THERE ARE TWO prominent findings from all the dietary studies done over the years. First: all diets work. Second: all diets fail.
What do I mean? Weight loss follows the same basic curve so familiar to dieters. Whether it is the Mediterranean, the Atkins or even the old fashioned low-fat, low-calorie, all diets in the short term seem to produce weight loss. Sure, they differ by amount lost—some a little more, some a little less. But they all seem to work. However, by six to twelve months, weight loss plateaus, followed by a relentless regain, despite continued dietary compliance. In the ten-year Diabetes Prevention Program,1 for example, there was a 15.4-pound (7-kilogram) weight loss after one year. The dreaded plateau, then weight regain, followed.
So all diets fail. The question is why.
Permanent weight loss is actually a two-step process. There is a short- term and a long-term (or time-dependent) problem. The hypothalamic region of the brain determines the body set weight—the fat thermostat. (For more on body set weight, see chapters 6 and 10.) Insulin acts here to set body set weight higher. In the short term, we can use various diets to bring our actual body weight down. However, once it falls below the body set weight, the body activates mechanisms to regain that weight—and that’s the long-term problem.
This resistance to weight loss has been proven both scientifically and empirically.2 Obese persons that had lost weight required fewer calories because their metabolisms had slowed dramatically and desire to eat accelerates. The body actively resists long-term weight loss.
THE MULTIFACTORIAL NATURE OF DISEASE
THE MULTIFACTORIAL NATURE of obesity is the crucial missing link. There is no one single cause of obesity. Do calories cause obesity? Yes, partially. Do carbohydrates cause obesity? Yes, partially. Does fiber protect us from obesity? Yes, partially. Does insulin resistance cause obesity? Yes, partially. Does sugar cause obesity? Yes, partially. (See Figure 17.2.) All these factors converge on several hormonal pathways that lead to weight gain, and insulin is the most important of these. Low-carbohydrate diets reduce insulin. Low- calorie diets restrict all foods and therefore reduce insulin. Paleo and LCHF diets (low in refined and processed foods) reduce insulin. Cabbage-soup diets reduce insulin. Reduced-food-reward diets reduce insulin.
Virtually all diseases of the human body are multifactorial. Consider cardiovascular disease. Family history, age, gender, smoking, high blood pressure and physical activity all influence, perhaps not equally, the development of heart disease. Cancer, stroke, Alzheimer’s disease and chronic renal failure are all multifactorial diseases.
Obesity is also a multifactorial disease. What we need is a framework, a structure, a coherent theory to understand how all its factors fit together. Too often, our current model of obesity assumes that there is only one single true cause, and that all others are pretenders to the throne. Endless debates ensue. Too many calories cause obesity. No, too many carbohydrates. No, too much saturated fat. No, too much red meat. No, too much processed foods. No, too much high fat dairy. No, too much wheat. No, too much sugar. No, too much highly palatable foods. No, too much eating out. It goes on and on. They are all partially correct.
So the low-calorie believers disparage the LCHF people. The LCHF movement ridicules the vegans. The vegans mock the Paleo supporters. The Paleo followers deride the low-fat devotees. All diets work because they all address a different aspect of the disease. But none of them work for very long, because none of them address the totality of the disease. Without understanding the multifactorial nature of obesity—which is critical—we are doomed to an endless cycle of blame.
Most dietary trials are fatally flawed by this tunnel vision. Trials comparing low-carb to low-calorie diets have all asked the wrong question. These two diets are not mutually exclusive. What if both are valid? Then there should be similar weight loss on both sides. Low-carb diets lower insulin. Lowering insulin levels reduces obesity. However, all foods raise insulin to some degree. Since refined carbohydrates often make up 50 percent or more of the Standard American Diet, low-calorie diets generally result in a reduced carbohydrate intake. So low-calorie diets, by restricting the total amount of food consumed, still work to lower insulin levels. Both will work – at least in the short term.
That is exactly what Harvard professor Dr. Frank Sacks 3 confirmed in his randomized study of four different diets. Despite differences in carbohydrate, fat and protein content, albeit relatively minor, weight loss was the same. Maximum weight loss occurred at six months, with gradual regain thereafter. A 2014 meta-analysis of dietary trials reached much the same conclusion.4 “Weight loss differences between individual diets were minimal.” Sure, sometimes one diet comes off as slightly better than another. The difference is usually less than 2 pounds (about 1 kilogram) and often fades within a year. Let’s face it. We’ve done low calories, low fat. It didn’t work. We’ve done Atkins, too. It didn’t produce the effortless weight loss that was promised.
Sometimes these results are interpreted to mean that everything can be eaten in moderation—which doesn’t even begin to address the complexity of weight gain in humans. “Moderation” is a cop-out answer—a deliberate attempt to evade the hard work of searching for dietary truths. For example, should we eat broccoli in the same moderation as ice cream? Obviously not. Should we drink milk in the same moderation as sugar sweetened beverages? Obviously not. The long-recognized truth is that certain foods must be severely restricted, including sugar-sweetened beverages and candy. Other foods do not need to be restricted: kale or broccoli, for instance.
Others have erroneously concluded that “it’s all about calories.” Actually, it’s nothing of the sort. Calories are only a single factor in the multifactorial disease that is obesity. Let’s face the truth. Low-calorie diets have been tried again and again and again. They fail every single time.
There are other answers that are not really answers. These include, “There is no best diet” or “Choose the diet that suits you” or “The best diet is one you can follow.” But if supposed experts in nutrition and disease don’t know the right diet, how are you supposed to? Is the Standard American Diet is the best diet for me because it’s the one I can follow? Or a diet of sugared cereals and pizza? Obviously not.
In cardiovascular disease, for example, “Choose the treatment that suits you” would never be considered satisfactory advice. If the lifestyle factors of stopping smoking and increased physical activity both reduce heart disease, then we would strive to do both, rather than try to choose one or the other. We would not say, “The best lifestyle for heart disease is the one you can follow.” Unfortunately, many so-called experts in obesity profess this exact sentiment.
The truth is that there are multiple overlapping pathways that lead to obesity. The common uniting theme is the hormonal imbalance of hyper- insulinemia. For some patients, sugar or refined carbohydrates are the main problem. Low-carbohydrate diets may work best here. For others, the main problem may be insulin resistance. Changing meal timing or intermittent fasting may be most beneficial. For still others, the cortisol pathway is dominant. Stress reduction techniques or correcting sleep deprivation may be critical. Lack of fiber may be the critical factor for yet others.
Most diets attack one part of the problem at a time. But why? In cancer treatment, for example, multiple types of chemotherapy and radiation are combined together. The probability of success is much higher with a broad- based attack. In cardiovascular disease, multiple drug treatments work together. We use drugs to treat high blood pressure, high cholesterol, diabetes and smoking cessation—all at the same time. Treating high blood pressure does not mean ignoring smoking. In challenging infections such as HIV, a cocktail of different antiviral medicines are combined together for maximum efficacy.
The same approach is necessary to address the multidimensional problem of obesity. Instead of targeting a single point in the obesity cascade, we need multiple targets and treatments. We don’t need to choose sides. Rather than compare a dietary strategy of, say, low calorie versus low carb, why not do both? There is no reason we can’t.
It is also important to tailor the approach individually to address the cause of the high insulin levels. For example, if chronic sleep deprivation is the main problem causing weight gain, then decreasing refined grains is not likely to help. If excessive sugar intake is the problem, then mindfulness meditation is not going to be especially useful.
Obesity is a hormonal disorder of fat regulation. Insulin is the major hormone that drives weight gain, so the rational therapy is to lower insulin levels. There are multiple ways to achieve this, and we should take advantage of each one. In the rest of this chapter, I will outline a step-by-step approach to accomplish this goal.
STEP 1: REDUCE YOUR CONSUMPTION OF ADDED SUGARS
SUGAR STIMULATES INSULIN secretion, but it is far more sinister than that. Sugar is particularly fattening because it increases insulin both immediately and over the long term. Sugar is comprised of equal amounts of glucose and fructose, as discussed in chapter 14, and fructose contributes directly to insulin resistance in the liver. Over time, insulin resistance leads to higher insulin levels.
Therefore, sucrose and high fructose corn syrup are exceptionally fattening, far in excess of other foods. Sugar is uniquely fattening because it directly produces insulin resistance. With no redeeming nutritional qualities, added sugars are usually one of the first foods to be eliminated in any diet.
Many natural, unprocessed whole foods contain sugar. For example, fruit contains fructose, and milk contains lactose. Naturally occurring and added sugars are distinct from one another. The two key differences between them are amount and concentration.