January 23, 2020
The process of gaining weight isn’t as simple as one might think. The model of “calories in/calories out” that many of us are familiar with is flawed, and doesn’t take into account the complex hormonal and biochemical pathways involved in energy balance, weight gain, and weight loss in the body.
The flaws of the calorie deficit model of weight loss can be pictured by imagining the human body as a car: The engine is our cells, the fuel tank is our fat stores, and the fuel within the tank is provided by the food we eat. As we drive the car along, the engine (cells) burns fuel (fat) to keep the car moving. By consuming food we "refill" the tank as we go, preventing it from running dry. In this analogy, if we want to deplete our fuel tank (fat stores), we can simply put less fuel in the tank (eat fewer calories) or drive the car faster (exercise more).
That's all quite straightforward and makes sense on first blush, but is it accurate? Is a car with just three components a reasonable way to represent the complexity of the human body? Moreover, is a car with three components even a reasonable way to represent the complexity of a real car? The answer is no, and here's why: A real engine does not just require fuel to run - it requires a precise blend of fuel and oxygen, along with a perfectly timed spark, controlled temperature and humidity, lubrication, and more. Furthermore, every engine model might be constructed slightly differently. Tip the balance on any of these mitigating factors and the fuel efficiency of the engine will change dramatically, if it manages to run at all.
The original thought experiment now seems a lot more complex. What happens if we are driving this more realistic car except this time debris has clogged the air filter, preventing oxygen from entering and making conditions impossible for the fuel to burn efficiently? What if the engine oil is depleted and there is excessive friction and wear on the engine parts? This is a more accurate representation of the human body and the hormonal mechanisms of weight and energy balance.
Amazingly, different types of foods eaten at different times of day and in different combinations can lead to completely unique hormonal responses in the body, and it is these hormones--in particular insulin--that determine what happens to the food molecules once broken down by the digestive system, and how efficiently they are processed. What’s more, different individuals can have highly variable glucose responses to the same food, regardless of calorie content.
Insulin is released in response to glucose in the blood (see Figure 1), and is the primary hormone involved in fat storage and weight gain. Though we often associate insulin with diabetes, it is a big contributor to weight gain for everyone--diabetic or not--and has to be tamed to successfully maintain a healthy weight.
Insulin is our body’s main anabolic hormone, meaning it promotes “building” in the body (e.g. the storage of fat), rather than breaking things down. Insulin tells our cells to take up glucose from the blood for use, or, if there’s excess, for storage. Because weight loss generally requires us to burn through fat stores, we need to control our insulin so that we signal to the body that it should burn fat, rather than store more of it.
When there is more glucose in the bloodstream than what the body needs to meet energy demands, increased insulin levels signal to the liver and muscles to store glucose in chains of glycogen. Once the liver and muscles are filled to the brim with glycogen, the excess glucose is turned into fat (triglycerides) and sent out in the blood to be stored in the fat cells around the body. You can think of the liver and muscle as short term, limited storage space for energy in the form of glycogen, and fat cells as long term, essentially unlimited storage space for energy in the form of triglycerides.
When we’re not eating-- if we’re between meals, sleeping, or fasting--the lack of dietary glucose causes insulin levels to fall. This signals to our body that we should burn stored energy, starting with glycogen. Once the stores of glycogen run out, we start burning fat (see Figure 2). The goal of weight loss is to burn excess stored fat by mobilizing it and bringing it to parts of the body that can use it for fuel. It’s important to note that the anabolic (storage) signal of insulin prevents the body from tapping into fat for energy as long as insulin levels are high.
This part of the story is simple: we need to lower our insulin levels to burn stored fat. But what if our insulin levels never really fall enough to signal that we should be burning through our stored fat? This is a similar scenario to the car with the clogged air filter - we can push the accelerator all we want but unless the oxygen (insulin) level is optimal, the engine (cells) cannot burn fuel (fat) efficiently. In the body, high insulin both impairs triglyceride breakdown in fat cells, and also inhibits fatty acids from entering into fatty acid oxidation in the mitochondria.
At Levels, we believe that a key to success is knowing exactly how your body responds to different foods. Fortunately, glucose levels tend to mirror insulin responses. If we know how much a food raises our blood glucose, then we have a more robust understanding of our body’s predicted exposure to insulin, and therefore gain a sense of whether our body is likely to be in a fat-storage or fat-burning mode.
Reading this, you might think that we should just eat very few carbohydrates and stick to high fat foods in order to decrease insulin and lose fat and weight. This may be part of the puzzle, but it’s not the only piece. It’s important to remember that there are many complex carbohydrates and healthy protein sources that can help our bodies function optimally, and which may not generate significant glucose and insulin spikes.
The concept of the “glycemic index” -- a ranking of foods based on how they affect blood glucose -- is a standardized tool to help understand this process, but it can also be a blunt instrument. A few problems have become increasingly clear regarding standardized glycemic indices:
Considering all these variables, how could someone possibly know how their day-to-day diet is affecting their glucose levels if they don’t have access to their glucose data? The answer is simple: They can’t.
Unfortunately, long term success rates with weight loss are dismal: despite the alarming statistic that 70% of Americans are overweight or obese, and nearly 50% of Americans have tried to lose weight in the past 12 months, only 15-20% of people who successfully lose weight are able to keep it off. As stated by Ochner, et al, “this almost ubiquitous weight regain is witnessed in virtually every clinical weight loss trial, including those specifically aimed at improving weight loss maintenance.”
Why do conventional attempts at weight loss fail? Three things: metabolism, hormones, and the brain. The reality is that our bodies have evolved to help us survive and hold on to energy in the face of starvation through a variety of complex mechanisms.
Simply eating less (ie, calorie deprivation) is a common approach to weight loss, but thwarts our efforts by reducing our resting metabolic rate. When the body senses an environment of food scarcity, it uses energy more efficiently and also reduces its use of stored energy. This translates to fewer calories expended per day.
The types of foods we eat after losing weight also seem to affect our ability to maintain weight loss. A study showed that people who adhere to low carbohydrate eating plans after weight loss burn ~200 kilocalories more per day than those on higher carbohydrate diets, and for those with the highest insulin secretion at baseline who subsequently adhere to a low carbohydrate diet, that difference widens to 400 kilocalories per day.
The brain is also affected by dieting in ways that promote weight regain. When we are calorie deprived, we see increased activity in areas of the brain that lead to increased attention, reward, and motivation related to food. In other words, calorie deprivation leads us to become hyper-focused on obtaining food.
Hormones, including those beyond insulin, play a major role as well. Leptin is one of our appetite-inhibiting/satiety hormones and is secreted by fat cells in response to eating. Its levels also increase as fat mass increases. It is thought that leptin signals to the brain to inhibit food intake in order to prevent overconsumption of dietary energy, and suppresses insulin production to discourage further fat storage in favor of fat burning.
Paradoxically, obese patients with higher levels of leptin (due to higher levels of fat mass) may suffer from “leptin resistance,” thought to be due to reduced transport of leptin across the blood brain barrier. High insulin levels are also thought to lead to leptin resistance, preventing appetite-inhibition, and leading to a cycle of increased weight gain.
It all starts with glucose levels - if they’re elevated, insulin is generally released. Increased insulin levels lead to fat storage and weight gain. Over time, if glucose is consistently elevated due to diet, and insulin production is therefore constantly active, our cells can become “numb” to insulin, a process called insulin resistance. This means that we need more and more circulating insulin to get glucose into cells, leading to higher baseline levels of insulin. This process directly counters weight loss efforts.
In obese individuals, high insulin levels also lead to impaired leptin signaling and “leptin resistance”, making it harder for us to feel full and more likely to continue consuming calories rather than burn stored fat for energy. On the other hand, decreased glucose levels lead to lower insulin levels, which can lead to weight loss and decreased fat mass.
Real-time glucose measurements give us the power to understand how the foods we eat affect the level of glucose in our blood, and by rough proxy, our insulin levels. Unlike traditional dietary strategies like calorie counting -- which have been shown time and again to be ineffective for sustained weight loss -- glucose monitoring provides insight into the underlying physiological processes that lead to fat storage.
Being overweight is a risk factor for a host of problems: cardiovascular disease, cancer, diabetes, and premature mortality. It can also exacerbate hypertension, arthritis, gallstones, high cholesterol, low back pain, bronchitis, and musculoskeletal problems.
Excess fat also acts as a source of many signaling molecules in the body, and is even thought to be an “endocrine organ” in its own right. Fat can secrete hormones (like those associated with appetite, i.e. leptin), but also pro-inflammatory chemicals called adipocytokines, which are associated with insulin resistance. Visceral fat -- the type that surrounds organs and is most dangerous in terms of risk for chronic disease -- is also known to harbor a large quantity of immune cells called macrophages, which in turn leads to further production of pro-inflammatory chemicals.
Given the relationship between glucose, insulin, and excess fat, real-time monitoring can provide a valuable tool to help individuals feel more empowered in their weight loss journey. Personal data helps individuals know specifically how their diet affects them, and can inspire behaviors that promote optimal weight and long-term health and wellness.
Disclaimer: The information on this site is intended to provide general educational information only, and does not constitute, nor is it a substitute for, medical advice.
Photo credit: Jamie Street
The rich text element allows you to create and format headings, paragraphs, blockquotes, images, and video all in one place instead of having to add and format them individually. Just double-click and easily create content.
A rich text element can be used with static or dynamic content. For static content, just drop it into any page and begin editing. For dynamic content, add a rich text field to any collection and then connect a rich text element to that field in the settings panel. Voila!
Headings, paragraphs, blockquotes, figures, images, and figure captions can all be styled after a class is added to the rich text element using the "When inside of" nested selector system.