Food addiction: Myth or reality

Animal models appear to show that certain foods (usually the so-called “high-fat, high-sugar and high-salt foods) can be addictive. However, this experimental model of addiction bears no relationship to addiction in humans. In his book “An End to Over-eating”, David Kessler comments on this animal model of food addiction, one he incidentally finds attractive to human obesity. Citing work from Italian researchers, which showed that in the short term, a cheese flavoured snack food increased levels of dopamine in rat brains he writes thus: “Over time, habituation set in, dopamine levels declined and food lost its capacity to activate their behaviour. But there’s more to the story. It turns out that if the stimulus is powerful enough, or administered intermittently enough, the brain may not curb its dopamine response after all. Desire remains high. We see this with cocaine use, which does not result in habituation”. Effectively one can trick the mouse and then make a quick jump to human cocaine addiction. Simple isn’t it?

Not so, according to a recent review by researchers at the Department of Psychiatry at the University of Cambridge[1]^,[2] In their review, they begin by distinguishing between behavioural addiction such as gambling, which doesn’t have an additive agent (betting slips per se are not addictive) and substance addictions, which are agent-dependent. Alcohol and cocaine are examples of agents that can be addictive. Thus the first challenge to the food addiction model is to identify the agent. It can’t be “fat” since effectively a totally fat-free diet is lethal to populations – reproduction becomes impossible. It can’t be “high-fat” since olive oil, the elixir of all our ailments according to many, is pure, 100% undiluted fat ~ the real thing. The normal brain relies solely on glucose as a fuel so if “sugars” are the agent, we have a problem. If it’s a specific cocktail of fat-sugar-salt, then that needs to be articulated in terms of the human diet and as of now, no such norms exist, let alone exist in some unproven state. So the putative addictive agent in food is utterly ill defined. The authors go on to point out that the so-called addictive hyperpalatable foods are widely available and widely consumed but as yet, are not a widespread public health problem. Thus they argue that in addition to some vague and as yet undefined cutoff above which addiction may occur, they will have to find other factors to explain why some people might become addicted whereas others will not. It could be a genetic factor or an addiction, dependent on alcohol intake, or on a sedentary life style or on stature or age or gender or all of the above. The concept of food addiction, particularly in relation to obesity might be popular with the wannabe celeb scientists but it is as imprecise a concept as one could possibly imagine.

 The clinical management of addiction uses a standardised guideline to define substance dependence based on the “Statistical Manual of Mental Disorders, fourth edition (DSM-IV)”. There are 7 criteria to be considered within this tool, all of which help in judgment on addictions. The first deals with “tolerance” and specifically the need for the user to seek ever-increasing amounts to reach the desired level of intoxication. This is impossible to apply to food addiction since we know neither the exact agent or its dose or its physiological, genetic, social or lifestyle dependencies. The second relates to withdrawal symptoms and no such data exists for humans and their food habits. The manual refers to symptoms such as shakes and sweats! The third is a persistent desire for and unsuccessful attempts to cut drug use. Overweight persons certainly wish to rid themselves of excess fat and try repeatedly to do so but linking this concept to a specific and putative food addiction agent is not supported by scientific data. The fourth describes the taking of larger amounts of the drug than intended. This is impossible in food since we don’t know the agent or its intoxicating dose. The fifth recognises that a great deal of time is spent getting, using and recovering from the drug. Take a walk in Tesco or Wal-Mart! The sixth deals with the effect the drug has on the pursuit of important social, occupational or recreational activities.  It’s hard to think of work absenteeism arising from the pursuit of highly palatable and putatively “addictive” foods. The seventh and final area deals with the continued use of the drug with the user well aware of its dire consequences for health and social well-being. Again, it is impossible to see how this can apply to food.

The authors do however, point out that certain eating patterns are nearing the DM-IV criteria, most specifically Binge Eating Disorders (BED) which they say is characterized by: “ …recurrent episodes (‘binges’) of uncontrolled, often rapid consumption of large amounts of food, usually in isolation, even in the absence of hunger. This eating behaviour persists despite physical discomfort and binges are often associated with feelings of guilt and disgust”. This is the closest that psychiatrists see food as approaching addiction but researchers in Yale are working on an adaptation of DSM-IV to score and quantify food addictions[3]. This blogger’s read of this adaptation of the DSM-IV clinical guidelines is that it will be quite significant adaptation, if not a total re-write. Like it or not, this will sustain the nutrition-psychiatry gulf in understanding and characterizing addiction.

Food addiction has now begun to attract the interests of other groups, most notably the legal & ethical researchers[4]. If, and it is a big if, research were to point to a possible addiction among some to a particular food or nutrient or cocktails thereof, then how do we deal with this legally? Do we expect to see certain foods removed from the supermarket shelves and driven into the underworld of dodgy dealing such as the illegal cheesecake (high fat, high, sugar, High salt food par excellence) the Cambridge scientists refer to? Of course this is farcical but where else would a regulatory and policy framework go to tackle this problem, if indeed, such behaviour is deemed to be a problem in the first place?  For those who want to explore this further, watch the You Tube video of a stand up comedian (lead author of references 1& 2 above) who is also a board certified psychiatrist on the subject of food addiction[5].

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[1] Ziauddeen H & Fletcher PC (2013) Obesity Reviews, 14, 19-28

[2] Ziauddeen H et al (2012) Nature Neuroscience, 13, 279- 286

[3] Gerhardt A et al (2009) Appetite, 52, 430-436

[4] Gearhardt A et al (2013) J Law Med Ethics. 41 Suppl 1:46-9

[5] http://www.youtube.com/watch?v=exJzI2LXh9k

Childhood IQ and maternal iodine status

About a year ago, I blogged on the subject of iodine and its increasing importance in public health nutrition in developed countries[1]. Of course, iodine deficiency is one of the three elements of global hidden hunger. According to a letter to the Lancet from the WHO “urinary iodine has been collected for 92% of the world's population and globally, more than 1·9 billion individuals have inadequate iodine nutrition (defined as urinary iodine excretion <100 (μg/L), of whom 285 million are school-aged children.”[2] In developing countries, iodine deficiency primarily affects energy metabolism and reduces the capacity for physical work. More recently, the spotlight has also been shone on the developed world where the role of iodine in brain development is the main concern. Iodine is a component of the thyroid hormones, which play a central role in the brain development of the fetal infant. In a recent Lancet paper[3], the offspring of 1040 women who had spot urine analysed for iodine during her first trimester were studied. Only those children who had an IQ test at 8 years and a reading ability test at age 9 years were included. The study drew on a longitudinal health study of mothers and their offspring, the Avon Longitudinal Study of Parents and Children.[4] The iodine to creatinine ratio, a measure recommended by the WHO was used to determine maternal iodine status and these levels were classified above or below a cut off point recommended by the WHO (150 μg/g). The average urinary value was 91 μg/g, which indicated that this population had a mild-to-moderate level of iodine deficiency (Two thirds of the population were below the WHO cut-off). The problem with cut off values is that they are often, if not always, set by scientists working in the relevant field who tend (in my view) to always go for the highest value so that their pet problem is seen to be a really important issue. This isn’t skeptism on my part. It is cynicism.

The research output of this paper would make me retract my cynicism because what the authors found was a direct association between cognitive performance and maternal iodine status. Looking firstly at the mothers themselves, those below the 150 μg/g cut off tended to be younger and to have had less education than mothers above the cut off.  For the children of these mothers below the cut-off, followed up at age 8 years, the IQ values were significantly lower for total function and for verbal and performance function. At 9 years of age, their reading ability was also lower: words per minute, accuracy, comprehension and reading score.  Clearly, a child’s cognitive function could be influenced by a wide range of confounding factors and the authors accounted for a total of 21 possible confounding factors such as maternal age, life events, breastfeeding, alcohol and tobacco intake, the use of fish oil supplements in pregnancy, birth weight, maternal depression and so on. The inclusion of all these variables did not alter the conclusions.

Using a simple cut off can sometimes be a bit too simple because it wont show if a trend exists so the authors re-analysed the data into a continuous regression analysis rather than the dichotomous cut off approach. In general they found a linear positive relationship between maternal iodine status and subsequent childhood cognitive function, again after allowing for all manner of confounding variables.

These findings are really very important. Basically, soil levels determine dietary iodine levels and there are many regions of Europe, which were known in the past to be “Goitrogenic regions” by virtue of low soil iodine levels. All that vanished when dairy farmers used iodophors to clean milking byres. That has now vanished and we are back to reliance mainly on soil levels. As I wrote in my previous blog: “Ironically, the many pregnant women who shift to organic foods in the belief that this will help ensure as healthy a baby as possible, will see a very significant fall in iodine intake.  Organic animal production greatly restricts the use of mineral and vitamin supplements in animal feeds.  Recent survey of the iodine content of milk from organic and conventional farms shows that the organic milk is 42% lower in iodine than conventional milk, and milk accounts for almost half the UK iodine intake. In fact, pregnant women should be counselled to avoid organic milk”.

Now here is an interesting question. Which would you rather have if you had the utterly unthinkable choice between an overweight 8 year old or a cognitively impaired 8 year old. Childhood obesity is very important. But there are other equally important if not more important issues for childhood nutritional wellbeing. Methinks iodine is top of the future list.

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[1] “Iodine, now a problem in developed countries July 23^rd , 2012 - http://tinyurl.com/ox3dloj.

[2]De Benoist et al (2003) Lancet, 362, (9398), 1859-1860

[3]  Bath SC et al (2013) , Lancet. 2013 May 21. E pub ahead of print

[4] http://www.bristol.ac.uk/alspac.

A greedy man in a hungry world

“A greedy man in a hungry world” is the title of a new book by Jay Rayner, an award winning author, journalist and most notably, restaurant critic. Anybody seriously interested in the food chain should read this book. It is highly informative, funny and embraces a fair degree of autobiography. There are a number of key points made by the author.

The first is the folly of the polarization of views in any discussion on food. Thus if you think supermarkets are a good idea, then you are seen to be opposed to local, slow food. If you are not convinced by the environmental or economic arguments for local farmers markets, then you are a supporter of global food trade. And if you eat food out of season, you are betraying the natural order of things. Rayner makes the point that you can see the great value of supermarkets while at the same time seeing the shortcomings of this sector. You can support local food suppliers but not accept the case of “food miles”. Thus food warriors who can only see slow, natural and local food are slated in his book and in my view, rightly so. In describing the case for only eating what is in season, he writes thus: ”Arguing for a food policy based on the kind of principles that would make the Amish look like a bunch of happy-go-lucky, profligate Sybarites may make a certain type of gimlet-eyed, self-regarding food warrior feel smug and self- righteous. It may make them glow with an inner purity. ‘Feel my deep well of virtue. Stroke my inner goodness”. And so on. But it will not provide a solution.”

Rayner, rightly, does not believe that the business-as-usual model will work and he recognises the need for reform of the present structure of the food chain. The UK’s capacity to feed itself, for example, fell from 70% efficiency in the mid-1990s to just 58% in 2011. In 2001, there were 2.25 million cows in Britain. By 2012, the dairy herd population had fallen to 1.85 million, all of 400,000 cows less. And the reason? Supermarket power was driving down prices paid to its suppliers such that farmers were being paid 25p per liter while the cost of production was 27p per liter. As a colleague of mine quips: “What is the difference between a supermarket buyer and a terrorist? Well, you can negotiate with a terrorist”!

Economics lies at the heart of many of the points made by the author and he has called for the establishment of a new branch of study, “gastronomics” combining gastronomy and economics. Take two examples.  In 1962 the average salary in the UK was £799 per annum. That increased 30 fold by 2012 to £26,000. In contrast, house prices in that period rose from an average of £2,670 to £245,000, an increase of 90 fold. Two incomes now became a necessity and the tedium of high street shopping in the green grocers, the grocers, the butchers, the egg man, the cheese man and so on became impossible. Welcome to the one stop shop the supermarket where you could buy everything at one visit at any time of the day. Supermarkets and women’s liberation are linked. On the other side of the coin, the global food chain has shown great vulnerability to natural and man-made events – a bad harvest in Australia, a cyclone in the Bay of Biscay, the US drive to supply the bio-ethanol industry with corn, a rise in the cost of oil which inflated farming input prices and the ever growing demand for meat and dairy products in China. In the space of 2 years between 2006 and 2008, the price of rice rose 217%, wheat by 136%, corn by 125% and soya by 107%. These massive fluctuations in food commodity prices will continue unless there is a move to ensure a stable and sustainable food chain. For supermarkets, the real problem will be supply. Local food production has fallen because supermarkets can buy the same products cheaper from elsewhere in the world where the natural advantage favours that particular food. Thus in New Zealand, the yield of apples is 50 tonnes per hectare while in the UK it is 14. However, the present monopoly of Western supermarkets might be challenged by the growing demand in economics such as China. The New Zealanders will sell apples to the buyer with the biggest purchase price, who are likely to be residents of the great Asian cities. Looking into the future, we can expect food prices to rise and we can expect some return to self-sustainability in food in individual EU states.

Prices are also a feature of his criticism of farmers’ markets: “Farmers’ markets are brilliant places. As are Ferrari showrooms, and glossy shops selling Chanel handbags. If you’ve got the cash, go right ahead. Knock yourself out”. Organic food is also slated for its feeble arguments and Rayner welcomes GM food but he states that “Biofuels are total bollocks”.

In addition to an excellent and amusing narrative about the food chain covering hunger, big agriculture and sustainable agriculture, Rayner also writes about his childhood growing up in London in a “culturally” Jewish family, his children and the hospitalization of his son with complicated appendicitis and of course his Mum, Clare Rayner the author and famous agony aunt, her life and death. This is a lovely book. Enjoy its facts, its humour and its pathos.

Vitamin D and breast fed infants

The diet of choice for infants during their first 6 months of life is exclusive breast milk. Not only is breast milk sterile and loaded with the exact nutrients an infant needs, but it also has an array of immune strengthening factors from maternal antibodies to complex carbohydrates, which promote a very health colonic microflora. Of late, however, breast milk has come under the spotlight of paediatric nutritionists because of concerns about vitamin D status in breast-fed infants. The level of exposure to sunlight largely determines vitamin D levels in blood. Thus vitamin D levels are highest as we enter winter following summer and autumn and are lowest as we enter summer following the darkness of winter and the emerging sunshine of spring. Given the high level of worry that people have about skin cancer, the use of sun blocks and possibly combined with poor dietary choices has led to quite a high frequency of low blood levels of vitamin D among adults. This has been linked to several metabolic disorders such as obesity and diabetes and these are topics, which have been extensively covered in previous blogs.

Whilst it may or may not be a problem for adults to have low levels of vitamin D in blood, it becomes an issue for mothers who are exclusively breast feeding their babies, particularly where infants are protected from UV sunlight with very high UV protection factors in sun blocks. In such cases, the infant may have insufficient dietary vitamin D and the American Academy of Pediatrics[1] have issued guidelines on the use of vitamin D supplements for exclusively breast fed infants recommending that they receive 400 International Units of oral vitamin D per day until they are weaned at 6 months.  This recommendation, issued in 2008, effectively doubled the previous recommendation and sought to ensure that the level of vitamin D in the blood of breast fed infants is at a level considered at the present time to be optimal to prevent rickets.

A recent paper published in the Journal of the American Medical Association[2] set out to directly explore the impact of varying oral doses of vitamin D on infant blood vitamin D levels. The infants were all breast fed and the study used four doses of oral vitamin D supplements (400, 800, 1200 and 1600 International Units) The study was a randomized double blind study in that infants were randomly assigned to one of the four treatments and neither the pediatric team nor the parents knew what actual dose was being given to each child. However, an independent safety monitoring officer was charged with inspecting all data as it emerged and on the instruction of this independent monitor, the dose of 1,600 IU per day was abandoned because this dose led to very high levels of blood vitamin D. Such high levels can cause calcification of soft tissue where calcium is inappropriately sequestered into non-bone or soft tissues such as the arteries and heart. All infants in this group were then re-assigned to the lowest group (400 IU/day).

The primary outcome expected by the researchers was to identify the level of vitamin D supplementation, which would lead to a blood level of vitamin D of 75 nano moles per liter in 97.5 % of infants. The results showed that this target was achieved by only 55% in those on the standard dose (400 IU/day). This % increased to 81% of infants on the 800 IU/d dose and 92% on those given 1,200 IU/d. The abandoned dose of 1,600 did achieve the target but of course was also found to increase the risk of soft tissue calculation. In effect, the study doses failed to deliver the expected outcome.

What does all this mean? To this blogger, sitting as I am now in a rare Irish heat wave, the sun is not evil. It should be respected but not feared. Obsessive use of sun protection by adults and by parents on their children and infants lies at the heart of this problem. Titrating the complex links between the levels of vitamin D in parental blood, in breast milk and in infant blood is just too complex even for clever pediatricians.  Mothers who use the sun sensibly and who allow some sun exposure to their infants, should have no problem with vitamin D deficiency in their exclusively breast fed babies. If they have any concerns, it is they who should take vitamin D supplements or enjoy butter, oily fish and liver. The level of vitamin D in plasma, which is the target of the American Academy of Pediatrics, is achieved by only 55% of infants. We urgently need studies to understand why this is so. How much is due to sun fear and how much is due to maternal nutrition? What do we know about formula fed infants? Why was such a group not included in this study? This is all a work in progress.

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[1] Wagner CL (2008), Pediatrics, 122, 1142-1152

[2] Gallo S et al (2013) JAMA, 309, 1785-1792