What Causes Metabolic Health Conditions?
It is estimated that 85% of the adult US population is not metabolically healthy. In our previous post, we discussed that there are numerous factors that can affect our metabolic health and our weight. It’s a complex interplay between our genetics, or biology, and our environment. The take-away message was that weight is complex and highly regulated by the brain, and that there are numerous factors that go far beyond calories-in-calories-out. I hope that this conveyed that obesity is not anyone’s fault, and that it is not about willpower but rather, it is about a complex interplay between our physiology, genetics and our environment. Whether you are part of the 85% of individuals who are struggling with your metabolic health, or if you are in the 15% of people who don’t, I think it’s important for all of us to understand how and why metabolic medical conditions develop.
In this second part of this three-part series, we will discuss what happens inside the body when we gain weight, or to state it more correctly, when we gain “adiposity”. Adipose tissue is the medical term for fat tissue, and adipocytes are the medical term for fat cells. I will use these terms interchangeably.
Prior to the 1990’s, our adipose tissue was simply seen as a reservoir for extra calories. There was some recognition of the role of adipose tissue to protect organs and to help with insulation, but for the most part, it was seen as a rather inactive tissue that just sat there collecting excess calories that we didn’t burn. Our eating and activity behaviors were viewed as mostly being under our voluntary, conscious control. If consumed too many calories, and didn’t burn off those extra calories, then any extra calories were stored as fat. Conversely, if we ate fewer calories than we expended, we lost fat. We continued this theory by declaring that one pound of fat contains 3,500 Calories, and as such, if we had 3,500 calories in excess, we gained a pound of fat, and if we were at a 3,500 calorie deficit, we lost a pound of fat. Does this sound familiar?
This is the over-simplified vision of weight regulation that is still perpetuated to this day, even though science has proven this to be incorrect, or at best, incomplete, for the past 20+ years. As discussed in our previous post, there are numerous factors, hormones, and neurotransmitters involved with energy and appetite regulation, and it’s not as simple as making personal decisions. It takes a long time for medicine and for the public to catch up with science, and my goal is to expedite this process by teaching all of you about the truth behind weight and appetite regulation, adipose tissue, and how all of this impacts our health.
Leptin is a hormone that is produced by our fat cells (adipocytes). It was discovered in 1994. The initial theory that there were hormones released from the fat cells that communicated with the brain about energy expenditure and appetite dated back to the 1950’s, but it wasn’t until some 40 years later that leptin was actually discovered. This discovery changed the way scientists thought about weight and appetite regulation and set off an explosion of research into this fascinating and misunderstood topic of energy regulation.
Fast-forward 26 years later, and we now know that the energy-regulatory system is extraordinarily complex and regulated by the brain, not by our own willpower. Numerous hormones have been discovered. These hormones are secreted by organs such as the stomach, the GI tract, the pancreas, adipocytes, and muscle tissue, and all of these hormones travel to the brain to inform our brain about our adiposity (our “energy stores”). This system is what allowed us to survive periods of famine and to encourage food-seeking behavior when food was plentiful.
We must remember that our bodies and brains were developed over millions of years of evolution, and that, for 99.5% of our human history, we lived as hunter-gatherers. It is the hunter-gatherer environment that our bodies and our brains were built for, not the environment that we live in today. It may seem to us that the agricultural revolution happened a long time ago, and that we should have adapted to having more reliable food sources, but 10,000 years is just a flash in the pan when you consider that humans have been around for about 2.5 million years.
Another thing we must recognize is that our bodies are designed to strongly protect us from weight loss, since this was a common reason for our demise, and weakly defend us from excess weight, since this was historically not a problem. The same is true of blood sugar and blood pressure. Your body will give strong signals when your blood sugar or blood pressure get too low- you feel dizzy, weak, sweaty, and in the case of low blood sugar, ravenously hungry, to signal to your body to get some glucose back into your blood stream. But when your blood sugar or blood pressure is too high? Most people can’t feel this, unless it becomes extreme. The body is not designed to know what to do with too much glucose or too many calories, because that simply didn’t exist in our hunter-gatherer days.
Obesity has been around since the beginning of mankind, but we didn’t see a rapid increase in the prevalence of obesity until around 40-50 years ago. Our environment has certainly shifted drastically since the agricultural revolution, and it has changed even more rapidly in the last 40-50 years. As much as we may try, there is no one thing that we can point to that triggered the weight gain that has steadily been getting worse. As we discussed in the last post, it’s not one thing, or even ten things. It’s thousands of little things that are all contributing to a disruption of our energy regulatory system.
Our discussion today is about what happens when the amount of adipose tissue starts to exceed our storage capacity. We all have a limited capacity for adipose tissue-storage and this capacity varies from person to person, and varies with gender, ethnicity, genetics, and other factors. Some people can safely store more adipose tissue than others, and therefore may not develop the metabolic signs and symptoms often seen with obesity. Others have a limited fat storage capacity and begin to develop signs of metabolic disease even before their BMI or body fat percentage classifies them as having obesity. Therefore, we see relatively lean people with metabolic disease such as type 2 diabetes, high blood pressure, or high cholesterol, and people with a high level of adiposity, without any of those medical conditions. Hence, we can’t judge somebody’s health by their body size.
There is another side of complications of weight that doesn’t relate to the metabolic conditions associated with excess adiposity, but rather to the biomechanical complications of excess weight. This includes medical condition such as acid reflux (GERD), obstructive sleep apnea (OSA), joint and back pain, hernias, urinary stress incontinence, and obesity-hypoventilation syndrome. These medical conditions are caused by the mechanical force that the weight places on organs and joints. Another component of our health that can be affected by our weight is the psycho-social aspect of our health. Both the biomechanical and the psycho-social impacts of weight are important, but today, we will focus primarily on the metabolic complications, since these are caused, in part, by what happens when we exceed our fat storage capacity.
When we gain adiposity, for whichever reason, we are increasing the amount of fat in our adipocytes (fat cells). Specifically, we gain fat in out white fat cells, which are the main fat cells for energy storage (we also have beige and brown fat cells, which serve a different purpose). We have white adipose tissue under the skin (subcutaneous) and within our abdomen, surrounding the organs in our abdominal cavity (visceral fat). While it used to be thought that white fat cells (aka white adipose tissue, or WAT) were just there for storage of energy, we now know that it is one of our most active endocrine organs, meaning that it is an organ that secretes numerous hormones and other substances, to communicate with the rest of the body.
Our WAT has a limit to how much fat it can store, and again, this storage capacity varies from person to person. When our WAT is forced to expand beyond its capacity, things start to go wrong, and our fat cells become “sick”. We develop what is known as “sick fat disease” or “adiposopathy”. The blood supply to this WAT becomes strained, and our fat cells start to secrete substances that cause inflammation. They start to leak “free fatty acids”, or fats that are not safely contained in our fat cells, into the blood stream. We get an immune response to these “sick fat cells”. Our once healthy fat cells that were doing their job by safely storing fat as an energy reserve, and communicating nicely with the brain and the rest of the body about our energy storage, are not well and can’t function the way they are supposed to.
But there is another problem. Once our WAT stores are full and can’t expand any further, and we continue to produce fat, this excess fat has to be stored somewhere. This excess fat will now start to be stored in places where we should not have any, such as in and around the heart, the liver, the pancreas, and muscle. This fat is called “ectopic fat” because it is fat that is stored somewhere where it is not supposed to be.
Fat that gets deposited in our pancreas causes disruption in the function of the pancreas. The pancreas, amongst other things, produces insulin. Insulin is the hormone that is needed to prevent our blood glucose (aka blood sugar) from getting too high. We can only tolerate about a teaspoon of glucose in our entire bloodstream, so any glucose that is not used in our cells must be stored for another time. We can store around 1,000-2,000 Calories of glucose in the form of glycogen (the storage form of glucose) in our muscles and in our liver, but once those stores are full, any extra glucose is sent to the liver to be converted to fat. Insulin is the hormone that controls this process. Insulin is the hormone that controls fat metabolism, which is why it’s a hormone that you will hear me talk about a lot. When insulin is high, the body is in “fat storage mode”. When insulin is low, the body is in “fat burning mode”.
You may also have heard of “insulin resistance”, which is when the body stops listening to the insulin signal, and as a result, the pancreas has to produce more and more insulin for insulin to be able to do its job. Think of it as the body becoming hard of hearing when it comes to insulin, so the pancreas has to yell louder and louder for insulin’s signal to be heard. When someone develops insulin resistance, and their pancreas is required to make more and more insulin, this can lead to chronically high insulin levels, also known as hyperinsulinemia. You can imagine, that when insulin is constantly high, the person is constantly in fat storage mode. Interestingly, and perhaps not surprisingly, many people with obesity have chronically high insulin levels.
Let’s get back to ectopic fat in the pancreas: This abnormal fat accumulation in the pancreas contributes to insulin resistance and dysfunction of the cells that produce insulin (the beta cells of the pancreas). Insulin resistance is the first step towards developing type 2 diabetes. The pancreas can over-produce insulin for only so long before it starts to wear out. Ectopic fat in the pancreas contributes to the dysfunction of the pancreas, until slowly and over many years (often 10-20 years after the onset of insulin resistance), the pancreas can’t keep up with the insulin production any more, and that is when we start to see blood glucose levels rise above what is considered “normal”, and we see the beginnings or pre-diabetes, and eventually, type 2 diabetes.
What happens when excess fat accumulates in the muscle? Well, when this happens in a cow, we get a nicely marbled, juicy steak. You can actually see the fat mixed in with the muscle in the raw piece of meat (sorry for the visual to all of the vegetarians out there). This is what happens when we give these cows hormones and antibiotics to make them gain weight, feed them a starchy diet of corn instead of grass, and then limit their movement by packing them together in a feedlot.
Unfortunately, the same thing can happen to our own muscles as well. When this happens, we can develop insulin resistance in our muscle cells (which are big consumers of glucose) and disrupt the way our muscle cells use fat and glucose as a fuel source. It causes a breakdown in the part of our cells called the mitochondria, which are the little energy factories inside of our cells that turn glucose and fat into usable energy called ATP. When our mitochondria become dysfunctional, we can’t use fuels such as glucose and fat efficiency, meaning we can’t produce energy for our body to do all of the things it needs to do to keep us alive and to allow us to be active. When these little energy factories break down, the result is fatigue, weight gain, hunger, and essentially, the breakdown of our whole energy regulatory system. As a side effect of becoming dysfunctional, these little factories start to produce reactive oxygen species (ROS), which damage our cells and cause a slew of health problems. The take-away here: marbled muscles are not a good thing when it’s happening to YOU!
You may have heard the term “fatty liver”, and this, as the name implies, is when ectopic fat accumulates in the liver. This causes, you guessed it, insulin resistance in the liver. It also causes inflammation of the liver, oxidative stress (those ROS particles again), and causes dysfunction in the way that cholesterol is made in the liver. Yes, cholesterol is made in the liver, Some people assume that the cholesterol in our blood comes from the cholesterol that we eat, but only a small percentage of the cholesterol in your blood comes from your diet. Most of it is actually produced in the liver. The process of how cholesterol is made in the liver is complicated and goes beyond what we are discussing today, but know that the liver plays an important role in all of this, and that when fat accumulates in the liver, the production of cholesterol is affected. When a person develops insulin resistance, and can’t use glucose efficiently, or is consuming excess glucose, the liver converts that glucose to triglycerides (a fat), which is then shuttled off to be stored away safely in our fat cells. Unless of course, our fat cells are full or can’t take in these triglycerides quickly enough, in which case these triglycerides end up in our blood stream, causing high triglyceride levels. In addition to producing lots of fat in the form of triglycerides, the liver starts to produce small, dense LDL and small HDL. All of these factors together, along with increased abdominal fat and elevated blood pressure, result in what is called “metabolic syndrome”, which is a major risk factor for heart disease, cancer, and many other medical problems.
When fat accumulates in the kidneys, it can lead to kidney damage and high blood pressure. When fat accumulates in the heart and around blood vessels, it causes inflammation, calcification, and defects of the heart and blood vessels.
All these effects and more help explain why sick fat disease, or adiposopathy, can have such wide-spread and devastating health effects. This is why is makes no sense to treat the 236 medical complications associated with excess adipose tissue, such as type 2 diabetes, hypertension, hyperlipidemia, heart disease, kidney disease, and over 22 kinds of cancer, without treating the root cause of these conditions. It also helps us recognize that a person’s weight, BMI, or even body fat percentage, is not the best indicator for who develops metabolic disease. What we really need to be looking at is whether an individual is developing ectopic fat and visceral fat, since THAT is what is causing the metabolic problems.
And here is the great news: by treating the adiposopathy, or “sick fat”, ALL the other medical conditions will improve as well. We have learned so much about adiposopathy over the past 20 years, and we now have real, science-based solutions to help people with this complex medical condition. We have learned that just a 5-10% weight reduction can significantly impact metabolic health, because your brilliant body will preferentially burn off that ectopic visceral fat FIRST when you begin to lose adipose tissue. There is research supporting that specific nutrition, activity, sleep, and stress reduction can target this ectopic visceral fat!
We haven’t gotten to the part yet where we talk about ways to improve our health, but I hope that you are developing a better understanding of a topic that is often so poorly understood, even by most medical providers. Once we understand what is broken and why, we start to fix it.
Stay tuned for part 3 of this 3-part series on understanding weight: What happens when we lose weight?
Subscribe to our website at www.gaininghealth.com to be notified of all of our new content, and join our Facebook page at www.facebook.com/MyGainingHealth.