While previous research has found that obesity could increase dementia risk, new research suggests being ‘skinny fat’—slender without muscle tone—is actually deadlier than obesity. And a new study shows that it could be as bad for your brain as it is for your body. James Galvin, associate dean for clinical research at the Florida Atlantic University College of Medicine, found that people with sarcopenia, the natural loss of muscle mass that comes with age, were three to six times more likely to experience memory and thinking problems; those with sarcopenia and obesity were even more likely to experience these issues. Galvin believes developing individualized nutrition and exercise programs that help people increase or stabilize their muscle mass and lose weight could help prevent cognitive decline.
- Because your muscles regulate insulin levels to reduce your chances of developing diabetes, a risk factor for Alzheimer’s, and release chemicals that help the brain grow, the loss of muscle mass could lead to cognitive decline
- Being ‘skinny fat’ causes people to experience a decline in their executive functions, including attention, problem solving and decision making skills, according to Galvin’s 350-person study
- Participants in Galvin’s study who followed a personalized nutrition and exercise plan that aimed to reduce their ‘skinny fat’ showed improvement in their memory
Being Patient spoke to Galvin about ‘skinny fat,’ how muscle helps the brain and the impact getting in shape could have on cognitive abilities.
Being Patient: From a scientific perspective, what does it mean to be ‘skinny fat’?
Dr. James Galvin: The medical term for that is called sarcopenic obesity. Obesity means that your percent body fat is above the normal range. The sarcopenic part is a little harder to understand. Sarcopenia is age-related degeneration of your lean muscle mass. Your muscles are important because they give you strength to get around, but they also serve other functions: They help regulate your insulin levels so they can reduce your chance of developing diabetes and they release growth factors that support your brain health. When we talk about sarcopenic obesity, it’s people who are gaining fat and losing muscle. We use the term ‘skinny fat’ to help people grasp the concept. But we’re not talking about a super skinny person who doesn’t have a lot of muscle; these are people who don’t look obese. They’re a little overweight, look a little doughy and not very toned, but the bad combination is that they have fat and a lack of muscle. That’s where the problems come in.
Being Patient: Are people born this way or do they become more susceptible as they age?
Dr. James Galvin: They generally become more susceptible as they age. Some people have trouble building muscle; it’s a lifelong problem. There are certain body types that make it very difficult to do this; they’re called ectomorphs. They have very little muscle mass and that’s a lifelong thing. But we’re talking about someone who had a fairly normal muscle mass and then as they age, they start to lose muscle and gain fat. Unfortunately, a lot of people gain fat as they get older, but this combination could be potentially problematic.
We know that as people develop Alzheimer’s disease, they become less physically functional. We want to answer the other side of the chicken-and-egg question: Does the lack of physical activity increase the risk of Alzheimer’s disease?
Being Patient: Your study looked at why this condition is bad for our brains. Can you tell us about your research?
Dr. James Galvin: Instead of waiting for people to develop the disease and trying to do something about it, one of our goals is to figure out what causes them to get the disease and try to attack from that end. We’ve been interested in physical performance and the risk of Alzheimer’s disease. We know that as people develop Alzheimer’s disease, they become less physically functional. We want to answer the other side of the chicken-and-egg question: Does the lack of physical activity increase the risk of Alzheimer’s disease?
In our first study, we looked at a condition called sarcopenia, so just muscle mass by itself, and we found that people who have sarcopenia had a three- to six-fold increased risk of having problems with their memory and thinking. We’ve looked at obesity and we saw a mild effect, not a very strong effect, and that was a little bit different than some studies that showed obesity was a risk factor for Alzheimer’s disease. What happens if we break people into four groups: people who have normal fat and normal muscle, who we’ll call ‘normals’; people who have normal fat, but low muscle, or sarcopenia; people who have normal muscle, but high fat, or obesity; and people who have both low muscle or high fat, or sarcopenic obesity. We found something really interesting: The people who are purely obese but had normal muscle mass were just a little bit different than the healthy controls, but not by very much. The people who had sarcopenia had more problems, but the people who had both sarcopenia and obesity had a greatly increased risk of having difficulties with various cognitive functions, particularly problem solving executive kind of functions. So we think a lot of the studies that talked about obesity before were really talking about sarcopenic obesity, rather than just pure obesity because they never considered the role muscle may play.
Being Patient: What role does muscle play?
Dr. James Galvin: Muscle does a lot of important things. It helps us be physically fit and active. The muscle also releases chemicals that may help support the growth and health of other organs, like the brain. These are called trophic or growth factors and a normal function of muscle is to release these factors. The brain releases growth factors that then support muscle, so it’s a bidirectional relationship. We think as you lose muscle, you also lose the production of these growth factors and that may have consequences on brain function. When you combine that with fat, the adipose tissue—we think of adipose tissue as just fat, but as a metabolically active organ, it releases inflammatory markers—the fat releases compounds that are inflammatory and the muscle releases compounds that support growth. If you have more inflammatory markers and less growth factors, this may have really bad consequences on your overall brain health. We think that that’s the key that puts people at a great risk for developing diseases like Alzheimer’s.
Being Patient: Do people have different types of fat?
Dr. James Galvin: Yes. You can think about the fat in three pools. There’s something called ‘brown fat’; babies have more of this and this is the fat that allows you to shiver and helps maintain your body temperature. As we get older, we use most of the brown fat, but the brown fat is actually good for us. The rest of us have fat. We can think about that in two places. So there’s body fat; that’s the fat that is under your skin, the subcutaneous fat, so around your face, under your neck, in the folds of your arms and in your legs, and that appears as cellulite. Then there’s the fat that’s around the organs, so it’s on the inside and surrounds the heart, the lungs, the liver, the kidneys, and is called visceral fat. If you had to find a real villain, it’s the visceral fat. That’s the one that’s really causing a lot of problems and is metabolically active and releasing all of these inflammatory markers. That’s the one that’s really hard to lose.
Being Patient: Is visceral fat also more dangerous for our brains?
Dr. James Galvin: Yes. When we looked at the difference between your subcutaneous fat and your visceral fat, the culprit was the visceral fat. That’s where the action is occurring and unfortunately, that’s also the hardest pool of fat to lose. You can diet and lose the subcutaneous fat, but it’s much more difficult and you really have to restrict calories to get down on the visceral fat. That makes it a very difficult thing to lose once you start to build it.
Being Patient: When you reduce calories and carbohydrates to a point where you’re starting to burn energy from your fat cells, like on the ketogenic diet, does that come from your visceral fat?
Dr. James Galvin: Some of it may come from the visceral fat, but the body is a smart thing and it’s going to get energy from the easiest source, so if you are very low carb and switching to largely fat to supply energy, it will go to the readily accessible pool or a lot of your subcutaneous fat. It’s not easy to utilize the visceral fat; that’s what makes it so hard to lose.
Being Patient: When you were conducting these studies, how did you measure cognitive ability?
Dr. James Galvin: We used two ways to measure cognitive ability. One was interviews. We did detailed interviews with people and an informant, or someone who knows them well, and tried to capture how different they are now from the way they used to be, so it was a report-based assessment. Then we gave them pencil and paper tests which captured different domains of memory and thinking—problem solving, visual construction skills, math and language skills. We looked at different measures and the ones that were most associated with the problems with ‘skinny fat,’ or sarcopenic obesity, were the executive function, which controls problem solving skills.
Being Patient: How can we relate this type of information to the onset of a disease like Alzheimer’s?
Dr. James Galvin: While most people think about Alzheimer’s disease as a memory problem, it’s not just a memory problem; it really is affecting lots of domains. When you carefully study people for a long period of time, and you see what’s changing in people even before they become symptomatic, those executive skills, like attention, problem solving and decision making skills are one of the first domains to change. People don’t necessarily recognize that early on. They do recognize when, “Oh, I can’t remember that piece of information,” but that may not necessarily be the first feature. It may be this executive attention change that’s occurring and that’s what we found associated with the changes in body composition. That tells us that if we could come up with an intervention that could fix the body composition, we might be able to head off the very early signs of a disease like Alzheimer’s.
Being Patient: What’s more important for the brain: putting on muscle or losing fat?
Dr. James Galvin: The more difficult answer is that it’s both, so what we do during our assessments is to measure body composition and figure out what the idealized weight is. Of course, no one can hit their ideal, but it gives us a target, so when we model out what you are and what we’d like you to be, we can get an equation of how much fat you need to lose and how much muscle you need to gain. And of course, as soon as you lose a couple of pounds of fat, the equation shifts, so it’s not a defined number, but we can get an idea of what we need to do. That is talking about nutrition. I don’t like the word diet. Diets ultimately fail. People can’t diet forever, but they can take on a nutritional plan. So we talk a lot about nutrition and then we talk a lot about lifestyle and how we can increase your physical activity, and that’s a combination of exercise like treadmill running and lifting weights or using those resistance bands, or flexibility training. If flexibility is not in there, so yoga and tai chi, then you really don’t maintain the gains that you get from lifting. We talk about a balanced approach to physical activity and nutrition.
Being Patient: Are some people more susceptible to ‘skinny fat’ than others, or is it something you have complete control over with diet and exercise?
Dr. James Galvin: I learned a long time ago that I’m in complete control of almost nothing, so there are a lot of factors that come into play. I’m going to talk about genes in two ways: There are some genes that cause things, but those are rare. Then there are genes that increase your risk of something, which means that it isn’t necessarily going to happen, but it predisposes you to it, so you need to take a more active approach to try to battle that. If your parents were thin and muscular, you’re predisposed to being thin and muscular, but that doesn’t mean you will be. Likewise, if your parents were obese, that predisposes you to being obese, but it doesn’t mean you will be. A simple analogy is that if you look at all of the professional football players, many of their children don’t become professional football players. So while they have the good gene pool, that doesn’t always translate into them being the offensive lineman that their father was. So you have some traits that you can build upon, but it’s not a guarantee. We try to look at each person as an individual and then figure out how we can adjust that person’s risk factors.
Being Patient: How many people were in your study and what was their profile?
Dr. James Galvin: We recruited about 500 people into the study, but some of them had missing data points, so the paper we published had 353 people in it. They were pretty diverse, so roughly a third were Caucasian, a third were African American and a third were Hispanic. We had a nice racial and ethnic mix that allowed us to look at some of those features. We also studied both men and women. The mean age was in the 60s and it ranged from people in the mid-40s up to people in their 80s. By and large, they were either cognitively normal or they had some very mild cognitive changes. For the most part, we did not have people who had Alzheimer’s disease in this project because we were trying to figure out risk for Alzheimer’s disease.
If they follow the nutrition and exercise plan, and do some of the other things we talked about in the project, then we’re seeing that their memory is stabilizing or showing some improvement, and their weight goes down.
Being Patient: How long did you track the participants for?
Dr. James Galvin: We’ve been following people for several years, but this report is looking at their baseline exam, so their first examination, trying to understand risk factors and whether they’re normal, sarcopenic, obese or have ‘skinny fat.’ At that point, when we see you for the first point in time, how does that relate to how you’re going to do on your test? The data was collected over several years because it takes a while to evaluate over 500 people, but this study is a one time point study. We are now continuing that study and looking at, if we put people on different plans—exercise or nutritional plans—what happens to them. What’s not published, and I can tell you a little bit about that, is that the more people adhere to the plan we’re giving them, the better they do. If they follow the nutrition and exercise plan, and do some of the other things we talked about in the project, then we’re seeing that their memory is stabilizing or showing some improvement, and their weight goes down. Muscle mass is harder to gain as you get older, but they’re not losing any muscle, so they’re stabilizing that. If their muscle’s stable and their fat’s going down, then their condition of ‘skinny fat’ starts to improve.
Being Patient: How do we know this is not just because exercise is supposed to prevent brain diseases like Alzheimer’s?
Dr. James Galvin: Exercise potentially is a risk reducer for Alzheimer’s disease. I think the flipside is that there are many people who are athletes and exercise their whole lives, but develop Alzheimer’s disease. So exercise by itself isn’t going to be a cure. I think if people haven’t exercised, putting them on an exercise program has clear brain health and protective or preventative effects, but the activity by itself is not sufficient to eliminate the disease because then no athlete would ever develop Alzheimer’s disease and that’s not true. I think it’s a combination. Just like there are people who eat vegan, plant-based diets, have very low body fat, and some of them still develop Alzheimer’s disease. So it’s not just exercise, it’s not just body fat, there are a lot of factors. People aren’t experimental mice or rats. You can’t control everything about them. We try to identify things that we can have an impact on and to design interventions that address those things we can change, realizing there are things that I can’t change. I can’t change your age, your sex or your family history, but I can change your body fat, your muscle mass, your glucose levels and your insolence resistance. Those things we can do so we try to do that and see which combination seems to be the most powerful.
Being Patient: A lot of scientists say it won’t be just one magic pill that will prevent brain disease. Do you think reducing ‘skinny’ fat is just one factor? How much more evidence do we need and what do your findings mean in terms of future research?
Dr. James Galvin: It’s one piece of a big puzzle and our research has really shifted to the prevention side. I think that diseases like Alzheimer’s will be difficult if not impossible to cure, but I think it’s very likely we can prevent them. Benjamin Franklin said an ounce of prevention is worth a pound of cure back in the 1700s, which is absolutely true. Why wait for a disease to happen and then try to do something about it? Why not try to figure out what puts people at risk for disease and do everything we can to reduce that risk? Our program has really become looking at the person as an individual. Each person is their own experiment, essentially, and we develop a personalized risk profile, and then we use the principles of precision medicine, like they do in cancer therapy, to try and design a personalized prevention plan. That includes nutrition and exercise, but also cognitive activities, and it may include vitamin replacement, depending on what their needs are. It includes social engagement, psychotherapy, and it may include medicines. We might identify conditions that we didn’t know about and have to treat them. I don’t think that just exercising is going to be a cure. I don’t think that just eating good, healthy food is going to be a cure. I think our approach to these diseases is going to be a multi-modal approach.