Trauma doesn't just live in memory. It lives in the body — in a nervous system that never got the signal that it was safe to stand down. 

You may have come to Dr. Deepti Sharma looking for answers about your weight, your energy, your hormones, or your metabolic health. But in Part 2 of this series, she's going to ask you to look a little further back. In this she picks up where the ACEs conversation left off and goes deeper into what trauma actually does to human physiology. From the way chronic stress hormones reshape the brain and gut, to the downstream effects on inflammation, metabolism, and chronic disease risk — this episode makes the invisible visible. Dr. Sharma explains how unresolved trauma can look like anxiety, emotional eating, fatigue, autoimmune flares, or a body that simply won't respond the way it "should" — and why none of that is a character flaw.

She brings together neuroscience, the metabolic science, and the human experience into a single cohesive picture that is as clinically grounded as it is compassionate. Whether you're a patient trying to understand why your health feels so complicated, or a provider looking to deepen your trauma-informed lens, this episode gives you the framework to see it clearly.

Because for many people, the missing piece isn't a lab value or a medication dose — it's an understanding of how their history shaped their biology.

In this foundational episode, Dr. Sharma — triple board-certified physician, certified Menopause Practitioner, and certified life coach — unpacks adverse childhood experiences from the ground up. What counts as an ACE. Why the metabolic consequences of early trauma can look like willpower problems, lifestyle failures, or "unexplained" disease — and why that framing is wrong. ACEs aren't just a childhood story. They reshape the stress response, dysregulate the HPA axis, and leave a biological fingerprint that shows up decades later as chronic disease, metabolic dysfunction, and yes — obesity. In this broad overview episode, Dr. Sharma breaks down what ACEs actually are, how they wire the nervous system for survival in ways that can work against us in adulthood, and why understanding this science isn't about blame — it's about finally having a framework that makes sense of so much suffering.

Whether you're a patient trying to understand your own health history, or a clinician looking to bring more trauma-informed care into your practice, this episode meets you where you are.

This is the foundation. Stay tuned — the next episode goes deeper into what we can actually do with this knowledge.

In the next few episodes, I want to talk about the contributing factors or causes of obesity in detail. The number one thing is genetics. Genetic predisposition plays a foundational role, influencing metabolic processes, fat storage, and appetite regulation. However, genetics alone do not dictate outcomes. This introduces the concept of epigenetics, which refers to changes in gene expression due to environmental factors like diet, stress, and even prenatal influences. Think of genetics as the blueprint or instruction manual. Epigenetics is like a light switch that turns certain genes on or off.

Dysfunction within neurohormonal pathways disrupts the delicate balance of hunger and satiety signals, metabolic rate, and fat distribution. Hormones like leptin, ghrelin, insulin, and cortisol interact in ways that can drive excessive weight gain when dysregulated. This brings us to the set point theory of body fat mass, which suggests that our body has a predetermined range of fat mass or weight that it naturally tries to defend. Fat mass is a physiologically regulated phenotype, tightly regulated just like body temperature and pH. Obesity results from abnormal regulation of body fat mass, meaning changes in underlying biology lead the body to an elevated fat mass. This is why obesity is a disease.

When you lose weight, your body activates mechanisms to regain it, such as increasing hunger, reducing energy expenditure, and increasing cravings. Adipose tissue is not just a blob of yellow cushiony tissue. It's a powerful and dynamic organ producing over 600 adipokines or hormones, including leptin, adiponectin, resistin, and TNF-alpha. They drive hormone regulation and dysregulation, contributing to metabolic processes involved in appetite regulation, insulin sensitivity, inflammation, and the pathogenesis of heart disease, chronic disease, and cancer. Leptin is the satiety hormone that helps us feel full. However, too much leptin leads to leptin resistance, where the brain becomes resistant to the hormone's message, resulting in reduced satiety, overeating, and weight gain. Research shows that calorie-dense processed foods impair the brain's leptin signaling.

Insulin is another key player. When we eat calorie-dense meals, glucose rises rapidly, making the pancreas pump out insulin. Over time, with too much glucose and fat accumulating, insulin doesn't work as well, resulting in insulin resistance, the precursor to pre-diabetes and type 2 diabetes. Insulin is an anabolic hormone that signals the body to store fat and increase hunger. Other important gut hormones include ghrelin (the hunger hormone), GLP-1 and GIP (satiety hormones targeted by medications like Ozempic, Wegovy, Mounjaro, and Zepbound), glucagon (maintains blood glucose levels during fasting), and amylin (suppresses appetite and slows gastric emptying).

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Let's talk about what obesity actually does to your body — not to shame or scare you, but so you understand what's really at stake.

In this episode, I walk through the hard science: obesity is an independent risk factor for sudden and premature death. All-cause mortality increases progressively with higher BMI, especially once you cross a BMI of 30. In the U.S. alone, obesity contributes to an estimated 300,000 deaths annually. For those with severe obesity (BMI over 40), life expectancy can be reduced by 5 to 20 years.

But it's not just about lifespan — it's about how you live those years. Obesity affects every single organ system and is a central driver in the development of chronic diseases and 13 different types of cancer.

We cover it all:

• Cardiovascular disease: hypertension, coronary artery disease, stroke, heart failure, atrial fibrillation, peripheral vascular disease
• Metabolic disorders: type 2 diabetes, dyslipidemia, metabolic syndrome
• Respiratory issues: asthma, sleep apnea, hypoventilation syndrome
• Gastrointestinal & liver disease: gallstones, reflux, IBS, fatty liver disease
• Musculoskeletal problems: osteoarthritis, chronic pain, mobility issues, increased fall risk
• Cancer: 13 confirmed obesity-related cancers, including colorectal, breast, endometrial, pancreatic, and more
• Reproductive health: fertility issues, PCOS, erectile dysfunction, pregnancy complications
• Mental health: depression, anxiety, body image struggles, stigma, and discrimination in healthcare

This episode isn't meant to overwhelm you. It's meant to help you see why addressing obesity isn't about vanity — it's about protecting your health, your quality of life, and your future.

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Let's talk about just how big this problem really is — because the stats are staggering.

In 2022, 1 in 8 people globally were diagnosed with obesity. Adult obesity has more than doubled since 1990. Adolescent obesity? It's quadrupled.

Here in the U.S., the numbers are even more alarming: more than 2 in 5 adults (42.4%) have obesity, and 1 in 11 adults have severe obesity. Among children and adolescents aged 2-19, nearly 1 in 5 (19.3%) have obesity, and 6.1% have severe obesity. If you include the overweight category, nearly 75% of U.S. adults are affected.

And here's the kicker: despite decades of education about healthy eating and exercise, the numbers keep climbing. In fact, no country in the world has made significant progress in tackling obesity over the last 40 years.

So what are we doing wrong? Why is this epidemic continuing to grow despite everything we know?

That's the question we need to answer — and it starts with understanding that this isn't about individual failure. It's systemic. It's biological. It's environmental. And it requires a complete shift in how we approach prevention and treatment.

In the next episode, we'll dive into the consequences of not addressing obesity — and why taking action matters now more than ever.

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In this episode, let's talk about stress eating, also called emotional eating. It's when you eat in response to emotions rather than physical hunger. It's usually a way to cope with stress, anxiety, sadness, boredom, or even excitement.

Why does it happen? Stress triggers the hormone cortisol in our body, which increases appetite and cravings, especially for sugary, salty, or high-fat foods. Eating releases dopamine, the brain's feel-good chemical, giving temporary relief from emotional discomfort. Once your brain recognizes this pattern and associates food with pleasure and comfort, it forms a habit loop. Signs you might be stress eating include eating suddenly and urgently without much thought, craving specific comfort foods rather than balanced meals, eating even when you're full, and feeling guilt, regret, or sluggishness afterward.

How do you break the cycle? First, pause and check for hunger signals. Ask yourself: am I really hungry or am I seeking comfort? Identify your triggers by keeping a journal of what situations or emotions spark eating urges. For example, many women crave sugar during the premenstrual phase. Then find alternative coping mechanisms like taking a walk, deep breathing, stretching, listening to music, or talking to a friend. Managing stress proactively through regular exercise, good sleep, and mindfulness practices like meditation or prayer reduces cortisol levels over time. Creating a supportive food environment also helps: keep tempting trigger foods out of immediate reach and stock easy, healthy snacks like dates, nuts, or dark chocolate instead of cookies.

The bottom line: think of your emotional hunger like a smoke alarm. It's a signal that something's off emotionally, and food is just one possible fire extinguisher. You can choose other options that won't leave a mess behind or feelings of guilt afterward.

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In this episode, I'm talking about glycemic index. The glycemic index is a system that ranks carbohydrate foods based on how quickly they raise your blood sugar levels after being eaten. The scale typically ranges from 0 to 100, with higher values indicating foods that cause a rapid increase in blood glucose.

Imagine your body as a fireplace and food as the logs you throw in it. The glycemic index tells you how quickly the food will burn. High glycemic index foods (70 or above) cause a rapid spike in blood glucose. They're often low in fiber and quickly digested and absorbed. This food burns like dry kindling: quick energy, but the flames die down fast, which means you'll feel hungry or tired sooner. Examples include white bread, sodas, sweetened coffees and teas, sugary snacks, and many processed foods. Medium glycemic index foods (56 to 69) cause a moderate increase in blood glucose, burning at a steady pace. Examples include whole wheat products, sweet potatoes, sweet corn, bananas, and some types of rice. Low glycemic index foods (55 or less) cause a slow, gradual increase in blood glucose. Examples include most fruits, vegetables, legumes, whole grains, apples, and oats.

Why does it matter? Stable blood sugar equals steady energy and fewer crashes. Low glycemic index foods help maintain steady blood sugar levels, leading to better satiety and easier weight management because they keep you fuller for longer. Diets rich in low glycemic index foods are also better for your heart, helping manage cholesterol levels and reduce the risk of cardiovascular disease. Factors that influence the glycemic index include the type of carbohydrate, fiber content, preparation and cooking methods (al dente pasta has a lower GI than overcooked pasta), ripeness of fruits (ripe bananas have a higher GI than unripe bananas), and fat and protein content (combining carbs with fat or protein slows digestion and lowers the GI).

The bottom line: understanding the glycemic index can help you make informed choices about your diet, particularly if you're managing blood sugar levels or optimizing energy throughout the day. Our goal is to mostly consume low or moderate GI foods, or combine high GI foods with fat and protein to slow digestion.

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In this episode, Dr. Deepti Sharma sits down with Erica Rooney from Walk West to pull back the curtain on why this podcast exists — and what drives her work in obesity and lifestyle medicine.

You'll hear Dr. Sharma get personal about the patient story that changed everything, the 30-year-old with undiagnosed diabetes who passed away suddenly, leaving behind young children. That moment shifted her focus from treating illness to preventing it — and it's the reason she's here today.

This conversation covers the real stuff: how to fit exercise into an impossibly busy life (spoiler: gardening counts), why mental health is the starting point for all health changes, the two core nutrition principles that actually matter, and how to stop treating movement like a separate chore on your to-do list.

Dr. Sharma also tackles the stigma around obesity head-on — why it's a chronic neurohormonal disease rooted in genetics and biology, not a moral failure. And why creating a safe, shame-free space for her patients is the foundation of everything she does.

If you've ever felt overwhelmed by conflicting health advice, stuck in patterns you can't break, or like you're failing because you "know what to do but can't do it" — this episode is for you.

🌐 Learn more at weightandmetabolism.com

In this episode, we're talking about metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO). These terms describe different metabolic profiles in people with obesity. Despite similar BMI, these two categories differ significantly in terms of their risk for developing obesity-related complications like cardiovascular disease, type 2 diabetes, and other metabolic disorders.

Individuals with metabolically healthy obesity have a BMI in the obese range, but they don't exhibit the metabolic complications typically associated with obesity. They have normal blood pressure, normal insulin sensitivity, normal blood glucose and cholesterol, lower levels of visceral fat (fat around internal organs), more subcutaneous fat (fat under the skin), and lower levels of inflammation. Although these individuals are at lower risk for metabolic complications than their metabolically unhealthy counterparts, they're still at higher risk than individuals with normal BMI. And over time, they can transition to metabolically unhealthy obesity.

Metabolically unhealthy obesity is characterized by elevated blood pressure, fatty liver, high cholesterol, borderline diabetes, elevated fasting glucose, higher levels of visceral fat, chronic inflammation, and insulin resistance. Individuals with MUO are more prone to develop obesity-related complications like type 2 diabetes and cardiovascular disease.

The bottom line: understanding the difference between MHO and MUO helps us tailor medical and lifestyle interventions. While metabolically healthy obesity might suggest a lower immediate health risk, it does not mean there's no risk at all. Both groups benefit from lifestyle changes like improved diet, increased physical activity, and weight management. From a treatment standpoint, metabolically healthy obesity is the right time to intervene and prevent metabolically unhealthy obesity. Our goal as physicians is to intervene before microvascular damage starts.

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Diagnosing and treating obesity is really challenging due to a variety of barriers that can be broadly categorized into patient-related, healthcare provider-related, and systemic barriers. Let's break them down.

Patient-related barriers include stigma and shame, which deter people from seeking help. Lack of awareness means some don't recognize they have obesity or underestimate the health risks. Psychological factors like depression, anxiety, and eating disorders complicate treatment. And misinformation makes it difficult to know what strategies are effective and safe. Healthcare provider-related barriers include lack of adequate training in obesity management, bias and stigma within the healthcare system, time constraints in busy clinical environments, and communication challenges because discussing weight is a sensitive topic.

Systemic and environmental barriers are significant. Insurance coverage for obesity treatment is often inadequate or nonexistent. Geographic, economic, and cultural barriers limit access to healthcare providers, healthy food options, and safe places for physical activity. Social determinants of health like poverty, education level, and food insecurity make it difficult to adopt healthy lifestyles. Cultural perceptions also play a role. In some cultures, higher body weight is not viewed negatively or is even considered desirable. For example, in the Indian community, an obese child is often considered a healthy child. Treatment-specific barriers include long-term adherence challenges, the complexity of obesity as a multifactorial condition, and side effects or complications from medications and bariatric surgery.

The bottom line: overcoming these barriers requires education and awareness to reduce stigma, provider training to improve care, policy and systemic changes to expand insurance coverage and access to healthy foods, and patient-centered care that tailors treatment plans to individual needs and provides ongoing support. By addressing these barriers, the healthcare system can more effectively diagnose, treat, and manage obesity, leading to better health outcomes for individuals and communities.

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