Saturday, January 31, 2015

Gluten-free January Participants: Take the Survey!

Matt Lentzner, Janine Jagger and I have designed a survey for participants of Gluten-free January, using the online application StatCrunch. Janine is an epidemiologist who studies healthcare worker safety at the University of Virginia; she has experience designing surveys for data collection so we're glad to have her on board. The survey will allow us to systematically gather and analyze data on the results of Gluten-free January. It will be 100 percent anonymous-- none of your answers will be connected to your identity in any way.

This survey has the potential to be really informative, but it will only work if you respond! The more people who take the survey, the more informative it will be, even if you didn't avoid gluten for a single day. If not very many people respond, it will be highly susceptible to "selection bias", where perhaps the only people who responded are people who improved the most, skewing the results.

Matt will be sending the survey out to everyone on his mailing list. Please complete it, even if you didn't end up avoiding gluten at all! There's no shame in it. The survey has responses built in for people who didn't avoid gluten. Your survey will still be useful!

We have potential data from over 500 people. After we crunch the numbers, I'll share them on the blog.

Why Do We Eat? A Neurobiological Perspective. Part III

In the first post, I explained that all voluntary actions are driven by a central action selection system in the mesolimbic area (the reward system).  This is the part of you that makes the decision to act, or not to act.  This system determines your overall motivation to obtain food, based on a variety of internal and external factors, for example hunger, the effort required to obtain food, and the sensory qualities of food/drink.  These factors are recognized and processed by a number of specialized 'modules' in the brain, and forwarded to the reward system where the decision to eat, or not to eat, is made.  Researchers divide food intake into two categories: 1) eating from a true energy need by the body (homeostatic eating), e.g. hunger, and 2) eating for other reasons (non-homeostatic eating), e.g. eating for social reasons or because the food tastes really good.

In the second post of the series, we explored how the brain regulates food intake on a meal-to meal basis based on feedback from the digestive system, and how food properties can influence this process.  The integrated gut-brain system that accomplishes this can be called the satiety system.

In this post, we'll explore the energy homeostasis system, which regulates energy balance (energy in vs. energy out) and body fatness on a long term basis.

The Energy Homeostasis System

Read more »

Friday, January 30, 2015

Paleo Diet Article in Sound Consumer

I recently wrote an article for my local natural foods grocery store, PCC, about the "Paleolithic" diet.  You can read it online here.  I explain the basic rationale for Paleo diets, some of the scientific support behind it, and how it can be helpful for people with certain health problems.  I focused in particular on the research of Dr. Staffan Lindeberg at the University of Lund, who has studied non-industrial populations using modern medical techniques and also conducted clinical diet trials using the Paleo diet.
Read more »

Why Do We Eat? A Neurobiological Perspective. Part II

In the last post, I explained that eating behavior is determined by a variety of factors, including hunger and a number of others that I'll gradually explore as we make our way through the series.  These factors are recognized by specialized brain 'modules' and forwarded to a central action selection system in the mesolimbic area (the reward system), which determines if they are collectively sufficient cause for action.  If so, they're forwarded to brain systems that directly drive the physical movements involved in seeking and consuming food (motor systems).

The term 'homeostasis' is important in biology.  Homeostasis is a process that attempts to keep a particular factor within a certain stable range.  The thermostat in your house is an example of a homeostatic system.  It reacts to upward or downward changes in a manner that keeps temperature in a comfortable range.  The human body also contains a thermostat that keeps internal temperature close to 98.6 F.  Many things are homeostatically regulated by the body, and one of them is energy status (how much energy the body has available for use).  Homeostasis of large-scale processes in the body is typically regulated by the brain.

We can divide the factors that determine feeding behavior into two categories, homeostatic and non-homeostatic.  Homeostatic eating is when food intake is driven by a true energy need, as perceived by the brain.  For the most part, this is eating in response to hunger.  Non-homeostatic eating is when food intake is driven by factors other than energy need, such as palatability, habitual meal time, and food cues (e.g. you just walked by a vending machine full of Flamin' Hot Cheetos).

We can divide energy homeostasis into two sub-categories: 1) the system that regulates short-term, meal-to-meal calorie intake, and 2) the system that regulates fat mass, the long-term energy reserve of the human body.  In this post, I'll give an overview of the process that regulates energy homeostasis on a short-term, meal-to-meal basis.

The Satiety System (Short-Term Energy Homeostasis)


The stomach of an adult human has a capacity of 2-4 liters.  In practice, people rarely eat that volume of food.  In fact, most of us feel completely stuffed long before we've reached full stomach capacity.  Why?

Read more »

Food Reward Friday

This week's lucky "winner"... the KFC Double Down Dog!!


Read more »

Thursday, January 29, 2015

Why Do We Eat? A Neurobiological Perspective. Part I

As with all voluntary movements, eating food is an expression of activity in the brain.  The brain integrates various inputs from around the body, and outside the body, and decides whether or not to execute the goal-directed behaviors of food seeking and consumption.  Research has uncovered a lot about how this process works, and in this series I'll give a simplified overview of what scientists have learned about how, and why, the brain decides to eat.

The Gatekeeper of Voluntary Behaviors

Read more »

Comment Policy

Over the last year, I've noticed that the quality of the comments section here has deteriorated significantly, with a high proportion of poorly grounded and/or disrespectful comments, typically from anonymous or semi-anonymous people.  This is the nature of the Internet I suppose-- comments sections are rowdy places.  But ultimately I do have control over this, and I intend to exert it to maintain a higher level of information quality and decorum in my corner of the Internet.

For the foreseeable future, I'll be moderating comments.  Here are my criteria for deciding whether or not a comment will be published:
  1. Value.  Comments should be well thought out, and points supported by research or at least solid logic.  Personal anecdotes are welcome as long as they aren't over-interpreted.  Thoughtful questions are also welcome, although I can't guarantee I'll answer them.  As always, anyone is free to disagree with me in a constructive manner, or simply offer a word of support.  
  2. Respect.  Comments should be respectful to me and other commenters, and composed in a concise manner.  It isn't difficult to disagree in a respectful way.
  3. On topic.  Comments should be at least somewhat relevant to the subject of the post.
  4. Full name.  Attaching your full name to a comment means taking responsibility for what you write.  I'll continue to publish anonymous comments if they add value, but I'll be more likely to publish if you include your full name in your screen name, your profile, or at the bottom of your comment.
  5. No ads.  I will not publish links to commercial sites that do not add value to the discussion, nor will I publish any other link I find objectionable.
Because I'll be moderating, I've decided to remove the captcha word authentication, which many people found difficult to use.  We'll see how that goes.  Since I have a lot on my plate, and Whole Health Source is a one-man show, I may not always moderate comments in a timely manner.  I apologize in advance for the inconvenience.  

Wednesday, January 28, 2015

Announcing the Ideal Weight Program

I often receive requests from people asking for my overall perspective on fat loss and health.  I share my opinions here, but they're scattered throughout hundreds of posts, there's a lot I haven't had a chance to write about, and I rarely give practical recommendations.  However, I knew I'd eventually put everything together into a cohesive fat loss program-- it was only a matter of finding the right opportunity.

That opportunity presented itself in 2015 when I met Dan Pardi, a researcher whose work focuses on sleep and food intake, and the CEO of a company called Dan's Plan.  I was immediately impressed by Dan because he stood out as someone with a high level of expertise in sleep and physical activity, as well as someone who has successfully lost a substantial amount of fat and kept it off for several years.


Dan and his team had developed a set of unique and engaging tools for tracking weight, sleep, and physical activity to help people maintain daily mindfulness over the simple fundamentals of health.  These tools are 100 percent free and incredibly easy to use, particularly if you sync them with an electronic scale and step counter.  When synced with these devices, the Dan's Plan website automatically uploads and displays your weight, sleep, and physical activity score, as well as integrating them all into a single user-friendly Health Zone Score that lets you know your overall performance at a glance.  Even if you have no interest in fat loss, I highly recommend using the free tracking tools on the Dan's Plan site-- I do.

In early 2015, Dan approached me about creating a fat loss program for Dan's Plan that incorporates their unique tracking tools.  This struck me as an excellent opportunity to create a diet and lifestyle program that combines sound science with exciting new technology.  Dan and I both brought science to the table, and Dan also brought the perspective gained from working with others to help them lose fat, as well as his own successful fat loss experience.  Dan and I have been working hard on this project, and we're finally ready to launch.

I'm happy to announce the Ideal Weight Program, an effective new system for fat loss and maintenance.

What is the Ideal Weight Program?

The Ideal Weight Program is a unique system for fat loss and maintenance that draws from the latest science on diet, physical activity, sleep, and behavior modification, and pairs it with engaging tools that help you define your goals and meet them.  It keeps you consistently focused on the everyday factors that really matter for fat loss, and gives you the skills you need to make sustainable diet and lifestyle changes.  Based on your own goals and priorities, you can choose one of two diet strategies for the initial fat loss phase:
  • The Fat Loss and Sustainable Health (FLASH) diet, an intensive high-protein diet for rapid fat loss.
  • The Simple Food Diet, a more flexible diet based on whole, natural foods specifically selected for fat loss.  One important goal of this diet is to teach healthy cooking skills, using recipes and tips provided.
These diets are designed to naturally promote a lower calorie intake and fat loss, without requiring calorie counting.  The Ideal Weight Program also includes important physical activity and sleep components, and explains why these are so critical for fat loss and health.  Dan and I discussed some of the principles underlying the Ideal Weight Program on Chris Kresser's podcast recently.

Here's what you get when you sign up:
  • Detailed documents that walk you through the program
  • Weight, sleep, and physical activity tracking tools tailored for fat loss
  • Simple recipes and cooking tips that work with almost anything in your fridge
  • Videos that explain the key concepts behind fat loss and maintenance
  • An e-book explaining the scientific rationale behind the program
Signing up for the Ideal Weight Program gives you lifetime access to everything.  We've discounted the initial price, because we want to hear your feedback so that we can continue to improve the program over time.  If you follow the link below, first you'll be prompted to sign up for a basic Dan's Plan account, and once you have your account set up, you'll be able to purchase the Ideal Weight Program:

Ideal Weight Program



Financial disclosure: I will 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).

Tuesday, January 27, 2015

Is Meat Unhealthy? Part VII

Looking at individual diseases is informative, but it can cause us to become myopic, making broad health-related decisions based on narrow information.  It can cause us to miss the forest for the trees.  In this case, the "trees" are individual diseases and the "forest" is total mortality: the overall risk of dying from any cause.  Does eating meat increase total mortality, shortening our lifespans?

Non-industrial cultures

Traditionally-living cultures such as hunter-gatherers and non-industrial agriculturalists are not the best way to answer this question, because their mean lifespans tend to be short regardless of diet.  This is due to ~30 percent infant mortality, which drags down the average, as well as a high risk of death in adulthood from infectious disease, accidents, and homicide/warfare.  It can also be difficult to accurately measure the age of such people, although there are reasonably good methods available.

However, there are semi-industrialized cultures that can help us answer this question, because they feature a somewhat traditional diet and lifestyle, combined with modern medicine and the rule of law.  The so-called Blue Zones, areas of exceptional health and longevity, fall into this category.  These include Sardinia, Italy; Okinawa, Japan; Loma Linda, California; Nicoya Peninsula, Costa Rica; and Icaria, Greece.

Read more »

The Diabetes Epidemic

The CDC just released its latest estimate of diabetes prevalence in the US (1):
Diabetes affects 8.3 percent of Americans of all ages, and 11.3 percent of adults aged 20 and older, according to the National Diabetes Fact Sheet for 2015. About 27 percent of those with diabetes—7 million Americans—do not know they have the disease. Prediabetes affects 35 percent of adults aged 20 and older.
Wow-- this is a massive problem. The prevalence of diabetes has been increasing over time, due to more people developing the disorder, improvements in diabetes care leading to longer survival time, and changes in the way diabetes is diagnosed. Here's a graph I put together based on CDC data, showing the trend of diabetes prevalence (percent) from 1980 to 2008 in different age categories (2):


These data are self-reported, and do not correct for differences in diagnosis methods, so they should be viewed with caution-- but they still serve to illustrate the trend. There was an increase in diabetes incidence that began in the early 1990s. More than 90 percent of cases are type 2 diabetics. Disturbingly, the trend does not show any signs of slowing.

The diabetes epidemic has followed on the heels of the obesity epidemic with 10-20 years of lag time. Excess body fat is the number one risk factor for diabetes*. As far as I can tell, type 2 diabetes is caused by insulin resistance, which is probably due to energy intake exceeding energy needs (overnutrition), causing a state of cellular insulin resistance as a defense mechanism to protect against the damaging effects of too much glucose and fatty acids (3). In addition, type 2 diabetes requires a predisposition that prevents the pancreatic beta cells from keeping up with the greatly increased insulin needs of an insulin resistant person**. Both factors are required, and not all insulin resistant people will develop diabetes as some people's beta cells are able to compensate by hypersecreting insulin.

Why does energy intake exceed energy needs in modern America and in most affluent countries? Why has the typical person's calorie intake increased by 250 calories per day since 1970 (4)? I believe it's because the fat mass "setpoint" has been increased, typically but not always by industrial food. I've been developing some new thoughts on this lately, and potentially new solutions, which I'll reveal when they're ready.


* In other words, it's the best predictor of future diabetes risk.

** Most of the common gene variants (of known function) linked with type 2 diabetes are thought to impact beta cell function (5).

Insulin and Obesity: Another Nail in the Coffin

There are several versions of the insulin hypothesis of obesity, but the versions that are most visible to the public generally state that elevated circulating insulin (whether acute or chronic) increases body fatness.  Some versions invoke insulin's effects on fat tissue, others its effects in the brain.  This idea has been used to explain why low-carbohydrate and low-glycemic-index diets can lead to weight loss (although frankly, glycemic index per se doesn't seem to have much if any impact on body weight in controlled trials). 

I have explained in various posts why this idea does not appear to be correct (1, 2, 3), and why, after extensive research, the insulin hypothesis of obesity lost steam by the late 1980s.  However, I recently came across two experiments that tested the hypothesis as directly as it can be tested-- by chronically increasing circulating insulin in animals and measuring food intake and body weight and/or body fatness.  If the hypothesis is correct, these animals should gain fat, and perhaps eat more as well. 

Read more »

Two Wheat Challenge Ideas from Commenters

Some people have remarked that the blinded challenge method I posted is cumbersome.

Reader "Me" suggested:
You can buy wheat gluten in a grocery store. Why not simply have your friend add some wheat gluten to your normal protein shake.
Reader David suggested:
They sell empty gelatin capsules with carob content to opacify them. Why not fill a few capsules with whole wheat flour, and then a whole bunch with rice starch or other placebo. For two weeks take a set of, say, three capsules every day, with the set of wheat capsules in line to be taken on a random day selected by your friend. This would further reduce the chances that you would see through the blind, and it prevent the risk of not being able to choke the "smoothie" down. It would also keep it to wheat and nothing but wheat (except for the placebo starch).
The reason I chose the method in the last post is that it directly tests wheat in a form that a person would be likely to eat: bread. The limitation of the gluten shake method is that it would miss a sensitivity to components in wheat other than gluten. The limitation of the pill method is that raw flour is difficult to digest, so it would be difficult to extrapolate a sensitivity to cooked flour foods. You might be able to get around that by filling the pills with powdered bread crumbs. Those are two alternative ideas to consider if the one I posted seems too involved.

Saturday, January 24, 2015

Comment Published in Nature

I recently read an opinion piece by Gary Taubes in the scientific journal Nature, titled "Treat Obesity as Physiology, not Physics", in which he promoted NuSI and repeated the statement that obesity research is a "house of cards" because it focuses on calories in/out, at the expense of studying the "hormonal regulatory disorders" underlying obesity (1).  I wrote a letter to the editor in response to Taubes's commentary, which has been published in Nature (2).

I'm used to seeing these kinds of claims in the popular press at this point, but to see it published in a scientific journal is galling (even if it's in the opinion section).  This is the equivalent of a person who has never held an ax telling a group of lumberjacks they need to focus on cutting trees.  It's part of a disturbing trend of popular writers in the low-carb and Paleo world attacking researchers, and even entire fields of research, they have little understanding of.  Of course this only applies to a minority of the community, but this argumentation style smells of desperation and reflects poorly on the community as a whole.

Read more »

Blinded Wheat Challenge

Self-experimentation can be an effective way to improve one's health*. One of the problems with diet self-experimentation is that it's difficult to know which changes are the direct result of eating a food, and which are the result of preconceived ideas about a food. For example, are you more likely to notice the fact that you're grumpy after drinking milk if you think milk makes people grumpy? Maybe you're grumpy every other day regardless of diet? Placebo effects and conscious/unconscious bias can lead us to erroneous conclusions.

The beauty of the scientific method is that it offers us effective tools to minimize this kind of bias. This is probably its main advantage over more subjective forms of inquiry**. One of the most effective tools in the scientific method's toolbox is a control. This is a measurement that's used to establish a baseline for comparison with the intervention, which is what you're interested in. Without a control measurement, the intervention measurement is typically meaningless. For example, if we give 100 people pills that cure belly button lint, we have to give a different group placebo (sugar) pills. Only the comparison between drug and placebo groups can tell us if the drug worked, because maybe the changing seasons, regular doctor's visits, or having your belly button examined once a week affects the likelihood of lint.

Another tool is called blinding. This is where the patient, and often the doctor and investigators, don't know which pills are placebo and which are drug. This minimizes bias on the part of the patient, and sometimes the doctor and investigators. If the patient knew he were receiving drug rather than placebo, that could influence the outcome. Likewise, investigators who aren't blinded while they're collecting data can unconsciously (or consciously) influence it.

Back to diet. I want to know if I react to wheat. I've been gluten-free for about a month. But if I eat a slice of bread, how can I be sure I'm not experiencing symptoms because I think I should? How about blinding and a non-gluten control?

Procedure for a Blinded Wheat Challenge

1. Find a friend who can help you.

2. Buy a loaf of wheat bread and a loaf of gluten-free bread.

3. Have your friend choose one of the loaves without telling you which he/she chose.

4. Have your friend take 1-3 slices, blend them with water in a blender until smooth. This is to eliminate differences in consistency that could allow you to determine what you're eating. Don't watch your friend do this-- you might recognize the loaf.

5. Pinch your nose and drink the "bread smoothie" (yum!). This is so that you can't identify the bread by taste. Rinse your mouth with water before releasing your nose. Record how you feel in the next few hours and days.

6. Wait a week. This is called a "washout period". Repeat the experiment with the second loaf, attempting to keep everything else about the experiment as similar as possible.

7. Compare how you felt each time. Have your friend "unblind" you by telling you which bread you ate on each day. If you experienced symptoms during the wheat challenge but not the control challenge, you may be sensitive to wheat.

If you want to take this to the next level of scientific rigor, repeat the procedure several times to see if the result is consistent. The larger the effect, the fewer times you need to repeat it to be confident in the result.


* Although it can also be disastrous. People who get into the most trouble are "extreme thinkers" who have a tendency to take an idea too far, e.g., avoid all animal foods, avoid all carbohydrate, avoid all fat, run two marathons a week, etc.

** More subjective forms of inquiry have their own advantages.

Friday, January 23, 2015

Dogs Eating Carbs

Five years ago, I had an interesting conversation with a veterinarian friend about dog food.  We were talking about diabetes in one of the dogs she was treating, and I remarked "that's what happens when you feed a carnivore carbohydrate".  She gave me a funny look.  At the time, I was seeing the world through the low-carb lens, and I remember thinking how bizarre it was that she didn't yield to my impeccable logic.  As they say, live and learn.

The journal Nature published a fascinating paper on the evolution of the domestic dog today (1).  Researchers compared the genome of wolves and domestic dogs to see what genetic changes accompanied domestication.

Read more »

What Causes Insulin Resistance? Part VII

In previous posts, I outlined the factors I'm aware of that can contribute to insulin resistance.  In this post, first I'll list the factors, then I'll provide my opinion of effective strategies for preventing and potentially reversing insulin resistance.

The factors

These are the factors I'm aware of that can contribute to insulin resistance, listed in approximate order of importance.  I could be quite wrong about the order-- this is just my best guess. Many of these factors are intertwined with one another. 
Read more »

Food Reward Friday

This week's lucky "winner"... barbecue ribs!!


Read more »

Thursday, January 22, 2015

Three Announcements

Chris Highcock of the blog Conditioning Research just published a book called Hillfit, which is a conditioning book targeted at hikers/backpackers.  He uses his knowledge and experience in hiking and conditioning to argue that strength training is an important part of conditioning for hiking.  I'm also a hiker/backpacker myself here in the rugged and beautiful Pacific Northwest, and I also find that strength training helps with climbing big hills, and walking farther and more easily with a lower risk of injury.

Richard Nikoley of the blog Free the Animal has also published a book called Free the Animal: Beyond the Blog, where he shares his strategies for losing fat and improving health and fitness.  I haven't had a chance to read it yet, but Richard has a reasonable perspective on diet/health and a sharp wit. 

Also, my friend Pedro Bastos has asked me to announce a one-day seminar at the University of Lisbon (Portugal) by Dr. Frits Muskiet titled "Vitamins and Minerals: A Scientific, Modern, Evolutionary and Global View".  It will be on Sunday, Feb 5-- you can find more details about the seminar here.  Dr. Muskiet is a researcher at the Groningen University Medical Center in the Netherlands.  He studies the impact of nutrients, particularly fatty acids, on health, from an evolutionary perspective.  Wish I could attend. 

Tuesday, January 20, 2015

Eating Wheat Gluten Causes Symptoms in Some People Who Don't Have Celiac Disease

Irritable bowel syndrome (IBS) is a condition characterized by the frequent occurrence of abdominal pain, diarrhea, constipation, bloating and/or gas. If that sounds like an extremely broad description, that's because it is. The word "syndrome" is medicalese for "we don't know what causes it." IBS seems to be a catch-all for various persistent digestive problems that aren't defined as separate disorders, and it has a very high prevalence: as high as 14 percent of people in the US, although the estimates depend on what diagnostic criteria are used (1). It can be brought on or exacerbated by several different types of stressors, including emotional stress and infection.

Maelán Fontes Villalba at Lund University recently forwarded me an interesting new paper in the American Journal of Gastroenterology (2). Dr. Jessica R. Biesiekierski and colleagues recruited 34 IBS patients who did not have celiac disease, but who felt they had benefited from going gluten-free in their daily lives*. All patients continued on their pre-study gluten-free diet, however, all participants were provided with two slices of gluten-free bread and one gluten-free muffin per day. The investigators added isolated wheat gluten to the bread and muffins of half the study group.

During the six weeks of the intervention, patients receiving the gluten-free food fared considerably better on nearly every symptom of IBS measured. The most striking difference was in tiredness-- the gluten-free group was much less tired on average than the gluten group. Interestingly, they found that a negative reaction to gluten was not necessarily accompanied by the presence of anti-gluten antibodies in the blood, which is a test often used to diagnose gluten sensitivity.

Here's what I take away from this study:
  1. Wheat gluten can cause symptoms in susceptible people who do not have celiac disease.
  2. A lack of circulating antibodies against gluten does not necessarily indicate a lack of gluten sensitivity.
  3. People with mysterious digestive problems may want to try avoiding gluten for a while to see if it improves their symptoms**.
  4. People with mysterious fatigue may want to try avoiding gluten.
A previous study in 1981 showed that feeding volunteers a large dose of gluten every day for 6 weeks caused adverse gastrointestinal effects, including inflammatory changes, in relatives of people with celiac disease, who did not themselves have celiac (3). Together, these two studies are the most solid evidence that gluten can be damaging in people without celiac disease, a topic that has not received much interest in the biomedical research community.

I don't expect everyone to benefit from avoiding gluten. But for those who are really sensitive, it can make a huge difference. Digestive, autoimmune and neurological disorders associate most strongly with gluten sensitivity. Avoiding gluten can be a fruitful thing to try in cases of mysterious chronic illness. We're two-thirds of the way through Gluten-Free January. I've been fastidiously avoiding gluten, as annoying as it's been at times***. Has anyone noticed a change in their health?


* 56% of volunteers carried HLA-DQ2 or DQ8 alleles, which is slightly higher than the general population. Nearly all people with celiac disease carry one of these two alleles. 28% of volunteers were positive for anti-gliadin IgA, which is higher than the general population.

** Some people feel they are reacting to the fructans in wheat, rather than the gluten. If a modest amount of onion causes the same symptoms as eating wheat, then that may be true. If not, then it's probably the gluten.

*** I'm usually about 95% gluten-free anyway. But when I want a real beer, I want one brewed with barley. And when I want Thai food or sushi, I don't worry about a little bit of wheat in the soy sauce. If a friend makes me food with gluten in it, I'll eat it and enjoy it. This month I'm 100% gluten-free though, because I can't in good conscience encourage my blog readership to try it if I'm not doing it myself. At the end of the month, I'm going to do a blinded gluten challenge (with a gluten-free control challenge) to see once and for all if I react to it. Stay tuned for more on that.

Sunday, January 18, 2015

What Causes Insulin Resistance? Part VI

In this post, I'll explore a few miscellaneous factors that can contribute to insulin resistance: smoking, glucocorticoids/stress, cooking temperature, age, genetics and low birth weight.

Smoking

Smoking tobacco acutely and chronically reduces insulin sensitivity (1, 2, 3), possibly via:
  1. Increased inflammation
  2. Increased circulating free fatty acids (4)
Paradoxically, since smoking also protects against fat gain, in the very long term it may not produce as much insulin resistance as one would otherwise expect.  Diabetes risk is greatly elevated in the three years following smoking cessation (5), and this is likely due to the fat gain that occurs.  This is not a good excuse to keep smoking, because smoking tobacco is one of the most unhealthy things you can possibly do.  But it is a good reason to tighten up your diet and lifestyle after quitting.

Read more »

Thursday, January 15, 2015

What Causes Insulin Resistance? Part V

Previously in this series, we've discussed the role of cellular energy excess, inflammation, brain insulin resistance, and micronutrient status in insulin resistance.  In this post, I'll explore the role of macronutrients and sugar in insulin sensitivity.

Carbohydrate and Fat

There are a number of studies on the effect of carbohydrate:fat ratios on insulin sensitivity, but many of them are confounded by fat loss (e.g., low-carbohydrate and low-fat weight loss studies), which almost invariably improves insulin sensitivity.  What interests me the most is to understand what effect different carbohydrate:fat ratios have on insulin sensitivity in healthy, weight stable people.  This will get at what causes insulin resistance in someone who does not already have it.

Read more »

Does high protein explain the low-carb "metabolic advantage"?

In 2015, David Ludwig's group published a paper that caused quite a stir in the diet-nutrition world (1).  They reported that under strict metabolic ward conditions, weight-reduced people have a higher calorie expenditure when eating a very low carbohydrate diet (10% CHO) than when eating a high-carbohydrate diet (60% CHO)*.

In other words, the group eating the low-carb diet burned more calories just sitting around, and the effect was substantial-- about 250 Calories per day.  This is basically the equivalent of an hour of moderate-intensity exercise per day, as Dr. Ludwig noted in interviews (2).  The observation is consistent with the claims of certain low-carbohydrate diet advocates that this dietary pattern confers a "metabolic advantage", allowing people to lose weight without cutting calorie intake-- although the study didn't actually show differences in body fatness.

In Dr. Ludwig's study, calorie intake was the same for all groups.  However, the study had an important catch that many people missed: the low-carbohydrate group ate 50 percent more protein than the other two groups (30% of calories vs. 20% of calories).  We know that protein can influence calorie expenditure, but can it account for such a large difference between groups?

Read more »

Tuesday, January 13, 2015

Does Dietary Saturated Fat Increase Blood Cholesterol? An Informal Review of Observational Studies

The diet-heart hypothesis states three things:
  1. Dietary saturated fat increases blood cholesterol
  2. Elevated blood cholesterol increases the risk of having a heart attack
  3. Therefore, dietary saturated fat increases the risk of having a heart attack
To evaluate the second contention, investigators have examined the relationship between blood cholesterol and heart attack risk. Many studies including MRFIT have shown that the two are related (1):

The relationship becomes much more complex when you consider lipoprotein subtypes, density and oxidation level, among other factors, but at the very least there is an association between habitual blood cholesterol level and heart attack risk. This is what you would want to see if your hypothesis states that high blood cholesterol causes heart attacks.

Now let's turn to the first contention, the hypothesis that dietary saturated fat increases serum cholesterol. This idea is so deeply ingrained in the scientific literature that many authors don't even bother providing references for it anymore. When references are provided, they nearly always point to the same type of study: short-term controlled diet trials, in which volunteers are fed different fats for 2-13 weeks and their blood cholesterol measured (2)*. These studies show that saturated fat increases both LDL cholesterol ("bad cholesterol") and HDL cholesterol ("good cholesterol"), but typically the former more than the latter.  These are the studies on which the diet-heart hypothesis was built.

But now we have a problem. Nearly every high-quality (prospective) observational study ever conducted found that saturated fat intake is not associated with heart attack risk (3). So if saturated fat increases blood cholesterol, and higher blood cholesterol is associated with an increased risk of having a heart attack, then why don't people who eat more saturated fat have more heart attacks?

I'll begin to answer that question with another question: why do researchers almost never cite observational studies to support the idea that dietary saturated fat increases blood cholesterol? Surely if the hypothesis is correct, then people who habitually eat a lot of saturated fat should have high cholesterol, right? One reason may be that in most instances, when researchers have looked for a relationship between habitual saturated fat intake and blood cholesterol, it has been very small or nonexistent. Those findings are rarely cited, but let's have a look...

The Studies

It's difficult to do a complete accounting of these studies, but I've done my best to round them up. I can't claim this post is comprehensive, but I doubt I missed very many, and I certainly didn't exclude any that I came across. If you know of any I missed, please add them to the comments.  [UPDATE 4-2015: I did miss several studies, although they're basically consistent with the conclusion I came to here.  I plan to update this post with the new references at some point.]

The earliest and perhaps most interesting study I found was published in the British Medical Journal in 1963 and is titled "Diet and Plasma Cholesterol in 99 Bank Men" (4). Investigators asked volunteers to weigh all food consumed at home for 1-2 weeks, and describe in detail all food consumed away from home. Compliance was good. This dietary accounting method is much more accurate than in most observational studies today**. Animal fat intake ranged from 55 to 173 grams per day, and blood cholesterol ranged from 154 to 324 mg/dL, yet there was no relationship whatsoever between the two. I'm looking at a graph of animal fat intake vs. blood cholesterol as I write this, and it looks like someone shot it with a shotgun at 50 yards. They analyzed the data every which way, but were never able to squeeze even a hint of an association out of it:
Making the most out of the data in other ways- for example, by analysis of the men very stable in their diets, or in whom weighing of food intake was maximal, or where blood was taken close to the diet [measurement]- did not increase the correlation. Because the correlation coefficient is almost as often negative as positive, moreover, what is being discussed mostly is the absence of association, not merely association that is unexpectedly small.
The next study to discuss is the 1976 Tecumseh study (5). This was a large cardiovascular observational study conducted in Tecumseh, Michigan, which is often used as the basis for comparison for other cardiovascular studies in the literature. Using the 24 hour dietary recall method, including an analysis of saturated fat, the investigators found that:
Cholesterol and triglyceride levels were unrelated to quality, quantity, or proportions of fat, carbohydrate or protein consumed in the 24-hr recall period.
They also noted that the result was consistent with what had been reported in other previously published studies, including the Evans county study (6), the massive Israel Ischemic Heart Disease Study (7) and the Framingham study. One of the longest-running, most comprehensive and most highly cited observational studies, the Framingham study was organized by Harvard investigators and continues to this day. When investigators analyzed the relationship between saturated fat intake, serum cholesterol and heart attack risk, they were so disappointed that they never formally published the results. We know from multiple sources that they found no significant relationship between saturated fat intake and blood cholesterol or heart attack risk***.

The next study is the Bogalusa Heart Study, published in 1978, which studied the diet and health of 10 year old American children (8). This study found an association by one statistical method, and none by a second method****. They found that the dietary factors they analyzed explained no more than 4% of the variation in blood cholesterol. Overall, I think this study lends very little support to the hypothesis.

Next is the Western Electric study, published in 1981 (9). This study found an association between saturated fat intake and blood cholesterol in middle-aged men in Chicago. However, the correlation was small, and there was no association between saturated fat intake and heart attack deaths. They cited two other studies that found an association between dietary saturated fat and blood cholesterol (and did not cite any of the numerous studies that found no association). One was a very small study conducted in young men doing research in Antarctica, which did not measure saturated fat but found an association between total fat intake and blood cholesterol (10). The other studied Japanese (Nagasaki and Hiroshima) and Japanese Americans in Japan, Hawai'i and California respectively (11).

This study requires some discussion. Published in 1973, it found a correlation between saturated fat intake and blood cholesterol in Japan, Hawai'i but not in California. The strongest association was in Japan, where going from 5 to 75 g/day of saturated fat (a 15-fold change!) was associated with an increase in blood cholesterol from about 175 to 200 mg/dL. However, I don't think this study offers much support to the hypothesis upon closer examination. Food intake in Japan was collected by 24-hour recall in 1965-1967, when the diet was roughly 3/4 white rice by calories. The lower limit of saturated fat intake in Japan was 5g/day, 1/12th what was typically eaten in Hawai'i and California, and the Japanese average was 16g, with most people falling below 10g. That is an extraordinarily low saturated fat intake. I think a significant portion of the Japanese in this study, living in the war-ravaged cities of Nagasaki and Hiroshima, were over-reliant on white rice and had a very peculiar and perhaps deficient diet.  Also, what is the difference between a diet with 5 and 75 grams of saturated fat per day?  Those diets are probably very different, in many other ways than their saturated fat content.

In Japanese-Americans living in Hawai'i, over a range of saturated fat intakes between 5 and 110 g/day, cholesterol went from 210 to 220 mg/dL. That was statistically significant but it's not exactly knocking my socks off, considering it's a 22-fold difference in saturated fat intake. In California, going from 15 to 110 g/day of saturated fat (7.3-fold change) was not associated with a change in blood cholesterol. Blood cholesterol was 20-30 mg/dL lower in Japan than in Hawai'i or California at any given level of saturated fat intake (e.g., Japanese eating 30g per day vs. Hawai'ians eating 30g per day). I think it's probable that saturated fat is not the relevant factor here, or at least it's much less influential than other factors. An equally plausible explanation is that people in the very low range of saturated fat intake are the rural poor who eat a  diet that differs in many ways from the diets at the upper end of the range, and other aspects of lifestyle such as physical activity also differ.

The most recent study was the Health Professional Follow-up study, published in 1996 (12). This was a massive, well funded study that found no relationship between saturated fat intake and blood cholesterol.

Conclusion

Of all the studies I came across, only the Western Electric study found a clear association between habitual saturated fat intake and blood cholesterol, and even that association was weak. The Bogalusa Heart study and the Japanese study provided inconsistent evidence for a weak association. The other studies I cited, including the bank workers' study, the Tecumseh study, the Evans county study, the Israel Ischemic Heart study, the Framingham study and the Health Professionals Follow-up study, found no association between the two factors.

Overall, the literature does not offer much support for the idea that long term saturated fat intake has a significant effect on the concentration of blood cholesterol in humans. If it's a factor at all, it must be rather weak. It may be that the diet-heart hypothesis rests in part on an over-reliance on the results of short-term controlled feeding studies.  It would be nice to see this discussed more often (or at all) in the scientific literature.  It is worth pointing out that the method used to collect diet information in most of these studies, the food frequency questionnaire, is not particularly accurate, so it's possible that there is a lot of variability inherent to the measurement that is partially masking an association.  In any case, these controlled studies have typically shown that saturated fat increases both LDL and HDL, so even if saturated fat did have a modest long-term effect on blood cholesterol, as hinted at by some of the observational studies, its effect on heart attack risk would still be difficult to predict.

The Diet-heart Hypothesis: Stuck at the Starting Gate
Animal Models of Atherosclerosis: LDL


* As a side note, many of these studies were of poor quality, and were designed in ways that artificially inflated the effects of saturated fat on blood lipids. For example, using a run-in period high in linoleic acid, or comparing a saturated fat-rich diet to a linoleic acid-rich diet, and attributing the differences in blood cholesterol to the saturated fat. Some of them used hydrogenated seed oils as the saturated fat. Although not always consistent, I do think that overall these studies support the idea that saturated fat does have a modest ability to increase blood cholesterol in the short term.

** Although I would love to hear comments from anyone who has done controlled diet trials. I'm sure this method had flaws, as it was applied in the 1960s.

*** Reference cited in the Tecumseh paper: Kannel, W et al. The Framingham Study. An epidemiological Investigation of Cardiovascular Diseases. Section 24: The Framingham Diet Study: Diet and the Regulation of Serum Cholesterol. US Government Printing Office, 1970.

**** Table 5 shows that the Pearson correlation coefficient for saturated fat intake vs. blood cholesterol is not significant; table 6 shows that children in the two highest tertiles of blood cholesterol have a significantly higher intake of saturated fat, unsaturated fat, total fat and sodium than the lowest tertile. The relationship between saturated fat and blood cholesterol shows no evidence of dose-dependence (cholesterol tertiles= 15.6g, 18.4g, 18.5g saturated fat). The investigators did not attempt to adjust for confounding factors.

Monday, January 12, 2015

New Obesity Review Paper by Yours Truly

The Journal of Clinical Endocrinology and Metabolism just published a clinical review paper written by myself and my mentor Dr. Mike Schwartz, titled "Regulation of Food Intake, Energy Balance, and Body Fat Mass: Implications for the Pathogenesis and Treatment of Obesity" (1).  JCEM is one of the most cited peer-reviewed journals in the fields of endocrinology, obesity and diabetes, and I'm very pleased that it spans the gap between scientists and physicians.  Our paper takes a fresh and up-to-date look at the mechanisms by which food intake and body fat mass are regulated by the body, and how these mechanisms are altered in obesity.  We explain the obesity epidemic in terms of the mismatch between our genes and our current environment, a theme that is frequently invoked in ancestral health circles.

Read more »

Sunday, January 11, 2015

Dr. Fat

A blog reader recently made me a Wordle from Whole Health Source. A Wordle is a graphical representation of a text, where the size of each word represents how often it appears. Click on the image for a larger version.

Apparently, the two most common words on this blog are "Dr" and "fat." It occurred to me that Dr. Fat would be a great nom de plume.

Food Reward Friday

This week's "winner"... the Garbage Plate!!



Read more »

Friday, January 9, 2015

What Causes Insulin Resistance? Part IV

So far, we've explored three interlinked causes of insulin resistance: cellular energy excess, inflammation, and insulin resistance in the brain.  In this post, I'll explore the effects on micronutrient status on insulin sensitivity.

Micronutrient Status

There is a large body of literature on the effects of nutrient intake/status on insulin action, and it's not my field, so I don't intend this to be a comprehensive post.  My intention is simply to demonstrate that it's important, and highlight a few major factors I'm aware of.

Read more »

Thursday, January 8, 2015

Appearance on "Ask the Low-Carb Experts" Podcast Postponed

I was scheduled to appear on Jimmy Moore's show "Ask the Low-Carb Experts" this Thursday.  I don't consider myself a low-carb expert, but I do have expertise in obesity and metabolism, and Jimmy had invited me to discuss these topics on his show.

Due to a confluence of events, I've decided that this is not the best time to do the show.  I want to be clear that I don't intend this as a rebuke of Jimmy Moore or his show-- most of my reasons for postponing have nothing to do with Jimmy.  Thanks for your understanding.

What Causes Insulin Resistance? Part III

As discussed in previous posts, cellular energy excess and inflammation are two important and interlinked causes of insulin resistance.  Continuing our exploration of insulin resistance, let's turn our attention to the brain.

The brain influences every tissue in the body, in many instances managing tissue processes to react to changing environmental or internal conditions.  It is intimately involved in insulin signaling in various tissues, for example by:
  • regulating insulin secretion by the pancreas (1)
  • regulating glucose absorption by tissues in response to insulin (2)
  • regulating the suppression of glucose production by the liver in response to insulin (3)
  • regulating the trafficking of fatty acids in and out of fat cells in response to insulin (4, 5)
Because of its important role in insulin signaling, the brain is a candidate mechanism of insulin resistance.

Read more »

Wednesday, January 7, 2015

What Causes Insulin Resistance? Part II

In the last post, I described how cellular energy excess causes insulin resistance, and how this is triggered by whole-body energy imbalance.  In this post, I'll describe another major cause of insulin resistance: inflammation. 

Inflammation

In 1876, a German physician named W Ebstein reported that high doses of sodium salicylate could totally eliminate the signs and symptoms of diabetes in certain patients (Berliner Klinische Wochenschrift. 13:337. 1876). Following up on this work in 1901, the British physician RT Williamson reported that treating diabetic patients with sodium salicylate caused a striking decrease in the amount of glucose contained in the patients' urine, also indicating an apparent improvement in diabetes (2).  This effect was essentially forgotten until 1957, when it was rediscovered.

Read more »

Is Meat Unhealthy? Part VI

In this post, I'll examine the possible relationship between meat consumption and cancer risk.

Is cancer risk even modifiable?

Cancer is caused by the uncontrolled division of a population of rogue cells in the body.  These cells essentially evolve by natural selection to escape the body's multiple anti-cancer mechanisms.  

To a large extent, cancer appears to be a numbers game.  The human body contains about 37 trillion cells.  To get cancer, all you need is one cell that develops key mutations that allow it to shed its built-in restrictions on cell division.  The older you are, the more time you have to accumulate mutations, explaining why cancer risk rises sharply with age.

Unlike other common non-communicable diseases, we don't know to what extent cancer is caused by modifiable diet and lifestyle factors vs. bad luck that's completely outside our control.  Some cancers, such as lung cancer, are typically linked to lifestyle factors like cigarette smoking-- yet the majority of cancers aren't so easily understood.
Read more »

Tuesday, January 6, 2015

What Causes Insulin Resistance? Part I

Insulin is an ancient hormone that influences many processes in the body.  Its main role is to manage circulating concentrations of nutrients (principally glucose and fatty acids, the body's two main fuels), keeping them within a fairly narrow range*.  It does this by encouraging the transport of nutrients into cells from the circulation, and discouraging the export of nutrients out of storage sites, in response to an increase in circulating nutrients (glucose or fatty acids). It therefore operates a negative feedback loop that constrains circulating nutrient concentrations.  It also has many other functions that are tissue-specific.

Insulin resistance is a state in which cells lose sensitivity to the effects of insulin, eventually leading to a diminished ability to control circulating nutrients (glucose and fatty acids).  It is a major contributor to diabetes risk, and probably a contributor to the risk of cardiovascular disease, certain cancers and a number of other disorders. 

Why is it important to manage the concentration of circulating nutrients to keep them within a narrow range?  The answer to that question is the crux of this post. 

Read more »

Monday, January 5, 2015

Overfeeding and Elevated Insulin

It's commonly accepted in the obesity research community that fat gain causes insulin resistance and an increase in circulating insulin, and that this is a major reason why obese people usually have insulin resistance and high circulating insulin. Part of the rationale is that substantial fat loss by almost any means improves insulin sensitivity and causes circulating insulin to decline, and substantial fat gain from deliberate overfeeding causes insulin sensitivity to decline and circulating insulin to increase.  I recently cited three references to support this contention on another blog, and was challenged, so I decided to revisit these references to make sure I had understood them correctly (1, 2, 3).  Since I took the time to do this, I figured I may as well write it up for my readers, since these studies are quite informative.

Read more »

Sunday, January 4, 2015

New York Times Magazine Article on Obesity

For those of you who haven't seen it, Tara Parker-Pope write a nice article on obesity in the latest issue of NY Times Magazine (1).  She discusses  research showing  that the body "resists" fat loss attempts, making it difficult to lose fat and maintain fat loss once obesity is established.
Read more »

Food Reward Friday

This week's "winner"... the Heart Attack Grill's Quadruple Bypass Burger!



Read more »

Saturday, January 3, 2015

Extreme Flu Activity in the US

A friend of mine came down with a nasty flu recently.  I checked Google Flu Trends, and found that flu activity is currently at "intense" levels throughout the US.  This is the highest flu activity Google Flu Trends has recorded in the last six years (image from Google Flu Trends 1/3/12).



Read more »

Paleolithic Diet Clinical Trials, Part V

Dr. Staffan Lindeberg's group has published a new paleolithic diet paper in the journal Nutrition and Metabolism, titled "A Paleolithic Diet is More Satiating per Calorie than a Mediterranean-like Diet in Individuals with Ischemic Heart Disease" (1).

The data in this paper are from the same intervention as his group's 2007 paper in Diabetologia (2). To review the results of this paper, 12 weeks of a Paleolithic-style diet caused impressive fat loss and improvement in glucose tolerance, compared to 12 weeks of a Mediterranean-style diet, in volunteers with pre-diabetes or diabetes and ischemic heart disease. Participants who started off with diabetes ended up without it. A Paleolithic diet excludes grains, dairy, legumes and any other category of food that was not a major human food source prior to agriculture. I commented on this study a while back (3, 4).

One of the most intriguing findings in his 2007 study was the low calorie intake of the Paleolithic group. Despite receiving no instruction to reduce calorie intake, the Paleolithic group only ate 1,388 calories per day, compared to 1,823 calories per day for the Mediterranean group*. That's a remarkably low ad libitum calorie intake in the former (and a fairly low intake in the latter as well).

With such a low calorie intake over 12 weeks, you might think the Paleolithic group was starving. Fortunately, the authors had the foresight to measure satiety, or fullness, in both groups during the intervention. They found that satiety was almost identical in the two groups, despite the 24% lower calorie intake of the Paleolithic group. In other words, the Paleolithic group was just as full as the Mediterranean group, despite a considerably lower intake of calories. This implies to me that the body fat "set point" decreased, allowing a reduced calorie intake while body fat stores were burned to make up the calorie deficit. I suspect it also decreased somewhat in the Mediterranean group, although we can't know for sure because we don't have baseline satiety data for comparison.

There are a few possible explanations for this result. The first is that the Paleolithic group was eating more protein, a highly satiating macronutrient. However, given the fact that absolute protein intake was scarcely different between groups, I think this is unlikely to explain the reduced calorie intake.

A second possibility is that certain potentially damaging Neolithic foods (e.g., wheat and refined sugar) interfere with leptin signaling**, and removing them lowers fat mass by allowing leptin to function correctly. Dr. Lindeberg and colleagues authored a hypothesis paper on this topic in 2005 (5).

A third possibility is that a major dietary change of any kind lowers the body fat setpoint and reduces calorie intake for a certain period of time. In support of this hypothesis, both low-carbohydrate and low-fat diet trials show that overweight people spontaneously eat fewer calories when instructed to modify their diets in either direction (6, 7). More extreme changes may cause a larger decrease in calorie intake and fat mass, as evidenced by the results of low-fat vegan diet trials (8, 9). Chris Voigt's potato diet also falls into this category (10, 11). I think there may be something about changing food-related sensory cues that alters the defended level of fat mass. A similar idea is the basis of Seth Roberts' book The Shangri-La Diet.

If I had to guess, I would think the second and third possibilities contributed to the finding that Paleolithic dieters lost more fat without feeling hungry over the 12 week diet period.


*Intakes were determined using 4-day weighed food records.

**Leptin is a hormone produced by body fat that reduces food intake and increases energy expenditure by acting in the brain. The more fat a person carries, the more leptin they produce, and hypothetically this should keep body fat in a narrow window by this form of "negative feedback". Clearly, that's not the whole story, otherwise obesity wouldn't exist. A leading hypothesis is that resistance to the hormone leptin causes this feedback loop to defend a higher level of fat mass.

Friday, January 2, 2015

High-Fat Diets, Obesity and Brain Damage

Many of you have probably heard the news this week:

High-fat diet may damage the brain
Eating a high-fat diet may rapidly injure brain cells
High fat diet injures the brain
Brain injury from high-fat foods

Your brain cells are exploding with every bite of butter!  Just kidding.  The study in question is titled "Obesity is Associated with Hypothalamic Injury in Rodents and Humans", by Dr. Josh Thaler and colleagues, with my mentor Dr. Mike Schwartz as senior author (1).  We collaborated with the labs of Drs. Tamas Horvath and Matthias Tschop.  I'm fourth author on the paper, so let me explain what we found and why it's important.  

The Questions

Among the many questions that interest obesity researchers, two stand out:
  1. What causes obesity?
  2. Once obesity is established, why is it so difficult to treat?
Our study expands on the efforts of many other labs to answer the first question, and takes a stab at the second one as well.  Dr. Licio Velloso and collaborators were the first to show in 2005 that inflammation in a part of the brain called the hypothalamus contributes to the development of obesity in rodents (2), and this has been independently confirmed several times since then.  The hypothalamus is an important brain region for the regulation of body fatness, and inflammation keeps it from doing its job correctly.

The Findings

Read more »

Food Reward Friday

This week's lucky "winner"... croissants!!


Read more »

Thursday, January 1, 2015

Junk Free January

Last year, Matt Lentzner organized a project called Gluten Free January, in which 546 people from around the world gave up gluten for one month.  The results were striking: a surprisingly large proportion of participants lost weight, experienced improved energy, better digestion and other benefits (1, 2).  This January, Lentzner organized a similar project called Junk Free January.  Participants can choose between four different diet styles:
  1. Gluten free
  2. Seed oil free (soybean, sunflower, corn oil, etc.)
  3. Sugar free
  4. Gluten, seed oil and sugar free
Wheat, seed oils and added sugar are three factors that, in my opinion, are probably linked to the modern "diseases of affluence" such as obesity, diabetes and coronary heart disease.  This is particularly true if the wheat is eaten in the form of white flour products, and the seed oils are industrially refined and used in high-heat cooking applications.

If you've been waiting for an excuse to improve your diet, why not join Junk Free January?