2010 March | Dr Briffa's Blog

Could advising people to eat less and exercise more INCREASE their risk of getting fatter?

Some time ago one of my blogs focused on the thoughts of Dr Andrew Wadge – Chief Scientist at the Food Standards Agency (FSA) in the UK. The blog specifically focused on his broadside at ‘detox’ regimes. I can understand that someone may be a bit sceptical of such regimes. However, if Dr Wadge wishes to express his withering attitude to such regimes, bearing in mind he is the CHIEF SCIENTIST (emphasis mine) at the FSA, would it be too much for him to use some actual science making his case? In reality, he uses none – not one study or citation. Nothing.

Earlier this week, I came across another of Dr Wadge’s blogs. It concerns a piece that appeared in the Daily Mail. The piece was an extract of a book entitled Big Fat Lies by Hannah Sutter. I know Hannah and like her. She started a company (Go Lower) that makes low carbohydrate foods. I’m generally supportive of low-carb eating, and am broadly supportive of Hannah’s work. I have not read Hannah’s book, but I did read the extract of it in the Daily Mail. You can read this piece here.

Dr Wadge’s blog post starts with this sentence

“Despite the absurdity of Hannah Sutter’s proclamation in Saturday’s Daily Mail that government advice to ‘exercise more and eat fewer calories’ is making people fat, I felt I had to respond.”

In his response, Dr Wadge invokes the calorie principle. He trots out the usual concept that weight control is all about calories in and calories out. Yet, in the Daily Mail piece, Hannah Sutter claims that we’re eating less and exercising more and actually getting fatter. She might be right. She might be wrong. According to Dr Wadge’s theorising, though, she must be wrong. And yet, he does not provide a single scientific study or piece of research that disproves Hannah Sutter’s assertion.

Central to Hannah Sutter’s argument is that carbohydrate is a major driver of obesity, because of its influence on the ‘fat-making’ hormone insulin. Dr Wadge does not engage at all with this key concept.

Hannah Sutter also takes a swipe at the oft-quoted idea that exercise promotes weight loss. For the most part, aerobic exercise is quite ineffective in this regard, and I think she’s right to point it out. You can read more about this here. Again, Dr Wadge does not engage with this from a scientific perspective.

What he does do, though, is draw our attention to the fact that Hannah Sutter owns a “website selling a weight loss programme”. This is a conflict of interest, I suppose. But such a conflict is most relevant if Hannah Sutter’s ideas can be demonstrated to be false. As yet, Dr Wadge seems unable to do this in any meaningful way.

It seems somewhat ironic to me that he appears to discredit Hannah Sutter by pointing out that she is a “lawyer and not a scientist”. But it’s clear from the extract that Sutter’s book refers copiously to the science. Dr Wadge does not. At all. Since when did scientists get a ‘free pass’ – a right to say what they like without validation just because they are a scientist?

The comments that come after this blog post are generally sharply critical of Dr Wadge and generally point to science which, again, Dr Wadge steadfastly refuses to engage in.

The fact is, there is a plausible way in which the advice that people should be eating less and exercising more might be fuelling the burgeoning rates of obesity. Eating less calories for a lot of people translates into ‘eat less fat’. Why? Well, because we’re constantly reminded that a gram of fat contains about twice as many calories as carbohydrate or protein. But a low-fat, high-carb diet (as encouraged by the FSA and most health professionals) tends, as Hannah Sutter points out, to disrupt blood sugar levels. The resultant surges of insulin are fat-making in the body. Plus, disruption in blood sugar can lead to blood sugar lows which cause us to be hungry – especially for carbohydrate (as so the cycle can repeat). Plus, carbohydrate foods, compared to those rich in protein, sate the appetite less overall. In short, encouraging people to eat a few calories and emphasise carbohydrates can drive people to overeating the very foods that are most fat-making in the body.

And what of exercise? Well, as I detail here, the calorie burn during exercise is generally quite modest. Plus, when people exercise more, they can find it quite difficult not to eat more as a result. A look at the evidences supports Sutter’s stance that conventional advice just doesn’t work.

Dr Wadge’s opinion appears to be that the failure of the advice stems from individuals not following that advice. His blog ends with this sentence:

“I’m surprised that Ms Sutter didn’t consider that perhaps it’s the people who aren’t following government advice are ones who are getting fatter.”

I wonder if Dr Wadge has ever considered the fact that its the advice and theories on which governement advice is based that might be flawed?

Dr Wadge has exposed himself here as he did before regarding detox regimes. So great appears to be his bias that he feels it unnecessary to engage with actual science to make his point. I notice that Dr Wadge’s blog goes under the name “hungry for science”. Yes, quite.

For more details on Hannah Sutter’s book see here.

Dr Briffa’s new book – Waist Disposal – the Ultimate Fat Loss Manual for Men – is now available. To learn more about the book click here.

To buy Waist Disposal from amazon.co.uk click here.

BMJ piece asks serious questions about the effectiveness of mammography

Last week one of my blogs focused on prostate cancer screening, and specifically the prostatic specific antigen (‘PSA’) test. For a variety of reasons, the doctor who discovered PSA says the practice of using it to detect cancer should be stopped. In that post, I mentioned that doubts have also previously been raised about the usefulness of mammography. Just a few days later, as it happens, the British Medical Journal published a paper which asks serious questions about the relevance of this practice.

The study in question focuses on breast cancer screening in Denmark. Mammography has previously been said to reduce risk of dying from breast cancer in Denmark by 25 per cent. However, as the authors of this recent study point out, just because breast cancer mortality fell after the introduction of mammography, does not mean that mammography is responsible. The reduction in mortality might be due to other factors, such as changes in risk factors or improvements in treatment.

To get a more accurate picture reading the effectiveness of mammography, the researchers compared changes in breast cancer deaths in regions where mammography had been introduced, and compared this with death rates in regions where mammography had not been introduced. Here’s what they found:

Over a 10-year period where screening could have saved lives, in women of an age who might benefit from screening (women aged 55-74), death rates from breast cancer fell by 1 per cent per year. This decline was not statistically significant.

In comparison, death rates in non-screened areas fell by 2 per cent per year over the same time period. And this fall was statistically significant.

The authors of this study also compared these findings with death rates in women too young to have benefitted from mammography. In the screened area, death rates fell by 5 per cent per year. In the non-screened areas, death rates fell by even more, though (6 per cent year).

The authors point out that their findings are not new, and in fact are in line with findings from other parts of the World. For example, they note:

“In the UK, where screening started in 1988, the decline in breast cancer mortality from 1989 until 2007 was 41% in women aged 40-49 years, who were not invited to screening, 41% in women aged 50-64 years, who were invited to screening from 1988, and 38% in women aged 65-69 years, who were invited from 2002. Furthermore, the drop in breast cancer mortality in the relevant age group began before the screening programme started, and was largest in the age group that was too young to be invited (40-49 years) if the whole observation period is considered (1971-2007).”

They also draw our attention to a European study that found that falls in breast cancer mortality in countries offering and not offering screening were of a similar size. The greatest declines were seen in women who were too young to be offered screening, which points to factors other than screening (such as improvements in treatment) as the real reason for declining breast cancer death rates.

Here are the conclusions from the BMJ study:

“We were unable to find an effect of the Danish screening programme on breast cancer mortality. The reductions in breast cancer mortality we observed in screened regions were similar or larger in non-screened regions and in age groups younger than that screened. The mortality reduction is therefore more likely to be explained by changes in risk factors and by improved treatment than by screening mammography. Our results are similar to what has been observed in other countries with nationally organised programmes. We believe it is time to question whether screening has delivered the promised effect on breast cancer mortality.”

Mammography on the outside appears so obviously the right thing to do to many. As a result, it perhaps has not been subjected to as much scrutiny as it should have been. It seems to me that there is at least some evidence which seriously calls into question the usefulness and appropriate of this practice. See here and here for more on this.

Mammography is, in my view, a highly politicised practice, and as with such things, there are always going to be individuals on both sides of the debate. For a long time it’s been ardent supporters of mammography that have largely had the floor. What is gratifying, I think, is that more and more the other side of the story is getting an airing. It is because of this that women may, eventually, be in a position to make a truly informed decision about whether to have a mammogram or not.

References:

1. Jørgensen KJ, et al. Breast cancer mortality in organised mammography screening in Denmark: comparative study Per-Henrik Zahl, Peter C Gøtzsche BMJ 2010;340:c1241

2. Levi F, et al. Monitoring the decrease in breast cancer mortality in Europe. Eur J Cancer Prev 2005;14:497-502

Study suggests high fructose corn syrup is uniquely fattening, a that a calorie is not a calorie after all

Variously on this site I’ve discussed the notion that ‘a calorie is a calorie’. Simply put, this concept, widely populated by doctors, dieticians and other health professionals, is that when it comes to their effects of weight, all forms of calorie are the same. In terms of its impact on body weight, a kilogram of fat will have the same as a kilogram of carbohydrate. Same for protein.

There is a certain logic to this, I suppose, but on the other hand, one could argue that it assumes that all forms of calorie are metabolised with equal efficiency. Imagine for a moment within your body you have a lit barbeque (this represents your metabolism). If you put petrol (gasoline) and charcoal briquettes on the barbeque, would they burn at the same rate and as completely? Of course not. Could this be at all true for fuel (food) in the body?

One way to test this theory is to feed individuals diets of the same calorific value but different composition (e.g. high-fat/low-carb, and low-fat/high-carb) to see if the effects on weight over time are the same. Some studies have yielded results which suggest that the composition of the diet does indeed have a bearing on their impact on body weight, while other studies have not. One of the problems with these studies is that it can be difficult to ensure individuals are eating what they’ve been instructed to eat, even when cooped up in a hospital ward. And even if the diet can be completely controlled, it can be difficult to conduct such studies for long enough for any real difference between the diets to emerge.

One way round such problems is to do relevant experiments in animals, as I describe here. In this post I describe and experiment in mice which shows very clearly that it is possible for a diet to offer weight loss advantages (a so-called ‘metabolic advantage) in a way that has to do with not just the number of calories it contains, but the form they come in [1]. Specifically, this study found that mice eating a high-fat, low-carb diet lost weight, while those eating a high-fat, high-sugar diet of the same number of calories gained weight.

One fundamental difference between these diets was the amount of carbohydrate (in the form of sucrose, maltodextrin and starch).

I was interested to read about a study published this week which assessed the effects of different dietary composition on weight in rats [2]. This study came in two parts. In the first part, rats were fed:

1. sucrose (table sugar) solution for 12 hours a day and rat chow in unlimited quantities

2. high fructose corn syrup (HFCS) for 12 hours a day and rat chow in unlimited quantities

3. high fructose corn syrup for 24 hours a day and rat chow in unlimited quantities

4. rat chow alone and in unlimited quantities

Rats eating the HFCS for 12 hours a day gained more weight than those consuming the sucrose solution, despite the fact that overall both groups of rats ate the same number of calories. The HFCS group did, however, consume fewer calories from HFCS than the sucrose-group consumed in the form of sucrose.

In the second part of this experiment, male rats were fed either diet 2, 3, or 4 (above) for a period of 6 months.

Also, female rats were fed one of diets 3 or 4 for a period of 7 months.
Over the same period, female rats were also fed either HFCS and chow for 12 hours or sucrose and chow for 12 hours.

In summary, compared to controls (chow only), male rats:

gained significantly more weight on both HFCS diets (diets 2 and 3).

gained significantly more fat on both HFCS diets.

this excess weight tended to accumulate around the abdomen (it is abdominal fat in humans that is most strongly linked with chronic diseases such as heart disease and type 2 diabetes).

saw significant rise in levels of unhealthy blood fats known as triglycerides on both HFCS diets.

In female rats, all the above was true for rats eating diet 3 (HFCS for 24 hours a day plus regular chow).

Overall, what these results suggest is that high-fructose corn syrup had special capacity to induce fat accumulation, particularly around the abdomen, as well as high levels of triglycerides in the bloodstream. Importantly, these effects (including those on weight) are to do with something other than mere calories.

How much relevance these results have to humans is not clear. However, my suggestion is that these results have at least some relevance, particularly as there is clinical research in humans which has linked fructose with adverse effects on health, and quickly too. See here for more about this.

What this study reminds us of is the potential hazards of consuming high fructose corn syrup, a sweetening agent that, increasingly, is pervading our diet. It should also remind us that, when it comes to the impact foods have on weight and fatness, a calorie is not necessarily a calorie, after all.

References:

1. Kennedy AR, et al. A high-fat, ketogenic induces a unique metabolic state in mice. Am J Physiol Endocrinol Metab 2007;292:E1724-E1739

2. Bocarsly M, et al. High fructose corn syrup causes characteristis of obesity in rats: In creased body weight, body fat and triglyceride levels

Coffee drinking has biochemical benefits for the body

Coffee, despite its not-so-healthy reputation, has been quite consistently linked in the scientific literature with benefits for health including a reduced risk of cardiovascular disease, diabetes and dementia. See here, here, here, and here.

While the research regarding the effects of coffee on health is voluminous, the great majority of it comes in the form of so-called epidemiological evidence. Such studies can identify associations between things, but that’s about all. If there were 20 studies showing that coffee-drinking is associated with a reduced risk of cardiovascular disease, say, then that still would not be enough to conclude that coffee protects against cardiovascular disease. It might turn out, for instance, that coffee drinkers happen to exercise more or eat more healthily than coffee abstainers, and these are the real reasons behind the association between coffee drinking and reduced cardiovascular disease risk.

The best test of an causal link between a foodstuff and health is a randomised controlled trial – preferably placebo-controlled. In this case, this would mean randomising a group of people to drink coffee or placebo (ideally an inert coffee-tasting beverage) over a period of time. If the coffee drinking group turned out to be less likely to succumb to cardiovascular disease (assuming the two groups were essentially the same in other respects), this would be very good evidence that coffee consumption does indeed reduce disease risk.

The problem is, the chances of such a study being undertaken are virtually nil.

However, what is much more realistic is to perform clinical studies (studies in people) which monitor not disease outcomes, but so-caled ‘surrogate’ markers of disease. In the case of cardiovascular disease, traditionally scientists would focus on cholesterol levels. Personally, I am doubtful about the relevance of cholesterol levels and the benefits of cholesterol reduction. There has for some time been emerging evidence that a true key underlying process in the development of cardiovascular disease is inflammation.

I was therefore interested to read a study published in the April edition of the American Journal of Clinical Nutrition which looked at the effect of coffee-drinking on a variety of biochemical surrogate markers for disease [1]. 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.

Not surprisingly, drinking coffee was found to lead to higher blood levels of a variety of coffee-derived substances including caffeine and chlorogenic acid.

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 (a hormone is secreted by fat cells, and has been shown to have generally beneficial effects on the body’s physiology including an anti-inflammatory effect). These effects may be relevant not just to cardiovascular disease, but diabetes too. The authors of this study point out that inflammation is a risk factor for type 2 diabetes.

For what it’s worth, the higher coffee consumption was also associated with lower ratios of LDL to HDL cholesterol and apolipoprotein B to apolipoprotein A1. These changes in the lipid levels in the blood would generally be taken as evidence of reduced cardiovascular disease risk.

This study provides evidence that coffee-drinking can affect the body’s biochemistry in a way that could explain the know association between coffee-drinking and reduced risk of disease. It also lends some support for the idea that coffee-drinking has genuine disease-protective properties.

References:

1. 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

Prostate cancer screening called into question

Screening for illness is based on a simple concept: catch the disease early and more timely treatment will (inevitably) lead to better outcomes. However, as with most things in life, things turn out to be not a clear-cut as they sometimes seem. Tests are not foolproof, of course. And sometimes tests can detect things that don’t necessarily matter. For example, mammography will inevitably detect breast cancers that are not destined to significantly compromise the quality or quantity of the life of the woman in whom it has been detected. What this means in this case is that women may be subjected to unnecessary debilitating and expensive treatment. You can read more about the issues surrounding breast cancer screening here and here.

The male counterpart of mammography is the PSA (prostate specific antigen) test – levels of which can go up when the prostate is affected by cancer. This test has been enthusiastically embraced by the American medical community, while here in the UK doctors have been more reticent about deploying this test. This might have something to do with the fact that running PSA tests and the treatment that may result is a potentially lucrative practice in the context of ostensibly-private system of medicine in the US.

In fact, this fact has recently been highlighted a one Dr Richard Ablin. Today’s British Medical Journal contains a piece which explores Dr Ablin’s many objections to PSA screening [1]. In fact, he thinks doctors should stop using it, a view he expressed in a recent New York Times article. What qualifies Dr Ablin to take such a broadside regarding PSA? Well, he discovered it.

Some of Dr Ablin’s reservations about PSA screening are:

1. It is not specific for cancer: the cut-off point for PSA is generally set at 4 ng/ml. 80 per cent of men with PSA values of 4-10 ng/ml actually have benign (non-cancerous) prostatic enlargement.

2. Even when it detects actual cancer, the test cannot be used to determine whether the cancer is slow-growing and non-life-threatening or more aggressive in type.

3. Evidence shows that for one life to be saved as a result of PSA screening, 48 men would have to be treated. This leaves 47 men who have had perhaps non-critical surgery, that can leave them impotent and maybe incontinent.

This last point reminded me of a client I saw recently who had, some time ago, been found to have a raised PSA. Prostate biopsy revealed genuine cancer, and he was offered (with different specialists) different treatments of varying aggressiveness for this. In all of this, though, doing nothing did not appear to be an option.

However, he was particularly concerned about the potential side-effects of treatment, and resolved to do some reading and research. In the end he elected not to have any conventional treatment. He actually ended up consulting a naturally-oriented doctor with a special interest in cancer.

The last I heard his PSA was back down in the normal range, with no sign of any further advancement in his disease. He’s had no adverse side-effects either. At this stage at least, it appears his decision to do nothing (regarding conventional treatment) was the right one.

Dr Ablin is scathing in his opinion of what drives PSA screening in the US. In ths BMJ piece today he is quoted as saying “It seems to me that financial motives have spurred a tsunami of testing,” adding “There’s an unbelievable industry behind this. Unfortunately we don’t practise evidence based medicine here; we do things and later rationalise what we’ve done by saying we thought it was the best thing to do at the time.”

The piece ends with this quote from Dr Ablin: “The medical community must confront reality and stop the inappropriate use of PSA screening. Doing so would save billions of dollars and rescue millions of men from unnecessary, debilitating treatments.” It’s one man’s view, but one that appears to be gaining considerable momentum.

References:

1. Hawkes N. Prostate screening: is the tide turning against the test? BMJ 2010;340:c1497

Why are melanoma survivors found to be at increased risk of other cancers?

Malignant melanoma is a form of skin cancer we are repeatedly warned about. As long as I can remember, just as things start to hot up, we are subjected to dire warning about the hazards of exposing ourselves to the sun’s rays. As a prelude to this this year, we have a recently published study which find that those that survive melanoma are at significantly increased risk of having another (compared to the general population) [1]. This study also found that melanoma sufferers are also at heightened risk of other cancers too, including those of the breast and colon, and several types of ‘lymph’ cancers referred collectively as non-Hodgkins lymphoma.

For a variety of reasons, I don’t think it comes as too much a surprise that melanoma survivors are at increased risk of a recurrence of this particular cancer. The effect of underlying factors such as environmental factors (e.g. sunlight exposure) and genetics do not go away overnight, if at all. And then we have the fact that melanoma sufferers are more likely than the general population to be repeatedly scrutinised for the presence of this cancer. In other words, some of the enhanced ‘incidence’ might be due to increased diagnosis, rather than increased risk per se.

But what about those other cancers? Why should melanoma survivors be at increased risk of cancers that have no directly link with melanoma?

One factor that demands our consideration, I think, is vitamin D. My overwhelming experience is that individuals who have had a diagnosis of melanoma become very sun-shy. They have usually been urged by medical professionals to take steps to minimise unprotected exposure to sunlight. This rationale is based on the widespread belief that sunlight causes melanoma. Actually, though, the link here is not as clear-cut as some would have us believe. See here for more about this.

Whether sunlight ‘excess’ is a potent factor in the development of melanoma is a moot point, I think. And what is all-too-often ignored is that fact that if we avoid the sun and slather ourselves in sunscreen when we’re in it, we run the risk of limiting the production of vitamin D in the skin. And higher levels of this nutrient and/or increased sunlight exposure are associated with a reduced risk of several cancers, including – as it happens – cancers of the breast and colon and non-Hodgkin’s lymphoma.

What this means is that when individuals become sun-shy, they are quite likely to increasing their long-term risk of several cancers, as well as several other conditions linked to sunlight/vitamin D including cardiovascular disease and multiple sclerosis.

I advise against burning, but I am vigorously opposed to the generally one-sided anti-sun propaganda we are fed on an annual basis.

One practice I question is the use of sunscreen. There is some thought that this might actually increase melanoma risk [2]. One reason for this is that use of sunscreen generally prolongs sunlight exposure. It has been suggested that while some sunscreens may block ‘tanning’ and burning UVB, they may allow enhanced overall exposure to UVA, excesses of which may induce skin cancer. In this way, some have suggested that sunscreens give a false sense of security.

One other potential issue with sunscreens is that they can stop an individual becoming habituated to the sun. I remember back in the 70s here in the UK using no sunscreen at all even during hot and sunny summers. Shade and appropriate clothing were used to avoid burning when necessary. And by the end of the summer I and my sun-loving would have turned deep brown. By the end of the summer, there seemed no need to take any precautionary methods at all against burning. Tanning is not just a cosmetic thing: it protects the skin and reduces the risk of damage and burning.

I may be looking back with rose-tinted spectacles, but what I see now is a vastly different relationship with sunlight. Even after a sunny holiday abroad I see many people, particularly kids, returning only marginally browner than when they left. Liberal use of sunscreen may well have something to do with this. The apparent lack of tanning is partly significant as it signifies skin that has not become used to sunlight. And this increases the apparent ‘need’ for sunscreen.

In a previous post I suggested that the preponderance of redheads in Scotland may be related to an evolutionary advantage with regard to vitamin D production in the skin. I also referred individuals to a book written by researcher Oliver Gillie which I think quite persuasively makes the point that some of the chronic disease burden in Scotland might be down to lack of sunlight. Oliver Gillie, like me, is concerned regarding the one-sided messages we tend to get re sunlight exposure. He has developed what he has coined ‘SunSafe’ advice.

Here it is:

1. Sunbathe safely and without burning – every day if you can.

2. The middle of the day is a good time for sunbathing in the UK.

3. Start by sunbathing for 2-3 minutes each side. Gradually increase for day to day.

4. Don’t use sunscreen while sunbathing.

5. If feeling hot or uncomfortable, expose a different area, cover up, move into the shade – or use sunscreen.

6. When abroad, where the sun is generally stronger, expose yourself for shorter times until you find out how much is safe.

7. Children benefit from sun exposure, but need guidance.

8. A tan is natural and is generally associated with good health.

The only part of this I personally disagree with is the suggestion in point 5 regarding resorting to sunscreen. Bearing in mind the potential hazards associated with sunscreen use, my preference would be to follow the preceding advice regarding covering up and/or seeking shade.

As I’ve stated before, I have not used sunscreen for over 20 years. My last recollection of sunburn was during a skiing holiday about 20 years ago. I sport a year-round tan and feel well habituated to the sun.

But I still have the capacity to burn, and I act accordingly. In the summer in southern Europe, for instance, I can often be found in middle of the day on a beach in a tee-shirt and straw hat. As the sun cools off during the afternoon, off come the tee-shirt and hat. I’ve learned over the years how to get my sun, and the benefits it promises, without sunscreen and without sunscreen. I have a strong sense I’m healthier for it too.

References:

1. Bradford PT, et al. Increased Risk of Second Primary Cancers After a Diagnosis of Melanoma. Arch Dermatol. 2010;146(3):265-272.

2. Garland CF, et al. Could sunscreens increase melanoma risk? Am J Public Health 1992;82:614-615

When is the best time to take your vitamin D supplement?

While walking the dog today, my mind wandered and I found myself thinking about nutrient absorption. I’d just had lunch (leftover roast pork from yesterday) and some veggies and salad including rocket (a type of lettuce). My girlfriend dished it up and all I had to do was add a drizzle of olive oil to the rocket before serving. I like the taste and texture of olive oil on salad leaves. However, there is another reason for adding oil to salad – it enhances the absorption of so-called carotenoid nutrients. See here for more on this.

Thinking about this as I walked the dog got me thinking about other nutrients. If someone supplements with nutrients, say, what factors might affect absorption? I generally advise individuals who take vitamin and mineral supplements to take them with food. My rationale is that supplements are more likely to be ‘digested’ and nutrients absorbed when the digestive tract is in the throes of digesting and absorbing food. It suddenly occurred to me to look to see if there was any research on this.

A cursory search of the literature did not immediately reveal anything noteworthy regarding the absorption of nutrients generally, but I did find one interesting study that caught my eye. It concerned the absorption of one particular nutrient – vitamin D [1]. It piqued my interest partly because vitamin D appears to be such an important nutrient. But also, I’m taking it myself, in an effort to optimise my vitamin D levels.

This study focused on a group of individuals who were taking 1000 – 50,000 IUs of vitamin D (that’s not a typo, this upper dose is indeed fifty thousand IUs) each day as part of the medical management advised at a bone clinic in the US. Mean levels of vitamin D at the start of the study were 30.5 ng/ml (76 nmol/l). This level of vitamin D would generally be considered ‘sub-optimal’.

In an effort to boost absorption of vitamin D, individuals were asked to take their vitamin D supplements with the largest meal of the day. After 2-3 months, vitamin D levels were checked again.

At the end of the study period, vitamin D levels had risen to an average of 47.2 ng/ml (118 nmol/l) – an average increase in vitamin D levels of about 57 per cent.

This study is somewhat hampered by the fact that it lacked a control group – in this case a group of individuals who continued to take their vitamin D ‘normally’ (not, explicitly, at the biggest meal of the day). It’s possible, for instance, that the individuals in this study got, say, more sun exposure during the study and it is this that accounted for the rise in vitamin D levels.

Nevertheless, it seems sensible, I think, for individuals who are currently supplementing with vitamin D to take this with their largest evening meal. It doesn’t cost anything, and may provide supplementers with more bang for their buck.

References:

1. Mulligan GB, et al. Taking vitamin D with the largest meal improves absorption and results in higher serum levels of 25-hydroxyvitamin D. J Bone Miner Res. 8th February 2010 [epud ahead of print publication]

Vitamin D supplementation found to help prevent flu in children

Back in February I wrote a post that was largely focused on my experience of supplementing with vitamin D, and specifically the fact that I had not had a single infection (e.g. cold or flu) since starting supplementation. I still, by the way, have not had an infection. Not even a hint of one. This might all be coincidental, but others (some of whom have commented on the site) do seem to have similar experiences. And given that there are plausible mechanisms through which vitamin D can afford relative protection from infection, there does seem to be mounting evidence that vitamin D can indeed help keep us infection-free.

This week saw the publication of a study which adds further support to the idea that vitamin D can help the body ward off infection. In a study, published in the American Journal of Clinical Nutrition, Japanese schoolchildren aged 6-15 years were treated from December through to the end of March with vitamin D (1200 IU per day) or placebo [1]. The outcome assessed was infection with the viruses influenza A and B (the two most clinically important of the three main types of influenza virus). As an aside, influenza A includes the H1N1 strain that last year was responsible for the ‘pandemic’ alerts of last year.

Whether a child had succumbed to influenza over the course of the study was tested microbiologically using swabs from the nose/throat.

Vitamin D supplementation was not associated with a reduced risk of infection with influenza B. However, for influenza A, the results were positive, with vitamin D reduces risk of infection by 42 per cent overall. The benefits were even more dramatic in children who had not been previously supplementing with vitamin D: in this group of children, risk reduction was 64 per cent.

Interestingly, in children with a history of asthma, there was no reduction in risk of flu virus infection. However, those taking vitamin D were at very significantly reduced risk of having an asthma attack.

What we have here is a placebo-controlled study which demonstrates that vitamin D supplementation has the power to protect against flu. This study, to my mind anyway, provides good scientific support for the anecdotal experiences of those, including myself, who have found that vitamin D supplementation has afforded protection against viral infection.

References:

1. Urashima M, et al. Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren. Am J Clin Nutr 10th March 2010 [epub before print publication]

Gluten and milk linked with constipation in kids

The natural food for human babies is breastmilk. However, at some point, children need to be weaned onto ‘solid food’. In the long term there is good reason, I think, for aiming for a childhood diet that is essentially ‘primal’ in nature. That means a diet based on foods like meat, fish, eggs, nuts, seeds, fruits and vegetables. What it doesn’t mean is a diet rammed full of starchy carbs and dairy products.

Some would counter such a diet with the claim that dairy products are essential for bone health, and that carbs supply valuable ‘energy’ for active, growing children. Let’s take the first of these assertions first – is milk and specifically the calcium it supplies really important for bone health. Thinking about this from an evolutionary perspective, this hardly makes sense. We probably haven’t been consuming dairy products in any meaningful way until a few thousand years ago. The paleontological record shows we, as a species, had a good, solid bone health until about 10,000 years ago (around the time we introduced grain). Apparently, we did fine without milk for about 2 million years, but now apparently we must have it for healthy bones. Seems a little odd.

The idea that milk and/or calcium do not play a huge part in bone building is also supported by some science. For example, in a review published in the journal Pediatrics, researchers cast a critical eye over 37 relevant studies, of which 27 found no relationship between dietary calcium or dairy product intake and measures of bone health [1]. Of the remaining studies, any apparent benefit was small. This review clearly deflates the notion that dairy products are ‘necessary’ for the normal growth and development of children.

Further evidence for the limited role of dairy products in building bone has come from a study published in the British Medical Journal which amassed evidence from 19 studies in the effects of calcium supplementation in children ranging from 3-18 years in age [2]. This mass of evidence found that calcium supplementation had no effect on bone density in the hip or spine, and very marginal benefits for bone density in the arm.

This study was accompanied by an editorial which highlighted the lack of evidence for the ‘benefits’ of not only calcium, but also dairy products, for bone health [3]. The editorial called for policy makers to revise calcium recommendations for young people and for a change in our assumptions about the role of calcium, milk, and other dairy products in the bone health of children and adolescents.

As for the idea that starchy carbs provide vital ‘energy’ for active growing bodies. Well, first of all, the body’s cells can run on carbohydrate (glucose), but this can be formed from other ‘macronutrients’ including protein. The absolute requirement for carbohydrate is, strictly speaking, none at all. Plus, if we were concerned about children getting enough calories, surely it’s fat we should be looking to to help here (seeing as it contains about twice as many calories per gram as carbohydrate). And finally, growing bodies rely mainly on protein to provide the raw materials necessary for this. The idea that children somehow ‘need’ starchy carbs just does not stack up.

Not only are dairy and starchy carbs of limited nutritional and health value, they can be positively problematic. For example, starchy carbs can upset blood sugar and insulin in a way that predisposes to issues such as weight gain and type 2 diabetes. And then we have the issue of ‘food sensitivity’.

Unwanted reactions to food can manifest in many ways including abdominal discomfort and bloating, irritable bowel syndrome, asthma, eczema and ear, nose and throat issues including enlarged tonsils, sore throat, glue ear and ear infections. While any food can, in theory, trigger such symptoms, experience (and some science) reveals repeat offenders to be dairy products and wheat. Within wheat, ‘gluten’ is often what gives rise to problem, and this protein is found in other grains such as oats, rye and barley.

Another potential symptom of food sensitivity is constipation. There is some evidence, for example, that milk can cause constipation in children [4,5]. And a study published recently has implicated gluten too [6]. In this study, researchers looked to see if the timing of introduction of gluten into a child’s diet appeared to have any bearing on risk of constipation at the age of 24 months. Timing may be important because, generally speaking, the sooner a foodstuff is introduced into a child’s diet, the more likely it is to provoke food sensitivity issues. Constipation was defined as less than 3 bowel movement per week or the presence of mainly hard stools for two weeks or longer.

Constipation was more likely in children who had been introduced to gluten at 6 months or earlier, compared to those who had later introduction of gluten to their diets. Earlier introduction was associated with a 35 per cent increased risk of constipation.

The researchers assessed the relationship between timing of introduction of cow’s milk and risk of constipation and found no association. However, they did find that a history of cow’s milk sensitivity in the first year of life was associated with a 57 per cent increased risk of constipation, which is consistent with other work linking cow’s milk with constipation (see above).

This study is epidemiological in nature, and cannot be used to conclude that gluten (or milk) causes constipation. However, my experience in practice leads me to believe that these foodstuffs are indeed a common cause of constipation and other gut symptoms in childhood (and in older individuals too). It is perhaps not too much of a surprise that these relatively recent additions to the human diet are common provokers of unwanted symptoms. And as I pointed out above, despite dietary dictats to the contrary, such foods offer relatively limited nutritional value. The problems with such foods and their lack of necessity in the diet should cause us to reconsider, in my opinion, if ‘cereal and milk’ really is a healthy, nutritious way to start the day.

References:

1. Lanou AJ, et al. Calcium, dairy products, and bone health in children and young adults: a reevaluation of the evidence. Pediatrics. 2005;115(3):736-43

2. Winzenberg T, et al. Effects of calcium supplementation on bone density in healthy children: meta-analysis of randomised controlled trials. BMJ 2006;333:775-778

3. Lanou AJ. Bone health in children. BMJ 2006;333:763-764

4. Heine RG, et al. Cow’s milk allergy in infancy. Curr Opin Allergy Clin Immunol. 2002;2(3):217-25

5. Daher S, et al. Cow’s milk protein intolerance and chronic constipation in children. Pediatr Allergy Immunol. 2001;12(6):339-42

6. Kiefte-de Jong JC, et al. Infant nutritional factors and functional constipation in childhood: the Generation R study. Am J Gastroenterol. 2 March 2010 [Epub ahead of print]

Why are there a lot of redheads in Scotland?

Earlier today, I came across this story in the on-line version of the Daily Mail (UK) which reports on a theory relating to why the Scotland enjoys a preponderance of redheads. The theory, which the originator herself describes as ‘speculation’, is that a combination of the ‘bad weather’ in Scotland, coupled with a genetic mutation, led to burgeoning in the numbers of those with red hair. What the piece does not mention, however, is why such a mutation should exist and then persist.

When a genetic mutation occurs there is sometimes a good reason for it: some benefit may be had from that mutation. So, what benefit might there to be had from having red hair? There probably isn’t one. But there probably is a significant advantage to be had from having the pale skin tone that invariably goes with red hair.

The action of sunlight on the skin can lead to the making of vitamin D – a nutrient which is linked with an ever-growing list of benefits for health including a reduced risk of multiple sclerosis, heart disease, diabetes, and several forms of cancer. Generally speaking, the lighter the skin tone, the more vitamin D is made for a given amount of sunlight. In other words, having pale skin is potentially advantageous, particularly in locations where sunlight tends to be in short supply (like Scotland).

And all this reminds me of a conversation I had recently with Oliver Gillie, a writer and research based in the UK who has a keen interest in vitamin D.

During our conversation, Scotland came up. Here in the UK, the Scots have a famously poor health record. This is very often put down to factors such as lack of exercise, alcohol excess and a generally poor diet including ‘deep-fried Mars bars’, as well as a certain social and class-related factors. However, according to Gillie, social and lifestyle factors such as these do not fully account for the health disparities that exist between the Scotland and more southerly parts of the UK.

It occurred to Gillie that at least one ‘missing’ factor might be vitamin D. Could the relative paucity of sunlight in Scotland lead to generally levels of vitamin D, in turn putting the Scottish at heightened risk of chronic disease?

Gillie then undertook an extensive review of the literature to see what evidence there is to support this theory. He distilled his extensive research into a book, which is available for free download here. In this book Gillie, in my view, makes a hugely compelling case for both the link between low vitamin D status and disease in Scotland. He supports his case with over 500 scientific references.

Among other things, Gillie draws our attention to the apparent folly of Cancer Research UK’s SunSmart campaign, which generally urges people to be wary of the sun. As Gillie points out, this advice may well be adding to the seemingly vast numbers of people who have suboptimal levels of vitamin D.

While too much sunlight can burn the skin and increase the risk of skin cancer, shying away from it has other hazards. Gillie promotes safe sunbathing and sun exposure (and so do I). While burning is to be avoided, he advocates that individuals generally get as much sun exposure as they can. His specific tips about how safe and effective sun exposure can be found in the book (see page 56 under ‘Sunbathing – the SunSafe advice’).

Resources:

Scotland’s Health Deficit: An Explanation and a Plan by Oliver Gillie