This morning, someone sent me a link to Gary’s latest article, and I’m passing it on to you here. In just two and a half thousand words Gary neatly, I think, reminds us of the fact that, repeatedly, eating less and exercising more has failed to have the desired effect, and the need for the scientific and medical community to embrace new concepts and new strategies.

I suspect Gary is on a bit of a mission to influence these communities and persuade them of his ideas. If this is the case, I wish him well on his quest.

I don’t want to be negative, but I’ve found changing doctors’ and scientists’ beliefs (actually, opinions) can be a bit of an uphill struggle, even when there’s plenty of evidence to support the alternative view. This is not always the case, but it is how things generally are.

I’ll happily discuss health issues and how we may best deal with them with anyone genuinely interested in this, including doctors, scientists and politicians. However, I am also mindful of the fact that some intransigence here might be the result of things that have less to do with true objections, but more to do with things like professional pride, conflicts of interest and ‘group-think’. Again, this is not universally true, but bias is more common that is healthy, I think.

I am not depressed about this, because I don’t think that persuading doctors and Governments of the merits of a particular way of eating is where the power is anyway. For me, the real power is in allowing individuals access to better information and advice. Then, if they wish they can ‘vote with their feet’ in terms of what they eat and how they lead their lives. And there’s nothing that any doctor or politician can do about that.

I came across this report today, which is about a study which assessed the association between the ‘benzophenone-type’ sunscreen ingredients and ‘endometriosis’. This condition is characterised by the finding of womb lining tissue (endometrium) outside the womb such as in the pelvis or fallopian tubes. It can be a painful condition, and can contribute to infertility.

Endometriosis is believed to be driven by the hormone oestrogen. Now, while benzophenone-type chemicals are helpful in terms of preventing sunburn, they also mimic the effects of oestrogen in the body. In this study, it was found that women with the highest levels of one particular benzophenone-type chemical were at 65 per cent increased risk of endometriosis compared to those with the lowest levels.

This sort of ‘epidemiological’ study does not prove that these chemicals cause endometriosis, but it might cause us to pause and think about the potential for chemicals in suncreens (and other skincare products) to cause harm. Of some concern here, is that oestrogen does not just drive endometriosis, but certain cancers too, including breast cancer.

I saw this story today which is concerned with the weight gain that often comes after stopping smoking. In this particular study, 3 months after smokers had stopped, their weight and fat mass had increased by 4 and 22 per cent respectively. At 6 months, these figures had risen to an average of 5 and 35 per cent. Not good. But the point of this study was to assess the mechanisms behind this phenomenon.

What this study showed is that insulin secretion after challenge with glucose rose. In all likelihood, this means when individuals ate food, they secreted more insulin than before – an insulin is a hormone which has a major role in determining how much fat gets stored in the body.

But there’s another problem with insulin, in that it lowers blood sugar levels. Now, while this is one of it’s jobs, surges of insulin run the risk of episodes of low blood sugar which can trigger ‘false’ hunger and food cravings (usually for chocolate or other sweet foodstuffs). Also, we don’t even need low blood sugar to trigger hunger – all is required is for blood sugar levels to be falling quite quickly. This is perhaps why individuals can sometimes feel a craving for sweet foods immediately after a meal.

Anyway, low and behold, it was found in this study that, in general, those who had stopped smoking were more drawn to eating carbohydrate at a free buffet (which is exactly what you expect in individuals secreting copious quantities of insulin.

What can individuals stopping smoking do to help this situation? I’d suggest as much as possible adopting a diet that is not going to compound the insulin surges and blood sugar disruption that they’re at increased risk of at least transiently after stopping smoking. This looks like a diet based on natural ‘primal’ foods including meat, fish, eggs, nuts, non-starchy vegetables and perhaps a little fruit. Who knows, such a diet may well not only help to prevent weight gain after stopping smoking, but will likely lead to healthier weight control and improved overall health in time too.

Now, if we have inherited some tendency to being overweight or obese, that does not mean we’re destined to be overweight or obese. Usually, there’s considerable potential for controlling body weight using lifestyle related approach which include diet, exercise, and some positive psychology.

It used to be thought that there was not much we could do about our genes, however, recent discoveries in the field of epigenetics reveal that the influence genes have on our health is more malleable than previously recognised. This is a good thing, because it affords the potential for considerable control over health and wellbeing through environmental (including lifestyle) factors.

I was interested to read a recent study which explored, among other things, the genetic influence on body weight, and its relationship with a key lifestyle factor – sleep [1].

The study involved assessing the sleep habits and weights of hundreds of pairs of identical and non-identical twins. Studies on twins, such as this one, allow researchers to assess the ‘heritability’ of certain characteristics. What they discovered is that the heritability of body weight is not fixed, but varies according to how long individuals sleep for.

Specifically, for individuals sleeping less than 7 hours a night on average, the overall influence of genes on weight was 70 per cent. In those sleeping for 9 hours or more each night, the influence of genetic factors on weight was less than half this (32 per cent). In other words, the longer individuals slept for, the less influence genetic factors had on their weight and, we assume, the greater the potential for regulating weight through lifestyle adjustment.

Quite what it is about sleep that has this effect is not known. The author of an accompanying editorial makes the point that individuals who sleep for longer are essentially better rested, and may be in a better position to influence weight through healthy lifestyle behaviours. He also makes the point that healthy lifestyle behaviours, like not eating too big an evening meal, may in turn help sleep.

It may take time to dissect the precise relationship between sleep and body weight, but the message from this study is that getting a decent amount of sleep is likely to make body weight more controllable. Chances are, of course, that optimising sleep will give us
more control over other aspects of our health too.

I recently wrote a blog post in which I suggested a range of strategies which tend to improve sleep for those who have trouble here.

References:

1. Watson NF, et al. Sleep duration and body mass index in twins: a gene-environment interaction. SLEEP 2012;35(5):597-603.

I suspect the panel, like a multitude of panels before it, will recommend that we keep strong downward pressure on our cholesterol numbers. But not all individuals in the medical and scientific community agree with this approach. One such dissenter is Professor Krumholz.

In this video below, Professor Krumholz does a good job, I think, of highlighting some of the major issues with current cholesterol policy. I advise you to watch the video but, for good measure, here’s a short summary of the salient points Professor Krumholz makes:

1. While targets are often based on levels of LDL-cholesterol, evidence shows that this is just one potential risk factor for cardiovascular disease. Many others exist, some of which are better predictors of cardiovascular disease than LDL-cholesterol.

2. Although it’s generally accepted that improvement in cardiac risk factors is beneficial, there is plenty of evidence that does not bear this out. He cites, for example, the example of the drug torcetrapib which lowered (supposedly unhealthy) LDL-cholesterol and raised (supposedly healthy) HDL-cholesterol. Torcetrapib, however, significantly increased overall risk of death in those who took it.

Professor Krumholz in his letter cites hormone replacement therapy as another example of a drug therapy that can ‘improve’ cholesterol numbers but that actually increases risk.

Other notable failures in terms of brining broad benefits to health include the drugs ezetimibe and fibrates.

3. Professor Krumholz speculates on why cholesterol ‘improvement’ may not actually improve health. One theory is that drugs which reduce cholesterol and have benefits (such as statins) do so through one or more mechanisms that are distinct from their cholesterol-lowering effects. Another is that even if cholesterol reduction is beneficial, this may be offset by the hazardous effects of a drug.

4. Professor Krumholz goes on to make the point that while we doctors are encouraged to treat peoples’ cholesterol down to a target level, not a single study has actually tested this approach.

5. He recommends an approach not based on cholesterol levels, but risk. He quite rightly points out that those at low risk of cardiovascular disease are unlikely to benefit much, but are still at risk of suffering from side-effects from treatment. He also points out the large ‘numbers needed to treat’ for relatively healthy people. Basically, about 50-100 people would need to be treated with a statin for 5 years to prevent on heart attack. This means, by the way, that 98-99 per cent of people treated will not benefit. People at higher risk stand to benefit more. However, it’s still true that the great majority who take statins will not benefit at all.

So there you have it, a neat summing up of the flaws in the conventional thinking regarding cholesterol lowering. And from a professor of medicine and cardiologist to boot. It’s a shame that the Professor Krumholz’s objectivity and ability to break out of the cholesterol ‘group-think’ is so rare in medicine. Many, many doctors would do well to follow his example.

However, the evidence base for the effectiveness of sunscreens in skin cancer prevention is scant to say the least. Back in 2000, the International Agency for Research on Cancer in Lyon, France, held a meeting to discuss the role of sunscreens in skin cancer prevention. Before we look at their findings, here’s a quick summary of the main forms of skin cancer.

There are 3 main sorts of skin cancer, squamous cell carcinoma (carcinoma is a type of cancer), basal cell carcinoma, and malignant melanoma.

Squamus and basal cells carcinomas are quite-strongly related to sunlight exposure, as partly evidence by the fact that they are most common in typically sun-exposed parts of the body like the face, ears and back of the hand. They make up about 90 per cent of skin cancers but are responsible for only about 15 per cent of skin cancer deaths. The relatively non-deadly nature of these cancers is essentially because they are not typically very aggressive and are often spotted quite early means that they usually won’t.

Malignant melanomas represent only about 10 per cent of skin cancers but account for about 85 per cent of skin cancer deaths. Most of them do not occur in typically sun-exposed parts of the body, though sunburn is a risk factor. When people use sunscreens to prevent skin cancer, it’s usually melanoma they’re thinking of.

Anyway, back to the International Agency for Research on Cancer meeting in 2000…

A report of the panel’s findings was published in the Scandinavian Journal of Work and Environmental Health [1]. The panel concluded that sunscreens could prevent sunburn (should hope so too), and that there was evidence that they could help prevent squamous cell carcinoma. There was a caveat though: protection was only evident where individuals had not used sunscreens to extend their time in the sun. Actually, a lot of people use sunscreens in this way. When people coat themselves in sunscreen on the beach or by the pool, one usual intention to allow themselves to stay longer in the sun without burning.

But what of the role of sunscreens in melanoma prevention? The paper refers to epidemiological evidence (studies that look at associations between things) that find sunscreen use was not associated with a reduction in the risk of moles (higher numbers of moles are a risk factor for melanoma). In their press release the panel members state this:

Several relevant epidemiological studies have shown significantly higher risks for melanoma in users of sunscreens than in non-users. This paradoxical observation could in part be due to the fact that users of sunscreens deliberately spend more time in the sun than they would otherwise have done. Thus, the protective effect of sunscreens can be outweighed by overexposure based on the false assumption that sunscreens completely abolish the adverse effects of UV light.

In light of these findings, the Working Group concluded that sunscreens prevent sunburns and may reduce the risk of squamous cell carcinoma, but only if they do not mislead people to extend their exposure to sunlight. The Working Group also put forward several recommendations in relation to the use of sunscreens. Principal amongst these is that use of sunscreens should be one part of a comprehensive sun avoidance strategy that includes moving into shade when the sun is near zenith and the use of protective clothing. As part of a comprehensive skin protection strategy, sunscreens with a protection factor of 15 or more should be used.

In other words, don’t rely on sunscreens to protect you from melanoma, because they probably won’t, and may actually increase risk. A more recent review concluded that studies link sunscreen use with increased risk of moles, malignant melanoma and basal cell carcinoma [2].

I have not used sunscreen for 20-odd years, opting to seek shade and wear appropriate clothing when the sun is at its hottest. Because sunscreens can give us a false sense of security, it might be wise to use it sparingly. One situation where it can come into its own is for the face and ears when swimming in a pool or sea. If protection is required elsewhere, I’d go for clothing designed to protect the body from UV rays.

References:

1. Vainio H, et al. Cancer-preventive effects of sunscreens are uncertain. Scandinavian Journal of Work and Environmental Health 2000;26(6):529-531

2. Autier P. Sunscreen abuse for intentional sun exposure. Br J Dermatol. 2009;161 Suppl 3:40-5

It turns out, that in the US, psychiatrists on these panels more often than not have conflicts of interest. For example, 70 per cent of the members of panels responsible for drawing up the most recent edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM – the ‘psychiatry bible’) have declared conflicts of interest. The actual number may be worse as certain sources of funding (including some research funding) does not need to be declared.

Now, it’s generally accepted in the medical and scientific communities that declaration of conflicts of interest is a good thing. But does it actually help to stamp out bias? A recent piece in the on-line journal PLoS Medicine [1] suggests that declaration of conflicts of interests does not get to the root of the problem, and may make bias worse, not better.

The piece cites arguments from ‘decision scientist’ George Loewenstein and his colleagues which apparently show that “disclosure can actually lead doctors to give biased advice, either through strategic exaggeration (whereby more biased advice is provided to counteract anticipated discounting), or “moral licensing” such that advice is legitimized because advisees “have been warned” (that is, caveat emptor or “buyer beware”).”

According to their experiments, bias is considerably greater when conflicts of interest are disclosed. In addition, it turns out that patients think their doctors would never intentionally mislead them and tend not to discount advice in light of conflicts. In this way, it is claimed, “disclosure policies will never be the solution and are very likely exacerbating the problem of bias in medicine.”

Perhaps the real remedy here is to make it mandatory for panel members to be free of conflicts of interest. It is sometimes claimed that this would not work, as such people with appropriate experience would be difficult to find. If this is true, it speaks volumes as to how effective the pharmaceutical industry is at identifying potential ‘key opinion leaders’ and striking deals with them.

References:

1. Clark J, et al. Does Conflict of Interest Disclosure Worsen Bias? PLoS Medicine 24 April 2012

Anyway, the BMJ article contained a lot of information about the management of this syndrome, including injecting botox into the bladder muscle to paralyse it. What the article did not do is mention the one approach which I find almost always reaps dividends in practice: magnesium supplementation.

The bladder is essentially a muscular bag. Magnesium is a nutrient that is important for proper muscle function. If magnesium levels are on the low side, this tends to make muscles prone to ‘tension’ and cramping. Low magnesium may there cause muscular cramps, as well as conditions such as ‘tension’ headaches, oesophageal spasm (spasm in the food pipe or gullet) and painful periods (the womb is made of muscle). It can also, in theory at least, cause ‘irritable bladder’.

As magnesium levels rise, the muscle is more likely to remain in an appropriately ‘relaxed’ state, and this can help relieve symptoms of ‘irritable bladder’. I’ve seen it work time and again in practice. There’s even some evidence for it. In one placebo-controlled study, magnesium supplementation was found to be quite effective for relieving the symptoms of irritable bladder [2]. This positive result was despite the fact that the form of magnesium used in this study was magnesium oxide – probably the least useful and absorbable form of magnesium.

In practice, I prefer to use other forms of magnesium such as magnesium citrate, taurinate, glycinate or succinate. A dose of around 400 mg of magnesium is usually what’s required to get good symptomatic relief.

References:

1. Marinkovic SP, et al. The management of overactive bladder syndrome. BMJ. 2012 Apr 17

2. Gordon D, et al. Double-blind, placebo-controlled study of magnesium hydroxide for treatment of sensory urgency and detrusor instability: preliminary results. Br J Obstet Gynaecol. 1998;105(6):667-9

Raised levels of ‘TSH’ (thyroid stimulating hormone, the hormone secreted by the pituitary gland at the base of the brain that stimulates the thyroid to produce thyroid hormones)

Low levels of thyroxine (one of the chief thyroid hormones – also known as ‘T4’)

My experience in practice tells me that the conventional way in which these blood tests are used to diagnose hypothyroidism is quite inadequate. The fact is, true hypothyroidism is not always reflected in a raised TSH and low thyroxine, and many individuals can suffer from hypothyroidism in the long term because their tests are ‘normal’. You can read about this here and here.

Even when tests yield abnormal readings, doctors can be reluctant to treat. For example, there is a recognised condition termed ‘subclinical hypothyroidism’ in which TSH levels are raised, but thyroxine levels are ‘normal’. Whether this condition should be treated with thyroid hormone is a moot point. Some doctors will treat. Many won’t, though, sometimes on the basis of the supposed risks associated with thyroid hormone treatment.

I was interested to read a recent study which looked women with subclinical hypothyroidism over time. Some of these women were treated with thyroxine, while some were not [1]. The researchers then looked at the women’s risk for ‘ischaemic heart disease’ events (fatal and non-fatal heart attacks). In women aged 40-70, thyroid treatment was associated with a 39 per cent reduced risk of heart events. In women over the age of 70, treatment was not associated with a reduction in risk.

Now this study was epidemiological in nature, and cannot be used to conclude that thyroid treatment reduces risk of heart attacks in ‘younger’ women. However, this idea is not far-fetched, seeing as subclinical hypothyroidism is associated with an increased risk of heart disease.

The results of this study suggest that treatment of subclinical hypothyroidism may benefit heart health, and that diagnosing the issue and initiating treatment earlier might be better than ‘watching and waiting’.

As will all things, there are risks associated with treatment. However, what sometimes is forgotten in thyroid management is that there is often a heavy price to pay for not treating too.

References:

Razvi S, et al. Levothyroxine Treatment of Subclinical Hypothyroidism, Fatal and Nonfatal Cardiovascular Events, and Mortality. Arch Intern Med. Published online 23 April 2012

The Atkins and other similar diets have often been classed as ‘high-protein’ diets. Some believe them to be high-fat too. Actually, when individuals adopt such diet they don’t tend to eat much more in the way of protein or fat – they just eat less carbohydrate. So, while the percentage of protein and fat will generally go up, the absolute amount of these ‘macronutrients’ stays more-or-less the same.

One of the rationales for eating a diet relatively rich in protein is that it is the macronutrient which, calorie-for-calorie, sates the appetite most effectively. What appears to be true is that individuals who adopt this type of diet almost always spontaneously eat less (often, several hundred calories a day less). This may have something to do with protein, but it might also have something to do with fat (which many people find is important for sating the appetite properly). It might also have something to do with the better blood sugar stability these diets tend to afford, which will help guard against episodes of low blood sugar which can trigger ‘false hunger’ and food cravings (usually for carbohydrate).

There is also a theory that higher protein diets may assist weight loss through increased ‘thermogenesis’. After eating, the metabolism will generally enjoy a ‘boost’ – a bit like what happens when you put fuel on a fire. The thermogenic effect of protein is greater for protein then it is for carbohydrate or fat. The effect is not huge, but might help weight control (and other things) over time.

This week, the European Journal of Clinical Nutrition published a review of the impact of protein content on a range of health parameters. The study was a ‘meta-analysis’ – a pooling together of similar studies. In this case, the results of 74 studies were lumped in together. These studies varied quite a lot in design. For example, in some studies individuals were left to fend for themselves food-wise, while in others they were supplied with food. Meta-analyses seem like a good idea, but something the fact that they lump together quite-different studies can make it hard to draw firm conclusions. Also, as usual, there can be a gap between what the diet was designed to test and what it actually tested, because not all people are utterly compliant of course. Many will misreport (deliberately or unconsciously) what they ate too.

Anyway, leaving these issues aside, what did the review find.

Well, overall, the prescribed diets has these macronutrient compositions (percentage of calories contributed by each macronutrient):

Lower protein:

protein – 18 per cent
carbohydrate – 55 per cent
fat – 26 per cent

Higher protein:

protein – 27 per cent
carbohydrate – 38 per cent
fat – 32 per cent

The diets in which higher protein was prescribed led to significant improvements, compared to lower protein, in a range of parameters, including:

Weight
Waist circumference
Systolic blood pressure (the higher of the two blood pressure readings)
Diastolic blood pressure (the lower of the two blood pressure readings)
HDL cholesterol levels
Triglyceride levels
Fasting insulin levels
Satiety

No parameter measured was improved by the lower-protein diet.

Overall adverse effects was the same between groups, and there was no difference detected in terms of bone and kidney health (high-protein diets are often claimed to be ‘bad for the bones’ or kidneys though, actually, there is no evidence for this for health people).

In general terms, one would have to chalk this up as a win for higher-protein, lower-carbohydrate diets. But actually, the authors of this review were quite dismissive of the results. They tell us that: “Higher-protein diets probably improve adiposity, blood pressure and triglyceride levels, but these effects are small and need to be weighed against the potential for harms.”

First of all, why “probably”? Their own meta-analysis shows that higher-protein diets do indeed induce these changes. And the authors left some of the other benefits out too. But what’s this “potential for harms” all about? The meta-analysis actually found these diets to be as safe as lower-protein ones, overall, so what could they be referring to?

When authors’ conclusions don’t match their very own results it sometimes pays to look for potential conflicts of interest (this can help explain authors’ bias). Well it turns out that one of the study authors is an employee of Barilla – an Italian company that makes pasta. Two of the other authors received “grant support” from Barilla to conduct the review.

Now, the relative popularity of ‘high-protein’ diets has not been particularly good news for companies like Barilla, essentially because these diets are lower in carbohydrate, and specifically encourage restraint in the consumption of starchy ‘staples’ including pasta.

My suspicion (this is just speculation) is that Barilla decided to go looking for evidence which was unsupportive of higher-protein and lower-carbohydrate diets. If so, it seems Barilla’s efforts here back-fired a bit it seems, so what to do? How about pouring cold water on the clearly positive findings and refer to the “hazards” of higher-protein diets for which there is no evidence?

References:

1. Santesso N, et al. Effects of higher- versus lower-protein diets on health outcomes: a systematic review and meta-analysis. Eur J Clin Nutr Epub 18th April 2012

The following year, flu hysteria had died down, and the new UK Government took, seemingly, a more relaxed attitude to flu. This is all documented in a study published recently which has been reported quite widely [1]. The study authors basically make the point that this supposedly ‘laissez-faire’ attitude led to an increase in hospital admissions for flu and death too.

The actual figures quoted in the study are (2009/10 versus 2010/11):

7879 versus 8797 hospital admissions (10 per cent rise)

361 versus 474 deaths (30 per cent rise)

Basically, the new Government is castigated for not dishing out Tamiflu like smarties and urging vaccination and, as a result, perhaps causing people to die.

Is it really that simple? First things first: Were the increases in hospital admissions and deaths due to a change in flu management policy or perhaps down to something else, like chance? We’ll never know, but we simply can’t assume it’s the former.

Did reduced vaccination cause the problem? Maybe, but let’s bear two things in mind. Firstly, flu vaccination is not nearly as effective as we’ve perhaps been led to believe. See here and here for some more information on this.

Secondly, according to the Government, vaccination rates were about the same in 2010/11 and 2009/10. It seems like a more relaxed attitude to pushing vaccination did not translate in to significantly reduced uptake anyway.

What about the fact that Tamiflu was not as widely ‘prescribed’? Well, the best available evidence suggests this drugs reduced symptoms of flu by about a day, and does not reduce the risk of complications. See here for more about this.

I have no particular political affiliation and am certainly not a closet supporter of the current Government or their health policies. However, the plain facts of the matter are that we really can’t tell from this recent study if the Government’s less aggressive approach to the containment of flu did us harm or good or neither.

One of the study authors turns out to be Sir Liam Donaldson, the Chief Medical Officer whose overblown estimates helped spark the pandemic pandemonium. And it was his decision, ultimately, to make Tamiflu available over the phone, even though this drug is virtually useless. Not surprisingly Professor Sir Liam took a little flack for his handling of the flu affair. He ‘stepped down’ from his Chief Medical Officer post unexpectedly in late 2009.

Seems to me that the point Sir Liam is making with this publication has not much to do with public health, and everything to do with politics.

References:

1. Mytton OT, et al. Influenza A(H1n1)Pdm09 In England, 2009 To 2011: A Greater Burden Of Severe Illness In The Year After The Pandemic Than In The Pandemic Year. Eurosurveillance, Volume 17, Issue 14, 05 April 2012

What is ‘earthing’?

Earthing is the practice of connecting the body with earth by touching skin to a conductive material such as grass (preferably wet), wet sand, a river, lake or sea.

Why would you want to do that?

When the body loses contact with the earth it can carry a positive voltage relative to the Earth. Some people believe this is not good for health and wellbeing. Earthing the body returns the voltage to zero which is, supposedly better for us.

Is there any ‘science’ to it?

Actually, yes. First of all, some theory…

During the normal processes of metabolism the body generates what are called ‘reactive oxygen species’ which are commonly referred to as ‘free radicals’. These compounds appear to be important, at least in part because they have the ability to attack and destroy unwanted things within the body including bacteria and viruses. However, too many free radicals are a bad thing, and have been implicated in chronic disease and well as the very process of ageing.

Free radicals are involved in the process known as inflammation, which is part of the healing process. However, low-grade inflammation throughout the body may lead to pain and other problems in the muscles and joints, and is also believed to be a key driving factor in many chronic diseases including heart disease and type 2 diabetes. In short, we want free radicals, but not too many.

Free radicals lack sparks of energy known as ‘electrons’. One way to quell them is to give them electrons, and these can be supplied by nutrients such as vitamins A, C and E, and plant substances known as ‘polyphenols’ (found in, among other things, tea, coffee, cocoa and apples). However, substances we eat and drink are not the only way to get electrons into the body: earthing does this too. If the body has a positive charge on it, earthing allows electrons to flow into the body where, in theory, they can neutralise overblown free radical and inflammatory damage.

Carrying a positive charge may well affect the body in lots of different ways, which means that earthing may offer a range of wellbeing benefits.

Any studies?

There is indeed some evidence that earthing can help people. For example, in one study earthing was studied in 60 people suffering form sleep disturbances and chronic muscle and joint pain for at least six months [1]. Subjects were randomly divided for the month-long study in which both groups slept on earthed mattresses. Half the pads were properly earthed and the other half while the other half were “sham” grounded (not actually earthed).

Most grounded subjects described symptomatic improvement while most in the control group did not. Some subjects reported significant relief from asthmatic and respiratory conditions, rheumatoid arthritis, sleep apnea, and hypertension while sleeping grounded. Here’s a table which summarises the results:

Other ‘blinded’ experiments have found earthing can induce significant changes in a range of objective parameters including heart rate, brainwave activity and skin conductance. You can access a pdf of a review article about earthing by clicking the following link earthing review article.

My own personal experience

I decided to give earthing a try.

First some background: On 3rd January this year I vaulted over a high gate and landed on some steps the other side, twisting my right ankle as I did this. I’ve had pain in this ankle ever since. Not enough to stop me walking, but running has been out of the question. Rushing down the stairs (as I like to do) has also been quite uncomfortable. I’ve also had a pain in the top of my left foot. Not sure when this started, but I first noticed it at least several weeks ago.

My earthing experiment started with me sitting with my bare feet on damp grass on 14th April. I lasted 20 minutes. Later in the day I noticed that the pain in my left foot and ankle had disappeared completely (and they have not returned since).

Another odd thing is that for the preceding few days I had been brewing an ingrowing toenail on my right big toe. I used to get these a lot when I younger, but they’ve been rarer since I’ve gotten older. The normal course for these is to get steadily worse over several days and then I’d perform a bit of DIY surgery (don’t ask) to relieve the issue. The morning after my first earthing escapade, I noticed that my ingrowing toenail had utterly resolved on its own.

That day I put my bare feet on the grass again, this time for 30 minutes. And then some earthing kit that I’d ordered arrived in the post and I’ve been using ever since (primarily an earthing mat which I put my feet on when I work).

OK, so the near miraculous resolution of my foot and ankle troubles could have been due to a lovely placebo response. I’m comfortable with this, if that’s the case (though I’ll never know). But one of my experiences I think points away from the improvement being purely placebo: For several months now I’d also had a niggly pain in my left elbow which is most noticeable when I wake up. While my ankle and foot pain (and ingrowing toenail) resolved, my elbow pain did not. This does not in any way disprove my foot/ankle improvement was not a placebo response, but the likelihood of it being placebo is diminished by the experience with my elbow I think.

Further reading

One of the biggest proponents of earthing is Clint Ober. He’s co-authored a book (Earthing – the most important health discovery ever?) which is worth a look for those who want to dig deeper and learn more.

References:

1. Ober C. Grounding the human body to neutralize bio- electrical stress from static electricity and EMF. ESD Journal January 2000.

1. Eat a ‘primal’ diet
I’ve found that a major cause of waking in the night and sleep disruption is episodes of low blood sugar (which turns on the stress response). Eating a ‘primal’ diet seems to guard against this and I’ve seen it improve sleep considerably and consistently.

2. Avoid alcohol in the evening
This is another consistent finding: individuals who avoid alcohol in the evening generally sleep better and feel more rested the following morning than when they drink. Avoiding coming into the evening very hungry can help here, as hunger is often a major factor in drinking. Keeping hydrated in the day and not being thirsty in the evening will generally help here too.

3. Avoid caffeine after lunchtime (or perhaps earlier)
Some people tolerate caffeine late in the day OK, but many don’t. Cutting out caffeine after lunch often helps.

4. Daytime light
Light appears to be important for the production of melatonin – a hormone that plays a key role in sleep. Light early in the day seems to be best here, so getting out in the morning or at least lunchtime for 20 minutes or so is a good idea. Alternatively, you might like to try a light device.

5. Turn the lights down low at night
Bright light in the evening can impair sleep, so try and get by with as little light exposure as possible for a couple of hours or so before bed.

6. Eyeshades
Total darkness seems to aid sleep, but who can ensure a totally dark bedroom? Not many of us. Eyeshades have potential value here. I prefer those made out of silk as I find these to be the most comfortable.

7. Earplugs
Noise is another common sleep-disrupter, whether this be traffic noise, a buzzing mini-bar in a hotel room or snoring partner. I think earplugs are an under-used Godsend. The best make I’ve found are foam plugs made by the company Quies.

8. Relaxation techniques
These can help calm the mind and body and smooth the transition into sleep. They can be used to get to sleep or help get back to sleep if you wake in the night. A couple of commonly used techniques (which can be applied together) are ‘progressive muscular relaxation’ and abdominal (‘belly’) breathing. There’s plenty of information about these techniques on the internet.

9. Magnesium
This mineral has a calming influence on the brain. It’s also a critically important nutrient for muscular functioning, and a lack of it (quite common) can cause symptoms such as restlessness, restless legs and muscular cramp. A lot of people find magnesium aids their sleep. Magnesium supplements come in many different forms and some are more bioavailable (absorbable and useful to the body) than others. One worth avoiding is magnesium oxide (cheap but not very absorbable). Better forms of magnesium include magnesium citrate, taurinate, glycinate and succinate. Personally, I suggest about 400 mg of elemental magnesium a day, perhaps best taken in the evening.

One class of medication with a range of known side-effects are the statins. These cholesterol-reducing drugs are known to have the potential to cause symptoms such as muscle pain and fatigue, as well as cause damage to organs such as the liver and kidneys. About a year ago I was at a medical lecture, and one (doctor) member of the audience commented that he felt his patients experienced side effects from taking statins far more commonly than official statistics suggested. My own experience supports this observation.
Could there be an explanation for this phenomenon?

One explanation has to do with the design of statin studies. Quite often, individuals who are in poor health and perhaps at increased risk of side-effects are automatically barred from entering a study. Yet, in the real world, even people who are poor candidates in this respect may end up being prescribed a statin. Individuals with a history of problems such as muscular pain or damage to the liver or kidneys (all of which can be exacerbated by statins) are typically excluded from studies too, further reducing the chance that side-effects will arise.

Even those who make it through this screening process, however, may be subjected to what is known as an ‘run in’ period prior to the study. Here, individuals may be treated with a statin with idea being that individuals who are ‘non-compliant’ (do not take their medication as instructed) are weeded out. However, the run-in period also affords the researchers the opportunity to detect individuals who are susceptible to statin side-effects and stop them getting into the study proper.

In other words, in formal studies participants are often at a significantly lower risk of side-effects than those in the general population.

Another problem with conventional studies is how side-effects are defined. Muscle pain is a quite-frequent side-effect of statins. In extreme cases, statins can cause a break-down of muscle tissue known as ‘rhabdomyolysis’ which can have potentially fatal consequences. In some studies, the focus has been on rhabdomyolysis, which means less severe side-effects such as muscle pain or fatigue may ‘go missing’.

Another way in which the bar for side-effects can be set very high concerns the blood parameters used to detect damage. For instance, in a recent study muscle damage was only deemed to have occurred when muscle enzyme levels (a marker for muscle damage) were at least 5 times the upper limit of normal [1]. In this same study, liver damage (another potential hazard of statins) was only deemed to have occurred when liver enzymes were at least 3 times the upper limit of normal. In both cases, a more logical approach would be to regard a rise of any amount above the top end of the normal range as abnormal and significant. This would be more how it is in actual clinical practice.

The elimination of individuals prone to side-effects and the setting of the bar very high for abnormalities help explain why the side-effects from statins seem much more common in the real world than officially quoted statistics.

However, even in the real world, there might be under-recognition of the damage statins can do. That’s because, quite often, doctors will dismiss the idea that statins might be the cause for someone’s symptoms, even when scientific evidence supports such as link. For more on this, see here.

References:

1. Nicholls S, et al. Effect of Two Intensive Statin Regimens on Progression of Coronary Disease. NEJM 2011;365(22):2078-87

The review, from scientists at Federal University in Sao Paulo, Brazil, refers specifically to a range of potential mechanisms here including:

1. Reduced insulin sensitivity
One of insulin’s jobs is to assist the transfer of nutrients in the bloodstream into the cells. If insulin does not do this effectively, cells can be effectively ‘starved’ of fuel. If, say, brain and muscle cells, are under-fuelled, the end result could be mental and physical fatigue. And under-fuelled brain would tend to predispose to heightened hunger too.

When the body is broadly resistant to insulin’s effects, then the pancreas will generally pump out more insulin in an effort to lower blood sugar levels. The problem here is that insulin has a range of biochemical effects that we’d expect to translate into increased fat accumulation in the fat tissues. Here are some of insulin key effects in this respect:

Insulin stimulates the uptake of fat into the fat cells
Insulin activates the enzyme ‘lipoprotein lipase’ that catalyses the conversion of fat in the form of triglcyerides into smaller molecules known as fatty acids. These fatty acids, unlikely triglyceride, can make their way into the fat cells.

Insulin increases the supply of glycerol for the ‘fixing’ of fat in the fat cell
Insulin also facilitates the uptake of sugar into cells where it can be converted into glycerol In combination with fatty acids, glycerol forms triglyceride again, effectively ‘fixing’ fat in the fat cells.

Insulin inhibits breakdown and release from the fat cells
Triglyceride in the fat cells is disassembled through the action of an enzyme known as ‘hormone-sensitive lipase’. Insulin inhibits this enzyme, and therefore slows fat release from the fat cells (lipolysis).

2. Raised levels of cortisol
Cortisol is a major ‘stress’ hormone secreted by the adrenal glands. It’s essential to life, but as with everything, too much can be a bad thing. Cortisol antagonises insulin, and may therefore contribute to ‘insulin resistance’ (see above). It also has the ability to predispose to fatty accumulation, particularly around the midriff.

3. Raised levels of ghrelin
Ghrelin is a hormone secreted by the stomach and the pancreas. It stimulates appetite thorough and effect on the brain. Higher levels of this hormone may drive us to overeat.

4. Lowered levels of leptin
Leptin is a hormone secrete by fat cells. It acts on the brain to quell hunger and stimulate the metabolism. Lower levels of this hormone, as induced by short sleep duration, might therefore increase hunger and put a brake on the metabolism – not ideal for someone seeking to maintain or attain a healthy weight.

5. Fatigue
Short sleep can cause us to be tired, which might contribute to obesity by reducing overall levels of activity.

The authors of this review conclude that: “…present literature highlights the importance of getting enough good sleep for metabolic health.” Here, here to that. Tomorrow, I’m going to write a post on some of the simple strategies I’ve found to be most useful for ensuring better sleep.

References:

1. Zimberg IZ, et al. Short sleep duration and obesity: mechanisms and future perspectives. Cell Biochem Funct. 2012 Apr 4 [Epub ahead of print]