Without further ado, here it is:
Whole Health Source, why did you choose that name for your blog and why did you decide to start a blog?
I began writing about seven years ago because I felt I had useful information to share. Whole Health Source was actually the name of my original website. It was intended to be a nutrition and health site, but due to my poor web development skills, it was very amateur looking! I took it down shortly after starting my blog because I felt the information was outdated. I chose the name Whole Health Source because it implies that health is more than just not having a disease, and that many factors converge to determine health.
What is the "state of the art" in nutrition science, what theories are right now more advanced?
I’m fairly specialized in my research so I’m perhaps not the best person to say what’s state of the art in the field as a whole, but I’ll give my perspective on a few things that I find compelling.
One of the things that I’ve found really gratifying is seeing the field move in the direction of studying foods rather than specific nutrients. Essential nutrients such as minerals and vitamins are obviously important, but now that we really understand the great biological complexity of whole foods, it’s becoming less and less plausible that we can accurately predict the biological impact of a food by understanding only a few of its chemical components. A number of prominent researchers understand this and are moving their research in that direction.
Another line of investigation that’s important is understanding how genes and environment interact to produce health or disease—this field will continue expanding and providing important insights. There is no one-size-fits-all solution for health.
Gut bacteria and digestive health have also generated a lot of interest lately.
There is a lot of cutting-edge research going into understanding the brain mechanisms that mediate food intake. We’re getting to the point where we can predict obesity risk to some degree just by measuring cognitive traits (e.g., ability to delay gratification, impulsiveness, susceptibility to reward), or brain responses to food stimuli. Also, understanding how the energy homeostasis system in the brain is altered during the development of obesity—this is my field.
What is the real role of physical activity? Some argue that the more you exercise the more hunger, is that correct?
I think a person would have to be pretty stubborn at this point to think that physical activity doesn’t help at all with body weight control and general health, given the state of the evidence. For obesity, it seems to work best as a preventive measure rather than as a treatment, and this has been strongly supported both by animal studies and observational studies in humans. It’s hard to return to true leanness once a person is obese, no matter what strategy they use. As we say, “an ounce of prevention is worth a pound of cure”. It is correct in a general sense that exercise increases hunger. However, on average it doesn’t increase hunger enough to make up for the calories you expended, and therefore you lose fat if you’re overweight.
There is a lot of individual variability here. Research has shown that some overweight people compensate for exercise by eating more, and others don’t, and in some cases they even eat less than if they hadn’t exercised. On average, exercise alone isn’t a very effective way to lose fat if you have a lot to lose, but it can increase the effectiveness of dietary interventions. However, some people respond exceptionally well to exercise and can lose 20, 30, 50 pounds. Regardless of whether or not it can turn people from fat to ripped, regular exercise is an absolutely essential component of a healthy lifestyle.
You have debated with Gary Taubes about the role of insulin and carbs in weight control, what is right or wrong with his view?
I think Taubes has been useful in the sense that he introduced many people to the low-carbohydrate diet, and the research challenging some of our conventional ideas about the health impacts of such diets. A number of studies on low-carbohydrate diets have shown that although they’re higher in fat and meat than most diets, when adopted by overweight or obese people they’re able to safely cause fat loss and health improvements over periods lasting up to two years. No one really knows what happens after that. They seem to cause more fat loss, and perhaps better metabolic improvements, than the conventional low-fat diet for periods up to one year. Although the ability of low-carbohydrate diets (and most diets in general) to cause fat loss is fairly modest in most clinical trials, some individuals respond extremely well to it and can lose large amounts of fat. For these people, the diet can be life-changing.
However, Taubes took this piece of useful information and stretched it much too far. He ditched most of the last 70 years of published research and constructed a mechanism whereby many of our modern health ills, particularly obesity and diabetes, are due to the ability of carbohydrates (particularly refined carbohydrate and sugar) to increase circulating insulin. It’s an extremely simple model if you think about it: carbs -> insulin acting directly on fat cells -> obesity. Much too simple in fact, given the many roles of insulin in various tissues including the brain, not to mention all the other processes that occur with food ingestion. Taubes has scathingly criticized seasoned researchers for not considering his hypothesis, which he felt was correct but ignored by researchers for non-scientific reasons (do I need to point out here that Taubes has virtually no training or experience in the biological sciences?). The reality is that researchers have not overlooked the hypothesis, they have tested it in many different ways and found that it does not explain obesity. As a scientist, I can’t say with 100 percent confidence that elevated insulin plays no role in obesity whatsoever, but what I can say with 99.99 percent confidence is that no single factor will ever be able to explain common obesity. I can also say with confidence that there are much more compelling explanations than excess insulin acting on fat cells, and these are currently being pursued by many brilliant researchers.
Is fructose a problem as Dr. Robert Lustig suggests?
Humans have a very long evolutionary history with fruit. Our ancestors were among the first organisms to eat fruit 55 million years ago, shortly after it evolved. Mammals likely evolved into primates specifically to access fruit, and our ancestors remained in trees eating fruit until relatively recently. Our closest living relatives the chimpanzees get most of their calories from fruit, and they therefore have a high-sugar diet. All human cultures that have access to fruit enjoy it and eat it regularly.
Studies suggest that fruit is healthy and can even aid fat loss a little bit under certain circumstances. However, most of the sugar people eat doesn’t come from fruit—it comes from processed corn or refined sugar cane juice. This poses a problem for several reasons. The first is that sugar and high-fructose corn syrup are virtually devoid of micronutrients and other beneficial substances, therefore they crowd out more nutritious food. The second is that sugar increases the energy density and palatability of foods, leading to increased meal size and eating/drinking between meals in the absence of hunger/thirst. This contributes to obesity and all the things that come along with it.
The third problem is that yes, in excess refined sugar can cause metabolic problems, and this is mostly due to its fructose content. To my knowledge, this has only ever been demonstrated with large amounts of refined sugar or fructose, and never with fruit. Lean people are more resistant to the insulin resistance and other metabolic problems that occur with fructose feeding, and this probably relates to the energy overload already present on the liver in obesity. It’s not clear whether or not the amount of fructose most people eat today is enough to cause these problems, however I suspect that for people eating more sugar than average, it is. Despite its ability to cause metabolic problems in excess, many studies have shown that fructose is no more fattening than other equally caloric sweet substances (such as glucose).
Is insulin the main problem? What about ghrelin, leptin and other hormones?
Insulin resistance (an inability of insulin to do its job properly) is definitely a central problem for health in the 21st century. It contributes to many different health conditions, particularly type II diabetes. The main cause of insulin resistance is excess body fat, plain and simple, although there are many other factors such as exercise and diet quality that also have an impact. To understand insulin resistance, we have to understand what causes excess body fat. Food intake is regulated by a “symphony” of signals that the brain receives and uses to determine whether or not a person will eat. Some of these signals are from sensory organs and the brain itself, while others are hormones in the circulation coming from the gut, body fat, the pancreas, and elsewhere. This finely tuned system is disrupted when a susceptible person is exposed to abundant, energy-dense, tasty food, in an environment that minimizes physical activity and sleep, and promotes psychological stress. Leptin is a key hormone that restrains food intake in this context, but it can only go so far. Eventually, leptin resistance develops, which makes it difficult to lose fat once obesity is established.
Is wheat that bad? If so, why?
Wheat is definitely bad for about one percent of Europeans and Americans who have celiac disease. This alone is a major public health burden attributable mostly to wheat. Beyond that one percent, I suspect that there are many other people who benefit from avoiding it for various reasons, but that is a supposition that will require more research to confirm. There are probably many people who can eat wheat with impunity.
I think one of the most problematic aspects of wheat is that it’s used to make things that are energy-dense and taste really good. Flour is a substance that can be homogenously mixed with fats, sugars, and flavorings, creating combinations that are virtually irresistible to the palate. Think brownies, cookies, cake, and even a hot loaf of crusty bread. Most people can find room for 200 calories of chocolate cake even when they’re stuffed at the end of a meal. Can you get that excited about a plain potato?
A fellow named Matt Lentzner organized something called “Gluten-Free January” last year where people gave up gluten for one month. An epidemiologist named Dr. Janine Jagger and I composed surveys to collect anonymous information from participants at the end of the month. We found that almost everyone who was overweight lost several pounds, and almost everyone with digestive problems and low energy noticed an improvement (1, 2). There was no control group so we don’t know how much of the improvement was due to avoiding gluten per se, how much was due to avoiding junk food and/or reducing carbohydrate, and how much was a placebo effect. However, it does suggest that many people benefit from giving up gluten, whatever the mechanism may be.
What about fats? Why they have been so criticized? What are the real dangerous fats?
Fats are energy dense, and saturated fats can increase circulating cholesterol in controlled trials, therefore it was thought that fats contribute to obesity and coronary heart disease. I think it’s still true that fat can contribute to obesity if it increases the energy density and palatability of food. However, paradoxically dietary fat is compatible with body fat loss in the context of a low-carbohydrate diet, so it’s not a simple relationship. The key in that context is that something is being restricted. High fat in combination with high carbohydrate will not cause fat loss.
Saturated fat has received a lot of blame over the years, but it’s becoming increasingly likely that it plays little or no role in heart disease in humans, in the context of a normal diverse diet. That doesn’t mean a person should put a huge amount of butter on everything or drink coconut oil, but in moderation as part of a mixed whole food diet, I don’t see any reason to be concerned about eating the natural fats contained in meat, dairy, eggs, and nuts, and to a lesser extent using fats like butter, unrefined coconut oil, red palm oil, and extra virgin olive oil in cooking.
I’m not a proponent of refined seed oils (“vegetable oils”). They’re refined and therefore contain virtually no nutritional value, and many of them (e.g. cottonseed and soy) are by-products of other industries. Furthermore, they tend to be high in polyunsaturated fat and are therefore susceptible to oxidation (rancidity) during cooking, and most of them contain a lot of omega-6 and very little omega-3, which can potentially disrupt many processes in the body (there are exceptions, such as canola oil). If you must use a refined seed oil for cooking, the best is probably high-oleic sunflower oil, a variety bred for low polyunsaturated and high monounsaturated fat content.
Do we have to be worried about cholesterol? Can we control it through diet or drugs?
Cholesterol in the blood is contained in particles called lipoproteins. Lipoproteins such as LDL (“bad” cholesterol) and HDL (“good” cholesterol) are causally related to the development of atherosclerosis (thickening and degeneration of the arteries), which increases heart attack risk. So yes, I think we should be worried about cholesterol. The ratio of total cholesterol to HDL cholesterol is a simple and effective indicator of risk. For people who are interested, the Framingham risk calculator can give an estimate of 10-year heart attack risk based on data collected from the Framingham study (3).
Diet and drugs do have an impact on lipoproteins. Excess body fat increases LDL and decreases HDL, and fat loss can reverse this to some extent. Polyunsaturated fat lowers LDL and HDL. Saturated fat increases LDL and HDL in trials lasting up to three months, although it’s not clear to what degree this effect persists in the long term (in any case, it appears to have little or no impact on heart attack risk). Dietary cholesterol has a modest ability to increase LDL and HDL. Moderate alcohol consumption and exercise increase HDL and reduce heart attack risk. Smoking cigarettes lowers HDL and greatly increases heart attack risk, while smokeless tobacco does not.
Drugs such as statins lower LDL and reduce heart attack risk. These drugs do have side effects for some people, but they’re probably worth it in high-risk individuals.
Your main point is that the reward and palatability plays a huge role in hunger and appetite? Why?
Food reward is the seductiveness of food—its ability to motivate you to seek it out and eat it. Palatability is a related concept—it’s the pleasure derived from eating a food. It’s really just common sense that if a food is seductive and tastes really good, you’re going to eat more of it, and you may even eat it between meals when you aren’t hungry.
Our ancestors lived in a world of simple foods. Even just a few hundred years ago, they didn’t have modern stoves, they didn’t have a spice rack, they often didn’t have cooking oils, sweeteners, or salt. They certainly didn’t have soda, candy bars, and French fries. They ate simply prepared whole foods, and this allowed their appetite control mechanisms to operate correctly, effortlessly matching energy intake to energy needs.
I won’t get into the details of the mechanism, but if food is highly rewarding and palatable, it modifies these appetite control mechanisms, allowing you to eat more and accumulate more body fat than you would if the food were more simple. In the US and globally we are increasingly surrounded by energy-dense, highly rewarding and palatable foods, and food cues in advertising that make us crave them. We eat less home-cooked food than ever before, instead outsourcing our food preparation to professionals who attempt to get our business by maximizing reward and palatability.
In Europe, the Dukan Diet is gaining traction as a way to lose weight, do you know it? What do you think?
The induction phase of the Dukan diet is basically a modified version of a protein-sparing modified fast (PSMF). PSMF diets have been around for a long time—they’re basically very high protein low-calorie diets that cause rapid fat loss while minimizing hunger and muscle loss due to the blandness, reduced carbohydrate, and high protein content. PSMF combines a low-fat and a low-carbohydrate diet. PSMF diets contain very little carbohydrate or fat, and in Dukan’s case they are also quite bland. This all contributes to the appetite suppressing effect of the diet, facilitating fat loss. It also resets the palate to some degree, diminishing psychological reliance on highly rewarding/palatable foods.
That’s OK for a while as long as you can tolerate the high protein and low calories, but obviously the diet is not nourishing enough to be a long-term solution, so it must give way to a maintenance phase. This is where things become difficult, because most people will rapidly regain lost fat. However, if you’re prepared to make positive and lasting changes to your diet and lifestyle, and never return to how you were living before, then it’s possible that you could maintain some or even most of the fat loss.