(I attended a virtual, sponsored session, A Journey from Conversation to Care: Shaping Communication on Obesity, sponsored by Novo Nordisk. I was not asked to write or compensated to write this post.)
I bet we all know someone who has been on the roller coaster of weight loss:
Step 1: Pick a diet from the hundreds that are popular at any moment (Paleo, Keto, Atkins, South Beach, WW, Nutrisystem, etc.)
Step 2: Lose weight.
Step 3: Regain weight.
Step 4: For many, repeat steps 1-3.
Motivation to lose weight was high, the plan was easy to stick to, but rarely do we stay “on” the diet. And, then after the initial weight loss, our lost weight finds us! Why?
Why do we eat?
We eat for three main reasons, and all are regulated by our brain. We eat for hunger (called homeostatic eating) and that is our survival mechanism. We also eat for pleasure (called hedonic eating). Under this heading I would lump recreational eating. Ask yourself how many social events (back when we had social events) centered around food? Or how many times has the smell of freshly baked cookies called your name, even though you were not hungry?) And third, is the brain’s executive function in deciding to eat or not eat.
What drives the brain to regulate our food intake? The answer is hormones. Hormones are chemical messengers produced in one part of the body that get transported to another part where they regulate functions. For eating, hormones influence the brain to trigger either hunger (telling us to eat) or satiety (telling us we are full). Satiety hormones are produced in the intestines, the pancreas, and even in fat tissue; hunger hormones are produced in the stomach. Sounds simple: our brain tells us to eat or not, but in the disease of obesity and especially after weight loss, a dysregulation can occur.
Dr. Gabe Smolarz, an endocrinologist and obesity specialists describes it as the “push-pull” of weight loss. After weight loss, metabolism declines (leading to less calories or energy burned), hunger hormones increase (making you hungrier) and satiety hormones decease (making you feel less full.)
Where does that leave us? It’s important to remember that obesity is a disease (click here a previous post on the disease of obesity) and is caused by many factors: societal, environmental, and genetic. Our genetics contribute 40 to 70% of our risk for overweight and obesity and our environment can influence the expression of those genes. There is no arguing that we live in an obesogenic environment…plentiful, inexpensive, good tasting food and little motivation to be physically active. Layer in societal issues, such as no or poor access to health care, racial injustice, and income inequality and it isn’t a surprise that 100 million Americans (or 2 in 5 adults in the US) are living with obesity.
What can we do? We can recognize that obesity is a disease that needs long-term management. Many people living with obesity find it hard to have a conversation with their healthcare provider because they are often dismissed or simply told to “eat less and move more.” But that is still a good first step. The website The Truth About Weight gives tips on how to start the conversation, along with more information on obesity treatments and science of the disease. We can also lean in by helping to change how society sees, prevents, and treats obesity.
Two recent initiatives (supported by Novo Nordisk) are worth checking out. Healthy Women and Black Women’s Health Imperative have teamed up to empower and educate women across diverse communities about obesity health risks and treatment options.
Another great partnership is with the NFL Alumni Association. Check out the video, “Huddle Up—Let’s Talk About Obesity” encouraging men to act on learning about and treating obesity.
As Obesity Week has just concluded, let’s remember their slogan, “Every Body Needs Everybody,” to successfully treat obesity.
Chris Rosenbloom is a registered dietitian and nutrition professor emerita at Georgia State University. Check out her book, Food & Fitness After 50 and click here to follow her blog.
