How to tackle obesity head-on

By Melanie Leyshon

25% of adults in the UK are already obese and two-thirds are overweight. Worrying statistics, which, according to Professor David Haslam, National Obesity Forum chair and Healthy Food Guide expert, means we could be facing a ‘doomsday scenario’. At the start of National Obesity Awareness Week (13–19 Jan), David wants to see campaigns for obesity becoming as hard-hitting as those against smoking.

‘There’s a lot more we can be doing by way of earlier intervention and to encourage members of the public to take sensible steps to help themselves,’ says David. ‘But this goes hand in hand with government leadership and ensuring responsible food and drink manufacturing and retailing. We need more proactive engagement by healthcare professionals on weight management, more support and better signposting to services for people who are already obese, and more importance placed on what we drink and how it affects our health.’

To tackle obesity successfully, health experts believe all the elements of the condition must be addressed. One successful scheme has been trialled in Rotherham, South Yorkshire.

The town’s weight management programme brought together health authorities and commercial enterprises such as WeightWatchers, with a focus on healthy eating and exercise. Its community approach encouraged overweight people to request a referral to the Rotherham Institute of Obesity from either their GP, nurse, pharmacist or dietitian, or to refer themselves.

Of the patients who completed the six-month weight-loss programme, 93% lost weight and 66% met or did better than their targets. Overall weight-loss results were up to 29% of the original starting weight.

‘It worked because once assessed, patients could see a weight management professional, dietitian, exercise physiologist or talking therapist, or whatever they needed,’ says David. There were three stages to the scheme: stage one identified people at primary care level; stage two was community based, where nutrition and lifestyle and exercise advice was given by trained staff; and stage three looked at specialist interventions, such as bariatric surgery. For children, this included residential weight management camps.

David believes the Rotherham approach is utterly cost effective and should be used across the country. ‘People are sitting in the wrong clinics. They’re in the cardiology clinic and the diabetes clinic or liver clinic, when really they should have started in the obesity clinic so that the problem could really be dealt with.’

‘If you rolled out the Rotherham programme everywhere, it would cost far less than the amount obesity is going to cost us in 25 years’ time, according to Government predictions,’ he says. The programme costs under £1m and if it were rolled out nationally, it would cost around £250m - a small fraction of the bill we will be faced with in 2050 if the obesity crisis continues at its current pace.’

For advice on tackling obesity, check out the National Obesity Awareness Week website www.noaw2014.org.uk/recipes - Healthy Food Guide has a week’s worth of recipes available for you to try.

For more everyday recipes - all 500 kcal or less - get a copy of Healthy Food Guide’s Make it Special 100 Speedy Suppers Recipe Collection (£3.99), out now at branches of Tesco, Sainsbury’s and WH Smith, or download the iPAD edition from iTunes. 

Public Talk at the University of Virginia on Friday, January 17

This Friday, I'll be giving an invited lecture at the University of Virginia, my undergraduate alma mater.  I was kindly invited by a medical student named Robert Abbott, and it worked out well because I was already traveling to Charlottesville.

The talk will be titled "Why Do We Overeat?  A Neurobiological Perspective".  Here's the teaser:

Obesity is a leading cause of morbidity and mortality in industrialized nations, yet this is a relatively recent phenomenon.  In the United States, increasing obesity prevalence has paralleled a gradual increase of daily energy intake.  Why do most Americans eat more than we used to, and more than we need to maintain a lean state, despite negative consequences?  This presentation will touch on the neurobiology of action selection, the neurobiology of energy homeostasis, and why our central nervous system hardware may not be up to the task of constructively navigating the modern food environment.

The talk will be attended by medical students, but I also hope to have some doctors and researchers show up, as well as people from the broader Charlottesville community.  It will be a thought-provoking talk regardless of your background, and it will touch on some of my own work.

The talk will be held in the main medical school auditorium, MEB 3110, on Friday, January 17 at noon.  You can find driving directions and parking information by following this link.  You'll probably have to park in a parking garage, either the Lee Street or Central Grounds garage (directions in the link).

For a map of the UVA health system, follow this link.  The Medical Education Building is number 44 on the map, and the talk will be in room MEB 3110 on the 3rd floor of the building.

See you there!

Sugar in our diets: what's the risk?

By Paul McArdle, British Dietetic Association dietitian and diabetes specialist

The newly launched Action on Sugar Campaign is pushing for a reduction of 20-30% in the amount of sugars in our diet – sugar hidden in products we buy and the sugar we add to our food and drink. Can our sweet addiction really put us at risk of obesity and type 2 diabetes?

It's true most of us are consuming too much sugar, and much of the sugar we consume is already in pre-packaged or convenience foods.

Although sugar has fewer than half the calories of fat, it's very easy to consume large quantities of it, especially in the form of drinks, which doesn't leave you feeling very full or satisfied. Often foods with added sugar provide very few nutritional benefits and, therefore, 'empty calories'.

The British Dietetic Association (BDA) supports the call by the campaign group Action on Sugar for the food industry to reduce the sugar added to foods. If successful, the reduction in sugar may contribute to cutting the number of calories people are eating.

This is the main problem: the sugar we eat is part of a diet which is already too high in calories – indeed it may be contributing to this, and therefore to the increasing numbers of people who are overweight and obese. Small amounts of sugar, as part of a balanced diet and in people who are successfully managing their weight, is not necessarily a problem. Moreover, there are no research studies that have proved eating sugar causes type 2 diabetes. However, there are studies that look at links between dietary patterns and the risk of developing type 2 diabetes.

One such link is sugar-sweetened beverages. A very large study of men found an association between drinking sugar-sweetened beverages and developing type 2 diabetes. Over a 20-year period, it showed a 24% increased risk for those with the highest intakes of these drinks. This doesn't demonstrate they are the cause of the diabetes in the study population, as different types of research studies would be needed to determine that. Watch this space.

Free e-Book and Ideal Weight Program 2.0 Announcement

I'm happy to announce that we're releasing a free e-book titled Why do We Gain Fat, and How do We Lose it? An Introduction to the Science of Body Fat, by Dan Pardi and myself. This is a slimmed-down version of the longer, fully referenced e-book we offer as part of the Ideal Weight Program. In it, we provide a succinct overview of the science of body fat gain and loss, and the evidence base for our program.  It also contains a schematic that ties together the various concepts in visual form. You can download it from the Dan’s Plan site by following this link to our program overview page.

Ideal Weight Program 2.0 Upgrades

Over the last year, Dan and I have been working hard to improve the Ideal Weight Program, both in response to user feedback and our own ideas for development.  Here are some of the new features we offer in 2014:

1. Four-week meal plans and shopping lists for the FLASH diet and the Simple Food Diet, as requested by Ideal Weight Program users.  This is in addition to the recipes and cooking guides we already provide.  
2. The Protein Unit system.  Research suggests there's an optimal amount of protein for appetite control and fat loss, depending on your height, weight, gender, and physical activity level.  Our fat loss diets are high in protein, but how do you know you're getting the right amount?  We've created a calculator that does it for you automatically, and explains how to apply your personalized Protein Unit value easily and intuitively using real food. 
3. Diet plates.  These are visual guides to following our diets, based loosely on the intuitive USDA MyPlate design.  
4. Cheat sheets.  Put these on your fridge to remind yourself of your diet and lifestyle guidelines, and daily protein unit goal.
5. Updated guidance.  We've refined a few things in the diet guidance documents. 

At a time of year when many people want to shed excess holiday pounds and start down a leaner, healthier path, we offer the Ideal Weight Program 2.0.  The program comes with a 30-day no-questions-asked refund policy so you can try it without risk.  We think you'll love this program, but if it doesn't work for you, we're happy to refund your purchase price. 

Financial disclosure: I receive a portion of the revenue from the sale of the Ideal Weight Program.  I do not receive revenue from the sale of other products associated with Dan's Plan or the Ideal Weight Program (such as the Fitbit, cooking tools, and other programs).

Does the Vitamin and Mineral Content of Food Influence Our Food Intake and Body Fatness?

The Claim: We Overeat Because Our Diet is Low in Vitamins and Minerals

We know that animals, including humans, seek certain properties of food.  Humans are naturally attracted to food that's high in fat, sugar, starch, and protein, and tend to be less enthusiastic about low-calorie foods that don't have these properties, like vegetables (1).  Think cookies vs. plain carrots.

In certain cases, the human body is able to detect a nutritional need and take steps to correct it.  For example, people who are placed on a calorie-restricted diet become hungry and are motivated to make up for the calorie shortfall (2, 3).  People who are placed on a low-protein diet crave protein and eat more of it after the restriction is lifted (4).  Humans and many other animals also crave and seek salt, which supplies the essential minerals sodium and chlorine, although today most of us eat much more of it than we need to.  At certain times, we may crave something sweet or acidic, and pregnant women are well known to have specific food cravings and aversions, although explanations for this remain speculative.  Research suggests that certain animals have the ability to correct mineral deficiencies by selecting foods rich in the missing mineral (5).

These observations have led to a long-standing idea that the human body is able to detect vitamin and mineral (micronutrient) status and take steps to correct a deficit.  This has led to the secondary idea that nutrient-poor food leads to overeating, as the body attempts to make up for low nutrient density by eating more food.  In other words, we overeat because our food doesn't supply the micronutrients our bodies need, and eating a micronutrient-rich diet corrects this and allows us to eat less and lose body fat.  These ideas are very intuitive, but intuition doesn't always get you very far in biology.  Let's see how they hold up to scrutiny.

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Does "Metabolically Healthy Obesity" Exist?

Obesity is strongly associated with metabolic alterations and negative health outcomes including diabetes, cardiovascular disease, and some types of cancer (1, 2, 3, 4).  Excess body fat is one of the primary causes of preventable health problems and mortality in the United States and many other affluent nations, ranking in importance with cigarette smoking and physical inactivity.  Obesity is thought to contribute to disease via the metabolic disturbances it causes, including excess glucose and lipids in the circulation, dysregulated hormone activity including insulin and leptin, and inflammatory effects.  This immediately raises two questions:

1. Does metabolically healthy obesity exist?
2. If so, are metabolically healthy obese people at an elevated risk of disease and death?

Does metabolically healthy obesity exist?

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Recent and Upcoming Appearances

Smarter Science of Slim

Jonathan Bailor recently released an interview we did a few months ago on the neurobiology of body fat regulation, and the implications for fat loss.  It's a good overview of the regulation of food intake and body fatness by the brain.  You can listen to it here.

Super Human Radio

Carl Lanore interviewed me about my lab's work on hypothalamic inflammation and obesity.  I'm currently wrapping up a postdoctoral fellowship with Dr. Michael Schwartz at the University of Washington, and the interview touches on our recent review paper "Hypothalamic Inflammation: Marker or Mechanism of Obesity Pathogenesis?"  Dan Pardi and I are frequent guests on Carl's show and I'm always impressed by how well Carl prepares prior to the interview.  You can listen to the interview here.

The Reality Check podcast

Pat Roach of the Reality Check podcast interviewed me about the scientific validity of the "carbohydrate-insulin hypothesis" of obesity.  The Reality Check podcast "explores a wide range of controversies and curiosities using science and critical thinking", and a dash of humor.  This one should be very informative for people who aren't sure what to believe and want a deeper perspective on the science of insulin and body weight regulation.  You can listen to it here.

Obesity Society conference

Next Thursday 11/9, I'll be speaking at the 2013 Obesity Society conference in Atlanta.  My talk is titled "The Glial Response to Obesity is Reversible", and it will be about my work on the reversibility of obesity-associated hypothalamic neuropathology in mice.  My talk will be part of the session "Neuronal Control of Satiety" between 3:00 and 4:30, specific time pending.  See you there!

A breakthrough for type 2 diabetes?

By Tracy Kelly

Can we put type 2 diabetes into long-term remission? It’s a question that’s asked often and to date we don’t have the answer – but that could all change within a few years. 

That’s because Diabetes UK has recently awarded a £2.4 million research grant to look into whether losing weight – and keeping it off – through a low-calorie liquid diet is a feasible long-term treatment for putting type 2 diabetes into remission.  

As part of the Diabetes Remission Clinical Trial (DiRECT) study, researchers will recruit 280 overweight people with type 2 diabetes and put them on two separate diets. This new trial follows a 2011 study that found that 11 overweight people with type 2 diabetes saw their insulin production return to normal and their type 2 diabetes put into remission after eight weeks on a low-calorie liquid diet. 

Following the huge media interest in this study, many people with type 2 diabetes were interested in this approach. But as exciting as these findings were, the study did not focus on the effects of the diet in the long term and there is still much about low-calorie diets that we are yet to understand.

As part of the new trial, one group of 140 people will spend between eight and 20 weeks on a low-calorie diet of 800 calories a day – mainly nutritionally complete diet soups or shakes, plus ample fluids. Then, as normal food is reintroduced, they will learn how to change their lifestyles permanently. 

The results of this group will be compared with an equal number in the second group, who will follow what is currently accepted as the best advice for weight loss and weight maintenance. 

Both groups will be monitored for two years to study the long-term effects of their diets on weight. MRI scans will look at what’s happening inside their bodies during the diet.

The aim is to see whether the stress and effort of following a restrictive diet for several months is beneficial in the long run. After all, 800 calories is not a lot – people following such a diet are likely to feel hungry quite a lot of the time. Also, will they be able to stick to it for long enough for it to be successful? Even more fundamentally, this kind of diet is not an easy option or a ‘quick fix’ and people will still have to follow a healthy lifestyle afterwards to stop their type 2 diabetes coming back. It’s a fact that weight regain after liquid diets is common.

Type 2 diabetes will always be a serious condition, but perhaps it won’t always be seen as a condition that people have to manage for the rest of their lives – and that inevitably gets worse. If this study shows that low-calorie liquid diets can be used safely, on a bigger scale and as part of routine care, it could completely change what we know about type 2 diabetes and how it is treated by the NHS. It could also provide an accessible way to help people with this condition live longer, with a better quality of life and a reduced risk of serious health complications.  

For more information about the trial visit www.diabetes.org.uk/DiRECT

Sleep and Genetic Obesity Risk

Evidence is steadily accumulating that insufficient sleep increases the risk of obesity and undermines fat loss efforts.  Short sleep duration is one of the most significant risk factors for obesity (1), and several potential mechanisms have been identified, including increased hunger, increased interest in calorie-dense highly palatable food, reduced drive to exercise, and alterations in hormones that influence appetite and body fatness.  Dan Pardi presented his research at AHS13 showing that sleep restriction reduces willpower to make healthy choices about food.

We also know that genetics has an outsized influence on obesity risk, accounting for about 70 percent of the variability in body fatness between people in affluent nations (2).  I have argued that "fat genes" don't directly lead to obesity, but they do determine who is susceptible to a fattening environment and who isn't (3).  I recently revisited a 2010 paper published in the journal Sleep by University of Washington researchers that supports this idea (4).

Read more »

Speaking in Lisbon on October 5

My friend Pedro Bastos graciously invited me to speak at a conference he organized in Lisbon on October 5 titled "Food, Nutrition and the Prevention of Chronic Diseases".  I will give two talks:

• "Ancestral Health: What is Our Human Potential?"  This talk will explore the health of non-industrial cultures in an effort to understand how much of our modern chronic disease burden is preventable, and it will briefly touch on one major aspect of non-industrial life that may protect against the "diseases of civilization".  This presentation will focus on age-adjusted data from high quality studies.  
• "Why Do We Overeat: a Neurobiological Perspective."  This talk will attempt to explain why most of us consume more calories than we need to maintain weight-- a phenomenon that is a central cause of morbidity and mortality in the modern world.  It will touch on some of the brain mechanisms involved in ingestive behavior, and outline a framework to explain why these mechanisms are often maladaptive in today's environment.

Pedro will speak about dairy consumption, vitamin D, and chronic disease.  

The conference is targeted to health professionals and students of nutrition, however it's open to anyone who is interested in these topics.  It's sponsored by NutriScience, a Portuguese nutrition education and consulting company.  Sadly, I don't speak Portuguese, so my talks will be in English.  

Access the full program, and register for the conference, using the links below:

Program

Registration

Is Refined Carbohydrate Addictive?

[Note: in previous versions, I mixed up "LGI" and "HGI" terms in a couple of spots.  These are now corrected.  Thanks to readers for pointing them out.]

Recently, a new study was published that triggered an avalanche of media reports suggesting that refined carbohydrate may be addictive:

Refined Carbs May Trigger Food Addiction
Refined Carbs May Trigger Food Addictions
Can You be Addicted to Carbs?
etc.

This makes for attention-grabbing headlines, but in fact the study had virtually nothing to do with food addiction.  The study made no attempt to measure addictive behavior related to refined carbohydrate or any other food, nor did it aim to do so.

So what did the study actually find, why is it being extrapolated to food addiction, and is this a reasonable extrapolation?  Answering these questions dredges up a number of interesting scientific points, some of which undermine popular notions of what determines eating behavior.

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More Thoughts on Cold Training: Biology Chimes In

Now that the concept of cold training for cold adaptation and fat loss has received scientific support, I've been thinking more about how to apply it.  A number of people have been practicing cold training for a long time, using various methods, most of which haven't been scientifically validated.  That doesn't mean the methods don't work (some of them probably do), but I don't know how far we can generalize individual results prior to seeing controlled studies.

The studies that were published two weeks ago used prolonged, mild cold exposure (60-63 F air) to achieve cold adaptation and fat loss (1, 2).  We still don't know whether or not we would see the same outcome from short, intense cold exposure such as a cold shower or brief cold water plunge.  Also, the fat loss that occurred was modest (5%), and the subjects started off lean rather than overweight.  Normally, overweight people lose more fat than lean people given the same fat loss intervention, but this possibility remains untested.  So the current research leaves a lot of stones unturned, some of which are directly relevant to popular cold training concepts.

In my last post on brown fat, I mentioned that we already know a lot about how brown fat activity is regulated, and I touched briefly on a few key points.  As is often the case, understanding the underlying biology provides clues that may help us train more effectively.  Let's see what the biology has to say.

Biology of Temperature Regulation

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AHS Talk This Saturday

For those who are attending the Ancestral Health Symposium this year, my talk will be at 9:00 AM on Saturday.  The title is "Insulin and Obesity: Reconciling Conflicting Evidence", and it will focus on the following two questions:

1. Does elevated insulin cause obesity; does obesity cause elevated insulin; or both?
2. Is there a unifying hypothesis that's able to explain all of the seemingly conflicting evidence cited by each side of the debate?

I'll approach the matter in true scientific fashion: stating hypotheses, making rational predictions based on those hypotheses, and seeing how well the evidence matches the predictions.  I'll explore the evidence in a way that has never been done before (to my knowledge), even on this blog.

Why am I giving this talk?  Two reasons.  First, it's an important question that has implications for the prevention and treatment of obesity, and it has received a lot of interest in the ancestral health community and to some extent among obesity researchers.  Second, I study the mechanisms of obesity professionally, I'm wrapping up a postdoc in a lab that has focused on the role of insulin in body fatness (lab of Dr. Michael W. Schwartz), and I've thought about this question a lot over the years-- so I'm in a good position to speak about it.

The talk will be accessible and informative to almost all knowledge levels, including researchers, physicians, and anyone who knows a little bit about insulin.  I'll cover most of the basics as we go.  I guarantee you'll learn something, whatever your knowledge level.

Brown Fat: It's a Big Deal

Non-shivering thermogenesis is the process by which the body generates extra heat without shivering.  Shivering is a way for the body to use muscular contractions to generate heat, but non-shivering thermogenesis uses a completely different mechanism to accomplish the same goal: a specialized fat-burning tissue called brown fat.  Brown fat is brown rather than white because it's packed with mitochondria, the power plants of the cell.  Under cold conditions, these mitochondria are activated, using a specialized molecular mechanism called uncoupling* to generate heat.

The mechanism of brown fat activation has been worked out fairly well in rodents, which rely heavily on non-shivering thermogenesis due to their small body size.  Specialized areas of the hypothalamus in the brain sense body temperature (through sensors in the brain and body), body energy status (by measuring leptin and satiety signals), stress level, and probably other factors, and integrate this information to set brown fat activity.  The hypothalamus does this by acting through the sympathetic nervous system, which heavily innervates brown fat.  As an aside, this process works basically the same in humans, as far as we currently know.  Those who claim that rodent models are irrelevant to humans are completely full of hot air**, as the high degree of conservation of the hypothalamus over 75 million years of evolution demonstrates.

Two new studies concurrently published in the Journal of Clinical Investigation last week demonstrate what I've suspected for a long time: brown fat can be 'trained' by cold exposure to be more active, and its activation by cold can reduce body fatness.

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The Genetics of Obesity, Part III

Genetics Loads the Gun, Environment Pulls the Trigger

Thanks to a WHS reader* for reminding me of the above quote by Dr. Francis Collins, director of the US National Institutes of Health**.  This is a concept that helps reconcile the following two seemingly contradictory observations:

1. Roughly 70 percent of obesity risk is genetically inherited, leaving only 30 percent of risk to environmental factors such as diet and lifestyle.
2. Diet and lifestyle have a large impact on obesity risk.  The prevalence of obesity has tripled in the last 30 years, and the prevalence of extreme obesity has increased by almost 10-fold.  This is presumably not enough time for genetic changes to account for it.

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The Genetics of Obesity, Part II

Rodents Lead the Way

The study of obesity genetics dates back more than half a century.  In 1949, researchers at the Jackson Laboratories identified a remarkably fat mouse, which they determined carried a spontaneous mutation in an unidentified gene.  They named this the "obese" (ob/ob) mouse.  Over the next few decades, researchers identified several other genetically obese mice with spontaneous mutations, including diabetic (db/db) mice, "agouti" (Avy) mice, and "Zucker" (fa/fa) rats.

At the time of discovery, no one knew where the mutations resided in the genome.  All they knew is that the mutations were in single genes, and they resulted in extreme obesity.  Researchers recognized this as a huge opportunity to learn something important about the regulation of body fatness in an unbiased way.  Unbiased because these mutations could be identified with no prior knowledge about their function, therefore the investigators' pre-existing beliefs about the mechanisms of body fat regulation could have no impact on what they learned.  Many different research groups tried to pin down the underlying source of dysfunction: some thought it was elevated insulin and changes in adipose tissue metabolism, others thought it was elevated cortisol, and a variety of other hypotheses.

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The Genetics of Obesity, Part I

Choosing the Right Parents: the Best Way to Stay Lean?

In 1990, Dr. Claude Bouchard and colleagues published a simple but fascinating study demonstrating the importance of genetics in body fatness (1).  They took advantage of one of the most useful tools in human genetics: identical twins.  This is what happens when a single fertilized egg generates two embryos in utero and two genetically identical humans are born from the same womb.   By comparing identical twins to other people who are not genetically identical (e.g., non-identical twins), we can quantify the impact of genes vs. environment on individual characteristics (2).

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