I opened the door and called her name as I scanned the backyard. Normally my 30-pound Border Collie mix would be bounding down the hill in response to my call, energized from her chipmunk escapades. “Coby. Cooooo – beeeeee,” I yelled. A light wind rustled the rust-colored aspen leaves, but there was no other movement. My stomach tightened and I briefly thought the worst. Coyotes. Then I had a thought. I suppressed my twinge of concern, jumped in my car and raced up the road.
Earlier that morning Coby and I strolled up the road, wet from the early morning fog. The sunrise glowed pink and orange and framed silky clouds resting on the lake below. As we turned the corner, we approached a group of large granite rocks and I spotted a pile of trash with beer bottles, soda cans, and fast-food wrappers limp from the fog. Without hesitation, Coby dove right in. I snapped at her, “Coby, no!” Licking her lips, she popped up and ran to my side, forming what I am sure was a large, satisfying grin.
The sight and smell of food initiates a cascade of hormonal responses in our body. These hormones trigger an intense desire for food and a strong motivation to seek and devour food. Dogs share this physiology with humans and Coby’s impulse to dive into the trash was a normal physiologic response to the fragrant pile.
In my car, I slowly approached the granite rocks for the second time that morning and spotted a black tail with a white tip wagging above the Manzanita bushes. Her head buried in the trash, Coby didn’t flinch when I pulled up beside her.
“Coby. Co – bee. No,” I shouted as I jumped out of the car.
Her head snapped up and a limp hamburger bun hung from her mouth. She stared at me. I stared back at her. Neither of us moved. I squinted my eyes and created my most menacing angry-at-my-dog face.
“No. Drop it. Come.”
Silent and still, she stood frozen with the bun dangling.
The oldest part of the brain in both dogs and humans is called the primitive brain, commonly referred to as the reptilian brain. This part of the brain is buried deep in our skull and is responsible for our survival instincts. Our reptilian brain controls our fight-or-flight response, drives us to desire sex, and motivates us to find food. For millions of years the primitive brain has kept us alive with immediate and automatic reactions to danger and food. We have been hardwired to search out high-calorie food, gorge on high-fat high-sugar food and defend this food to ensure our survival. Coby’s primitive brain was in action, creating an intense desire to seek out this food and a fierce motivation to devour the food before someone, or something, tried to take it away.
Have you ever found yourself in the freezer section of the grocery store looking at fancy ice creams when not only are you not hungry, you had only hours earlier promised yourself that you would not eat sweets for a month? That was your reptilian brain at work, driving you to search for high-fat high-sugar food. Have you had the urge to stab a friend’s hand with your fork when she reached for your last French fry? That was your reptilian brain at work, defending your last bite of food. Our most irrational thoughts are derived from our reptilian brain, which is operating as if we are hunter-gatherers. Our food environment has changed rapidly over the last one hundred years, while our brain has been slowly evolving over the past two million years. Our primitive brain doesn’t understand that we are surrounded by high-calorie food and that we no longer need to hunt for, feast on, and protect our food.
Coby dropped the bun and ran to my side. I scolded her and she did her best to apologize by squirming on the ground by my feet. I opened the back door of my car and instructed her to, “load up”. Before she jumped into the car she glanced at the pile of trash, looking longingly at the tasty heap. She looked up at me and I stared back with narrowed eyes and a frown. Eyes averted and head down, her ears flattened against her head and she jumped into the car. A more advanced part of her brain quieted her reptilian brain and she curled up into a ball as we drove back home.
Heart failure is a condition in which the heart muscle is not strong enough to pump enough blood to the body. Heart failure affects about 6.5 million adults in the United States.
Study results presented at the American Heart Association annual scientific meeting found correlations between heart failure development in those without heart disease and eating patterns. Researchers identified five main eating patterns in the United States:
The only eating pattern associated with a lower risk of heart failure was a plant-based diet eating pattern
According to a new study published in the Journal of Clinical Oncology, a low-fat diet with increased fruit, vegetable, and grain intake reduces the risk of death after breast cancer.
The trial followed 48,835 postmenopausal women without breast cancer for 8.5 years. The participants were randomly assigned to one of two diets, a low-fat diet and a standard diet. The dietary goal for the low-fat group was to achieve less than 20% of total calories from fat and to increase intake of fruits and vegetables to five servings a day, and grains to six servings a day. The remaining participants in the control group ate their usual diet, which resembled the standard American diet (SAD).
According to the US Dietary Guidelines, the standard American diet has too much fat and too few fruits and vegetables. Most fat is consumed as oils in packaged foods such as salad dressing, mayonnaise, prepared vegetables, corn and potato chips, and as saturated fat from meat, cheese, and other dairy products.
After 8.5 years, there were fewer deaths in the low-fat group, but the difference was not statistically significant. During the 16-year follow-up period, the number of deaths after breast cancer was significantly reduced in the group following the low-fat diet.
The authors concluded that a low-fat high-fruit-vegetable-grain eating pattern may lower the incidence of death after breast cancer.
Research presented at this year’s European Association for the Study of Diabetes (EASD) in Lisbon, Portugal suggested that artificial sweeteners may increase the risk of type 2 diabetes by changing the body’s response to glucose.
Twenty-seven healthy individuals were given a placebo or two noncaloric artificial sweeteners, sucralose and acesulfame-K, in an amount equivalent to drinking four 12-ounce cans of a diet beverage. After two weeks, the participants were tested for rates of glucose (sugar) absorption, insulin levels, and gut hormones levels that control food intake.
This small study determined that it took two weeks of consuming an equivalent of four cans of diet beverage to increase the rate sugar is absorbed into the bloodstream and increase the body’s response to sugar. The participants had an increase in blood sugar, as opposed to a decrease in blood sugar as would be expected with the consumption of a beverage containing no sugar.
Despite the growing evidence that nonnutritive sweeteners may not be healthy substitutes for sugar-sweetened beverages, popular health websites, such as the Mayo Clinic, suggest that individuals with diabetes use nonnutritive sweeteners. Sweeteners in their list include saccharin (Sweet'N Low), aspartame (NutraSweet, Equal), acesulfame potassium (Sunett), sucralose, (Splenda) and stevia (Pure Via, Truvia).
The author of the Mayo Clinic page on nonnutritive sweeteners mentions that recent studies have cast doubt on recommending these sweeteners, and the benefits of making these substitutions are not clear.
* Pepsi no longer uses sucralose in their diet soda.
Poor sleeping habits are associated with an increased risk of weight gain and obesity. Short sleepers (< 7 hours/night) and long sleepers (> 9 hours/night) are more likely to be obese. Other sleep characteristics associated with obesity include daytime napping, working night shifts, poor sleep quality and evening chronotype (being a “night person”). Individuals who tend to stay up late at night, and sleep during the morning hours, are more likely to have poor eating habits, engage in late-night snacking, have sleep apnea and higher levels of stress hormones. Night owls are also more likely to develop diabetes and metabolic conditions.
A study in the April 2017 issue of the American Journal of Clinical Nutrition evaluated sleep patterns in those with a genetic risk for obesity. Among individuals at risk for obesity, short sleepers and long sleepers had a greater body mass than normal sleepers, those who sleep between seven and nine hours per night. Sleep duration was not significantly associated with body weight in individuals with a low genetic risk for obesity. Sleep behaviors are more likely to affect individuals who are at risk for obesity based on their genes.
This study sheds light on the interactions between our genes and our lifestyle. Sleeping behaviors influence our genes, and those at risk of obesity may be able to moderate weight gain by changing their sleeping habits.
A new study in the Journal of the American College of Nutrition set out to determine the nutrient content of preschoolers' lunches. Researchers studied the contents of 607 parent-packed lunches for preschool children. They found that only one quarter of lunches packed by parents contained adequate fiber. Only half of the lunches contained adequate vitamin A and calcium. Less than one in eight lunches contained adequate potassium. On average, thirty percent of the total calories in the lunches came from sugar.
The researchers concluded that lunches packed by parents do not consistently provide adequate nutrients. This may be one reason children age 3-5 are not consuming adequate essential nutrients.
To send your preschooler to daycare with a healthy lunch, avoid prepackaged lunches, include whole fruits and vegetables and check nutrition labels for added sugar.
You stopped snacking after dinner, eliminated mindless munching, and have been avoiding the white stuff, but the pounds just won't come off. Despite putting your best effort into your new diet, you can't seem to lose any weight! You are not alone, many people have the same frustrating experience with dieting, and scientists are searching for explanations.
A new study from researchers at the Washington University School of Medicine evaluated the impact of dieting on two groups of mice. One group of mice was accustomed to the Standard American Diet (aka SAD diet), while the other group was accustomed to a low-calorie plant-based diet. We’ll call this group VEGGIE mice. When fed the same restricted diet, the SAD mice lost less weight compared with the VEGGIE mice. Both groups of mice went on the same diet, but the mice used to eating a low-calorie plant-based diet lost more weight.
Many of us can relate to these diet-challenged SAD mice. Despite multiple attempts at dieting, passing on warm french bread and mac n’ cheese, we cannot seem to drop those extra pounds. Two weeks without any weight loss? Forget it! Where’s the Ben & Jerry’sⓇ?
The standard American diet is high in refined carbohydrates, simple sugars, saturated fat and low in whole fruits and vegetables. Those of us who have spent our lifetime eating a SAD diet have fewer types of bacteria in our guts. In scientific terms, our microbiota lacks diversity. This lack of bacterial diversity lowers our response to positive dietary changes. Our gut bacteria prevent us from losing weight. Blame the bacteria!
In their study, researchers noted that the SAD mice had fewer types of bacteria in their gut. They decided to see if cohousing SAD mice and VEGGIE mice would impact the response to the diet. They found that when the diversity-challenged SAD mice mingled with their VEGGIE-mice friends, their gut bacterial colonies became more diverse. Incredibly, after mingling with the VEGGIE mice, the SAD mice started to respond to the restricted diet. The bacteria from one group of mice ended up in the other group of mice, increasing the diversity of the bacteria in the SAD mice, resulting in weight loss.
A shared space led to a greater variety of gut bugs, which led to more weight loss
Does this mean we should make more vegan friends and put away our antimicrobial sanitizer to lose weight? Possibly. But, despite our continuous shedding of bacteria, the rate at which we exchange bacteria, and the effect this has on weight loss and health is not yet clear.
What we can take away from this research is that poor food choices over the long term will negatively influence the bacteria in our gut, limiting responses to positive short-term dietary changes. If you've been eating packaged food and fast food for decades, you may not see an immediate response to a new diet. But this doesn't mean you shouldn't try! We should still make improvements to our diet, making efforts to eliminate processed foods and refined carbohydrates and adding more whole fruits and vegetables to our daily menu. But, perhaps we should abandon "dieting". Instead of multiple short-term diet attempts, a better approach may be to make a few positive dietary changes that will last a lifetime.
Creating a healthy dietary pattern will result in greater gut bacterial diversity. This diversity gives us a better chance of losing weight and will lead to long-term health benefits.
In Dr. Sandra Aamodt’s new book, Why Diets Make Us Fat: The Unintended Consequences of Our Obsession With Weight Loss, she discusses the neuroscience behind our repeated and unsuccessful diet attempts. Dr. Aamodt, a self-admitted, yo-yo dieter and neuroscientist, describes her personal history with weight cycling, binge eating, and obsessive dieting. She explains the science driving these behaviors and the reasons for our inevitable diet failures.
Short-Term Success, but Long-Term Failure
Diets may work in the short-term, but almost all diets fail in the long-term. Studies have shown that 80-100% of dieters who have successfully lost weight gain back the weight within a few years. This is in part due to the body’s drive to keep weight stable. Unfortunately, chronic dieting and weight cycling many times results in weight gain.
The Body Defends its Perceived Set Weight
The key concept outlined in her book is the idea that the brain defends the body’s perceived appropriate weight, called the set-point theory. The brain keeps body weight within a particular range, which Dr. Aamodt terms the “defended weight range”. The defended weight ranges between 10 to 15 pounds. The brain will always strive to keep weight within this range. Fluctuations can happen within the weight range and it is easier for weight to move up than down. If weight goes above or below the defended weight range, the brain will do everything possible to return to the body’s perceived appropriate weight.
The Struggle to Lose More Weight
To demonstrate why weight loss, or gain, within the defended weight range is possible, but weight loss below the range can seem nearly impossible, let's take an example of a 150-pound woman. Let’s say our 150-pound woman gains ten pounds over six months due to a busy period at work. Once the stressful work situation eases, she can lose those ten pounds by returning to her previous, regular eating habits and by making healthy food choices. If this same woman goes on a diet, restricting calories and increasing exercise, it’s very likely she could lose ten pounds and reach 140 pounds. Within the defended weight range, the body will adapt to these changes in weight loss or weight gain. But trying to lose more weight, to drop to 130 pounds, is more challenging.
If this same woman loses more weight to reach a 130-pound goal, the body will feel deprived, even starved. The brain will not adapt to this new weight, and instead, it will fight to return to the defended weight range, making further weight loss almost impossible and weight maintenance, at 130 pounds, incredibly challenging. Even small deviations from her diet will quickly result in weight gain.
The Brain’s Response to Starvation
It’s easier to understand the body’s desire to limit weight loss outside a set range if we think about it as a survival mechanism. Throughout human history, humans have had to endure periods of food scarcity, and we have survived many famines because of the body’s natural protective mechanism. When the brain perceives starvation, it immediately responds with the following:
• slowing down metabolism
• decreasing the drive to exercise
• increasing efficiency
• increasing hunger
These responses increase our desire to eat and limit our use of energy. This incredible mechanism has helped us survive famines and recover from periods of starvation. Unfortunately, this mechanism works against us in a world of food abundance. Our body’s natural drive to keep weight on, and to resist weight loss, has led to an epidemic of obesity and a nation full of obsessive dieters.
Effects of the Self-imposed Famine
Dr. Aamodt terms food restriction via dieting a "self-imposed famine" and states that this famine triggers the body’s survival mechanism. The brain perceives food restriction as starvation, particularly when the body is below the defended weight range, and it immediately attempts to protect itself. The body slows down metabolism, using as little energy as possible. Muscles become more efficient, capable of doing more work with less energy. The drive to eat is incredibly strong and hunger is intense. Dieting turns on the brain’s starvation mode.
Factors Contributing to Weight Gain and Weight Loss
Dr. Aamodt discusses other factors that contribute to weight gain, including environmental chemicals, sleep loss, stress, and social stigmas. She reviews the research and techniques for mindful eating (i.e.: the first bite will always taste better than the fifth bite) and mindless eating (i.e.: changing plate and glass size can help you unconsciously eat less).
Healthy is Better than Thin
After decades of dieting and weight cycling, Dr. Aamodt resolved not to diet for one year, to focus on healthy foods and exercise daily. She lost ten pounds. Pleased with the results, she now gives talks on diet avoidance and emphasizes a focus on health. She reviews research supporting her theory that being healthy, both with diet and lifestyle habits, but also by exercising daily, is more important than being thin. Adopting healthy eating habits and a healthy lifestyle will lower the risk of death from chronic disease in all individuals, regardless of weight.
Helpful Eating Tips and Strategies
Despite the dismal statistics on weight loss, Dr. Aamodt offers practical advice:
Two Dietary Goals
Two uncontroversial dietary goals:
1. Eat more whole vegetables
2. Minimize added sugar, refined grains and processed foods
If you are trying to lose weight, are a yo-yo dieter, have weight cycled over the years or have an interest in metabolism and energy balance, you will thoroughly enjoy the personal accounts by Dr. Aamodt as well as her explanation of the neuroscience surrounding weight loss.
Proposition 65 requires California businesses to post a list of chemicals that cause cancer, birth defects, or reproductive harm. Bisphenol A (BPA) is one of over 900 chemicals listed on California's list of chemicals known to the state to cause cancer or reproductive toxicity (1,2).
The Toxicant Identification Committee (DARTIC) reviewed more than 300 human and laboratory studies on the female reproductive effects of BPA. The committee concluded that BPA can harm the female reproductive system.
There is widespread exposure to BPA. When CDC scientists measured BPA in the urine of 2,517 people, almost all of the individuals tested had BPA in their urine (3).
BPA is found in plastic products, as well as food and drink packaging. Epoxy resins containing BPA are found in the metal coating in food cans and bottle tops. BPA can leach into food from the canned food coating.
Women in their childbearing years should take steps to limit exposure to BPA. Choose BPA-free cans, plastic bottles and beverage containers. Choose fresh, whole food and limit consumption of canned and packaged food.
Cow’s Milk, Sugar Overload, Weight Gain and Environmental Toxins All Risk Factors for Type 1 Diabetes in Children
There has been a dramatic increase in the incidence of type 1 diabetes in the past 30 years. Although there is no single cause of type 1 diabetes, a recently published article in The Lancet identifies the dietary and environmental triggers contributing to the development of this devastating disease (1).
Interaction Between Genetics, Diet and the Environment
The main risk factor for type 1 diabetes is genetics, but an environmental trigger is necessary to initiate the disease process (2). The authors categorize risk factors based on childhood stage.
Viral infections, changes in the microbiota (the microorganisms in the gut), a lack of physical activity, rapid weight gain and psychological stress are also all risk factors. These factors can trigger the disease process in children who have a genetic risk for type 1 diabetes (1, 2).
Environmental Risk Factors for Type 1 Diabetes Infographic
Type 1 Diabetes - The Immune System Attacks The Pancreas
Type 1 diabetes is an autoimmune disease that typically develops during childhood and is characterized by high blood glucose (3). Glucose is a sugar that is the end product of starch digestion as seen in the diagram below. Glucose is also the main sugar in our bloodstream and main carbohydrate stored in our body.
Type 1 diabetes results when the immune system mistakenly identifies the beta cells in the pancreas as foreign invaders. The immune system attacks and destroys the insulin producing beta cells. Insulin is the hormone that moves glucose, our main energy source, from the bloodstream into our cells. Without insulin, not only does blood glucose rise to dangerous levels, the body’s cells are deprived of energy. An individual with type 1 diabetes must administer insulin daily (3).
Cause of Type 1 Diabetes is Unknown: Genes Play a Role
The cause of type 1 diabetes is unknown (4) but it is generally accepted that multiple genes are involved in its development. In addition, many dietary and environmental risk factors have been identified. One important group of genes associated with type 1 diabetes is the human leukocyte antigen (HLA) gene complex (5). The HLA complex provides the body’s immune system with a set of tools to help it differentiate between our own proteins and proteins made by bacteria or viruses (5). Variations in this gene complex are linked to chronic diseases.
The Immune System - Identifying a Foreign Invader
Although our immune system is intended to attack viruses and bacteria, it is designed to respond specifically to proteins on the surface of these microorganisms, not the entire microorganism. Using the HLA complex, the immune system can distinguish between our own proteins (self) and proteins on the surface of microorganisms (foreign) (6). This allows the immune system to adapt to a variety of invaders, neutralizing and destroying foreign proteins on microorganisms, but ignoring the proteins that make up our organs. Variations in the HLA gene complex can create confusion for the body’s immune system, making it difficult to tell the difference between a foreign protein and a protein that is part of our own body.
The Immune System - Creating a Specialized Army
The immune system is designed to respond to foreign proteins that enter the body. Bacteria and viruses, common foreign invaders, have proteins on their surface which can be identified by our immune system. When presented with a foreign invader, the immune system launches its attack. The first line of defense attacks the foreign invaders, neutralizing or destroying them. But, these invaders usually attack again.
Fortunately, after the first strike a strategic mission is in the works by the immune system. Upon first exposure, the immune system sizes up the foreign invader and creates an antibody specifically designed to neutralize it. The immune system assesses the enemy and creates a small army of specialized soldiers ready to attack when the bacteria or virus invades again (6).
The Innocent Invader - Food Protein
When we consume protein, our digestive system breaks down the protein into individual amino acids as seen in the image to the right. The amino acids are then absorbed into our bloodstream and utilized by the body. Occasionally, a protein, or a protein fragment, escapes digestion and ends up in the bloodstream (7). Once in the bloodstream, the immune system might identify this food protein as a foreign invader and launch an attack. This is how a food protein, for example protein from peanuts, can result in an allergic reaction (8). With repeated exposures, the body will build up its specialized army, preparing itself for the next attack.
Mistaken Identity - If Food Protein Looks Like Body Protein
When protein sneaks across the intestines into the bloodstream, it can induce an immune response. This may initiate an allergic response or it may initiate an autoimmune response. In some cases, a section of a food protein is identical, or nearly identical, to a section of protein in an organ in our body. The body may mistakenly identify the protein in an organ, for example the pancreas, as a foreign invader.
The immune system rounds up its specialized antibodies. These specialized antibodies, created to attack the similar food protein, now attack the cells in the pancreas. It's a case of mistaken identity.
Milk Protein Mistaken for Beta Cells in the Pancreas
A small section of a protein in cow’s milk appears just like a small section of protein in the beta cells (insulin-producing cells) of the pancreas (9). A study in the New England Journal of Medicine in 1992 tested 142 children with type 1 diabetes for antibodies to a protein in milk (bovine serum albumin) and compared the results to 79 healthy children without diabetes. All of the children with type 1 diabetes had the antibody to the specific milk protein, whereas only two of the healthy children had the antibody (9). This study demonstrates that the children with type 1 diabetes had exposure to cow’s milk. This exposure resulted in the creation of a specific antibody designed to neutralize and destroy the milk protein. The authors theorized that this anti-milk protein antibody mistakenly identified the pancreas as foreign and destroyed the beta cells. Not all studies have reproduced these results (10) and this theory of the role of cow’s milk as a causative agent in the development of type 1 diabetes remains controversial. Cow’s milk remains a risk factor, but not necessarily a cause of type 1 diabetes.
Environment and Diet Increase Risk For Type 1 Diabetes
The recent two-part article in The Lancet (1, 2) demonstrates the importance of understanding the interaction between diet, environment, and genetics. Although certain individuals may be genetically susceptible to type 1 diabetes, an environmental or dietary trigger is needed to initiate the disease process. The infographic above provides a visual representation of the dietary and environmental factors triggering the disease during various phases of childhood. Important dietary risk factors and dietary protective factors are summarized below (1).
Dietary Factors Influencing Development of Type 1 Diabetes
The incidence of type 1 diabetes has increased over the past three decades. The exact cause of type 1 diabetes has not been identified because there are many factors influencing the development of the disease. Changes in our diet, our environment and our lifestyle over the past 30 years have contributed to the increase of this disease. In children who have a genetic risk for type 1 diabetes, the foods they eat, the amount of activity they engage in and the amount of weight they gain can trigger the onset of the disease. Children with a genetic risk have variations in their genes that increase the likelihood that the immune system will mistakenly identify the insulin producing cells in the pancreas as foreign invaders, destroying these cells slowly over time. Once destroyed, the cells in the pancreas can no longer produce insulin. This causes elevated blood sugar and type 1 diabetes results.
Christine Dobrowolski is a nutritionist and whole-foods advocate.