopping the consumption of eggs yolks after a stroke or myocardial infarction [heart attack] would be like quitting smoking after a diagnosis of lung cancer: a necessary action, but late.”

The review focuses on so of the biochemical changes induced by egg eating that might, in theory at least, cause cardiovascular disease. Cholesterol, inevitably, features heavily. The authors can’t quite bring themselves to be up front about the fact that egg eating does not raise cholesterol levels. The focus is shifted to things like cholesterol oxidation, raised fat levels in the blood after meals, and the idea that cholesterol “potentiates the adverse effects of dietary fat.”

Well, saturated fat doesn’t appear to have any adverse effects regarding cardiovascular disease risk, so that idea is essentially dead in the water. And so what if eating food with fat in it causes blood fat levels to go up? It’s what you’d expect. What is really important is the impact a food has on health and disease risk. ‘Surrogate markers’ such as blood fat levels are not to be relied upon to judge the impact of any factor on health. If arsenic or cyanide reduced cholesterol levels, would we recommend that everyone swigs back these poisons everyday?

To really judge the impact of eggs on health we require intervention studies. For example, we could take a group of individuals and instruct them to eat lots of eggs over a long period of time and then assess their health compared to a group eating fewer eggs. We don’t have such studies.

So, inevitably, scientists have turned to ‘epidemiological evidence’. This sort of evidence at best can tell us about relationships between things. It cannot prove that one thing causesanother (or that one thing does not cause another, for that matter).

Anyway, the point is there have been some epidemiological studies that have found in healthy individuals, higher egg consumption is not associated with an enhanced risk of cardiovascular disease [2,3]. The authors are dismissive of this finding though, and suggest it’s most likely caused by the studies lacking the ‘statistical power’ to detect a link.

Interpretations of this type, in my mind anyway, smack of ‘bias’. It’s just the sort of comment authors who have made up their mind about what they want to find make. Is there any other evidence of bias in this review? You bet.

For a start, the authors are dismissive of these epidemiological studies ‘lacking statistical power’, but quote one of these studies as evidence of a link between egg eating and cardiovascular risk in diabetics (suggesting that the power here was sufficient).

They also do not pause to think about what might have led up to such a finding. It could be that individuals who are not very health conscious continue to eat relatively large amounts of eggs, and it’s not the eggs, but the laissez faire attitude about their health that explains this association. I wrote about this recently here.

The authors also quote a study which found that eggs eating was not linked with an increased risk of cardiovascular disease [4], but was associated with an increased risk of death. Now the authors spend a lot of time highlighting the supposed perils of eggs with regard to cardiovascular health. And then quote a study linking eggs are linked with an increased risk of death but not cardiovascular disease. So if it’s not cardiovascular disease that’s killing people, what is it? The authors don’t even suggest an explanation here, so let me do their job for them: the likely explanation is that egg eaters are, generally speaking, less health conscious (see above), and are at increased risk of dying as a result of other lifestyle factors associated with not being very health-conscious (such as being sedentary and smoking).

More evidence of bias in this review comes in the form of the language the authors sometimes use. Look at these two sentences:

“A recent re-analysis of the smaller Physician’s Helath Study…[showed] that regular egg consumption doubled all-cause mortality.”

“Two recent studies also showed that consumption of eggs increased new-onset diabetes, independent of other dietary factors.”

To read these sentences you’d think that the observations they refer to had been made via intervention studies that can discern cause and effect. But, in reality, they refer to epidemiological studies, the results of which we can be circumspect about at best. Essentially the authors of review have taken some quite weak evidence, and expressed in a way that suggests eggs cause diabetes and can kill.

Bias creeping into science is not a good thing, and it’s sometimes useful to ask where such bias may come from. Well, here’s the conflict of interest statement from this review:

“None of the authors receives funding from purveyors of margarine or eggs. Dr Spence and Dr Davignon have received honoraria and speaker’s fees from several pharmaceutical companies manufacturing lipid-lowering drugs, and Dr Davignon has received support from Pfizer Canada for an annual atherosclerosis symposium; his research has been funded in part by Pfizer Canada, AstraZeneca Canada Inc and Merck Frosst Canada Ltd.”

Seems like two of the authors of this review have some potential interest in keeping the cholesterol theory alive and well.

Look, we simply don’t have definitive evidence which tells us whether eggs are healthy or not. But in the presence of evidence which does not incriminate them, as well the weak and inconsistent nature of evidence used to damn them, I’ll continue to ‘take my chances’ with this natural and nutritious food.

References:

1. JD Spence, DJ Jenkins, J Davignon. Dietary cholesterol and egg yolks: Not for patients at risk of vascular disease. Canadian Journal of Cardiology, 2010; 26 (9): e336-e339

2. Hu FB, et al. A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA. 1999;281(15):1387-94.

3. Quereshi AI, et al. Regular egg consumption does not increase the risk of stroke and cardiovascular diseases. Med Sci Monit. 2007;13(1):CR1-8.

4. Djousse L, et al. Egg consumption in relation to cardiovascular disease and mortality: the Physicians’ Health Study. Am J Clin Nutr 2008;87(4):964-9.

--   Norma Bridge, Dip ION FdSc   Essentia Nutrition  +44 (0)7791 890 541 www.essentianutrition.co.uk  Member of the British Association for Applied Nutrition & Nutritional Therapy (BANT) Nutritional Therapy Council Registered Practitioner (NTC) Complementary and Natural Healthcare Council Registered Practitioner (CNHC) Clinical Studies Tutor, Dip NT - Premier International www.premierglobal.co.uk 

Soy: thyroid problems a flash in the pan

Soy: thyroid problems a flash in the pan

By Benjamin Brown N.D

 

A recent 3 year safety study has found that the soy isoflavone genistein does not affect thyroid function adding to a growing body of evidence that dismisses previous concerns about soy and thyroid health.

 

Soy foods and supplements have been shown to be useful for improving hot flashes in postmenopausal women yet there are still concerns around effects on thyroid gland function. In a safety investigation a group of postmenopausal women receiving 54 mg of the soy isoflavone genistein were assessed for thyroid function after three years of treatment.

 

Circulating thyroid hormones (TSH, free T(3), free T(4)) and autoantibodies (thyroid peroxidase, thyroglobulin, and thyroid microsomal antigen) were assessed after the three years of treatment and did not differ from women receiving placebo. This report suggests that genistein at a dose of 54 mg per day over three years has no effect on the development of clinical or subclinical thyroid disease.

 

Comment:

Early concerns about the safety of soy for thyroid health came from experimental studies however the largest review of the hormonal effects of soy to date found no evidence of an effect of soy protein or soy isoflavones on thyroid hormones in women. The review and meta-analysis (Hum Reprod Update. 2009 Jul-Aug;15(4):423-40.) included some 47 published human clinical studies.

 

This recent study adds to evidence in support of the safety of soy and thyroid health. Good for hot flashes and not harmful for the thyroid it seems.

 

Source:

Bitto A, et al. Genistein aglycone does not affect thyroid function: results from a three-year, randomized, double-blind, placebo-controlled trial. J Clin Endocrinol Metab. 2010 Jun;95(6):3067-72.