When it comes to choosing the best diet for overall health, the Mediterranean diet has topped the list again in 2025. It’s easy to see why: it’s simple, it’s sustainable, and it delivers proven health benefits. Are you looking to manage your weight, reduce your risk of heart disease, or improve your gut health?  The Mediterranean diet offers a balanced, flexible approach to eating.

The Mediterranean diet was originally based on the eating habits of countries like Greece, Italy, and Spain. But here’s the key: it’s not just about eating food from these regions. The Mediterranean diet is more of an eating pattern—one that focuses on fresh, whole foods, a variety of plant-based ingredients, lean proteins, and healthy fats. This diet encourages you to eat fruits, vegetables, whole grains, legumes, nuts, and seeds while making olive oil your primary fat source. Fish is a star in this diet, while dairy and red meat are enjoyed in moderation.

The Mediterranean diet isn’t about following a strict menu or buying expensive specialty ingredients. It’s about focusing on whole, nutrient-dense foods and following an algorithm: more plants, more healthy fats, and fewer processed foods. It’s not a fad—it’s a way of life that’s been proven to improve long-term health.

So, why is the Mediterranean diet still ranked #1 for 2025 by experts like U.S. News & World Report? Here’s why:

1. Supports Heart Health
2. The Mediterranean diet is packed with healthy fats, like olive oil and fatty fish (think salmon and sardines), which are known to reduce inflammation and lower cholesterol levels. Studies have shown that this diet can lower the risk of heart disease and stroke by improving blood pressure and supporting healthy arteries.
3. Controls Blood Sugar
4. If you have diabetes or prediabetes, the Mediterranean diet is a fantastic choice. It helps regulate blood sugar levels, improving insulin sensitivity, and preventing blood sugar spikes that can cause problems over time.
5. Improves Gut Health
6. The Mediterranean diet is rich in fiber from fruits, vegetables, and whole grains, which are essential for a healthy gut. A healthy gut microbiome can help with digestion, boost immunity, and even improve your mood.
7. Fights Inflammation
8. Chronic inflammation is at the root of many diseases, including arthritis and certain cancers. The Mediterranean diet’s focus on antioxidant-rich foods (like leafy greens, tomatoes, nuts, and fatty fish) helps reduce inflammation in the body.

The Mediterranean diet isn’t just popular because it sounds good—it’s backed by science. Multiple studies have shown its effectiveness in:

• Lowering Cholesterol
• The diet’s high intake of heart-healthy fats like olive oil and fatty fish helps reduce LDL (bad) cholesterol while increasing HDL (good) cholesterol. This supports better heart health and lowers the risk of heart disease.
• Preventing Cognitive Decline
• Research has shown that the Mediterranean diet may help protect against Alzheimer’s disease and other forms of cognitive decline by promoting brain health with its antioxidants and healthy fats.
• Maintaining a Healthy Weight
• While the Mediterranean diet isn’t necessarily a “weight loss diet,” it encourages eating nutrient-dense foods that keep you feeling fuller for longer. This can help prevent overeating and support long-term weight maintenance.

It’s easy to get started with the Mediterranean diet. Here’s how you can structure your meals:

• Fruits and Vegetables: Aim for at least 9 ounces (250 grams) of vegetables and 2 servings of fruit per day. Vegetables should be the focus of your meals, while fruits can be enjoyed as snacks or desserts.
• Whole Grains: Consume 9 ounces (250 grams) of whole grains daily. Choose options like brown rice, quinoa, and whole wheat bread for fiber and energy.
• Legumes: Incorporate at least 2 ounces (56 grams) of beans, lentils, or chickpeas into your meals every day. These are a great source of plant-based protein and fiber.
• Healthy Fats: Use olive oil as your primary fat source—about 2 to 4 tablespoons per day. Also, aim for two servings of fatty fish per week, like salmon or sardines.
• Dairy: Dairy is allowed but should be moderate. Stick to low-fat options like Greek yogurt and cheese, and limit portion sizes.
• Alcohol: If you drink alcohol, limit it to one 5-ounce pour of red wine per day, preferably with meals. Excessive alcohol consumption is discouraged in the Mediterranean diet.

While the Mediterranean diet is all about variety and balance,unlike the Carnivore Diet.  The Carnivore diet focuses on eliminating most food groups entirely—specifically plant-based foods. The Carnivore Diet is an extreme approach that promotes only animal products, which means no fruits, vegetables, grains, or legumes.

Despite its growing popularity, the Carnivore Diet is not recommended for long-term health. Here's why:

• Lacks Nutrients
• The Carnivore Diet lacks many essential nutrients found in fruits, vegetables, and grains, including fiber, vitamins, and minerals. Over time, this can lead to deficiencies and negatively impact your health.
• Increases Risk of Chronic Diseases
• Diets high in red and processed meats are linked to an increased risk of heart disease, cancer, and diabetes. The Carnivore Diet’s heavy reliance on meat and fat can lead to elevated cholesterol and higher inflammation levels in the body.
• Not Sustainable
• The Carnivore Diet is extremely restrictive and difficult to follow long-term. Most people don’t want to give up entire food groups, especially ones that offer important health benefits.

The Carnivore Diet is a fad diet at best. It’s not based on science and doesn’t provide a balanced approach to long-term health. For a diet that’s sustainable, nutritious, and scientifically backed, stick to the Mediterranean diet.

Myth: The Mediterranean Diet is Just About Olive Oil and Fish

• Olive oil and fish are key components, but the Mediterranean diet is much more. It’s about eating more fruits, vegetables, legumes, and whole grains. These foods provide the bulk of your daily nutrition.
• Myth: It’s Too Expensive
• Do you think Mediterranean-style means spending a fortune? Some ingredients like olive oil and fatty fish can be expensive, you don’t need to break the bank. Buy seasonal, local produce and canned legumes to keep costs low.
• Myth: Mediterranean Cuisine is Only for Mediterranean Countries
• You don’t need to live in the Mediterranean to follow this diet! Adapt Mediterranean principles to any cuisine. Make a fish taco made with whole grain tortillas, grilled fish, and fruit salsa and you have a  Mediterranean-inspired meal. Even Indian cuisine can be adapted to the Mediterranean diet with dishes like Chana Masala made with chickpeas, spices, and whole wheat roti.

The Mediterranean diet continues to be the best choice for 2025 and beyond. Its benefits for heart health, weight management, and disease prevention are backed by science, and its flexibility makes it easy to follow long-term. Plus, it’s not about eliminating food groups—it’s about making healthy, sustainable food choices that nourish your body.

So, if you’re looking to improve your health and eat a balanced, flavorful diet, the Mediterranean diet is the way to go. It’s not just a trend—it’s a lifestyle that’s proven to work.

Bird flu, or highly pathogenic avian influenza (HPAI), has far-reaching effects on public health, the food supply, and even the global economy. While human-to-human transmission hasn’t occurred, its potential to mutate poses significant concerns. Understanding how bird flu impacts us today — and how science is working to mitigate its risks — is essential.

In this blog post, we’ll explore the realities of bird flu, its effects on food prices, the role of vaccines, and practical tips to stay safe. Let’s break it down into manageable pieces so you’re fully informed.

Bird flu primarily affects birds, especially poultry, like chickens and turkeys. However, certain strains, such as H5N1, have occasionally infected humans. While these cases are rare, they carry a high mortality rate of over 50%, making the virus particularly dangerous if contracted.

Here’s the good news: Bird flu isn’t currently spreading from person to person. The bad news? Experts worry about a process called reassortment, where bird flu and human flu viruses could mix in someone infected with both. This could result in a highly contagious and deadly strain capable of causing a pandemic.

Despite some conspiracy theories, no laboratory is working on gain-of-function research to make bird flu more transmissible. These myths are counterproductive, distracting from real medical efforts to monitor and control the virus.

If you’ve noticed higher prices at the grocery store, bird flu is partly to blame. The virus has disrupted the poultry industry and the broader food supply chain.

When bird flu outbreaks occur, millions of chickens are culled to prevent the virus from spreading. This reduction in supply causes egg prices to skyrocket, leaving many of us paying more for our morning omelets.

Bird flu also affects dairy products. The demand for poultry feed drives up costs for dairy farmers, who often rely on the same feed. Additionally, in rare cases, parts of the bird flu virus have been detected in raw milk. This is yet another reason to avoid raw, unpasteurized milk and stick to pasteurized dairy products for safety.

Vaccines are at the heart of our response to bird flu, but they serve different purposes for birds and humans.

Scientists are developing vaccines for poultry to control the virus in bird populations. These vaccines could:

• Reduce the need for mass culling.
• Lower the economic impact on the poultry industry.
• Decrease the risk of the virus spilling over into humans or other animals.

While these efforts are promising, it will take time before poultry vaccines are widely implemented.

For humans, H5N1 vaccines are available for at-risk workers like poultry farmers and wildlife handlers. However:

• These vaccines are strain-specific and may not protect against a mutated strain.
• They are not available to the general public.
• In the event of a pandemic, new vaccines would need to be developed, which takes time.

You might wonder, “If the flu shot doesn’t protect against bird flu, why get it?” The answer lies in preventing co-infections.

When someone is sick with both seasonal flu and bird flu, there’s a risk the two viruses could mix, creating a new, more dangerous strain. By getting your flu shot, you reduce your chances of catching seasonal flu, which helps minimize this risk. Remember, vaccines are not about completely preventing illness; they’re about reducing severe outcomes like hospitalization and death.

Whether you’re a hunter, backyard birder, or just someone who loves eggs, here’s how to reduce your risk:

• Avoid handling sick or dead birds. Report them to local authorities.
• Use gloves and masks when field dressing game, and disinfect tools afterward.
• Cook wild birds to an internal temperature of 165°F (73.8°C) to kill viruses.

• Clean bird feeders and baths regularly with soap and disinfectant.
• Avoid contact with bird droppings; wear gloves during cleaning.
• Keep pets, especially cats, away from areas frequented by wild birds.

Cats are surprisingly vulnerable to bird flu. They can contract the virus by hunting infected birds or contacting bird droppings. To protect your pets:

• Keep cats indoors during outbreaks.
• Monitor them for symptoms like lethargy or respiratory distress.
• Consult a vet if your cat shows any signs of illness.

• Always cook poultry and eggs thoroughly to an internal temperature of 165°F (73.8°C).
• Avoid raw, unpasteurized milk and stick to pasteurized dairy products.
• Wash your hands thoroughly after handling birds or poultry products.

In science, recommendations change as we learn more. This isn’t a sign of uncertainty but a testament to how science adapts to new evidence. The same applies to vaccines — their primary purpose is to prevent severe illness and death, not to guarantee you won’t get sick. Trust in the scientific process is vital as we navigate complex challenges like bird flu.

Bird flu isn’t just a health issue; it’s a food and economic issue, too. The virus has already disrupted poultry and dairy markets, and its potential to mutate keeps public health experts on high alert. Fortunately, science is actively working on solutions, from vaccines to monitoring programs.

For regular updates on bird flu, follow me on TikTok and Instagram at @drterrysimpson, where I share timely insights and tips. And don’t forget to subscribe to my podcast, Fork U, for in-depth discussions about science, health, and smart eating.

Bird flu poses significant challenges, but by staying informed and following practical steps, we can protect ourselves and our communities. Whether it’s understanding vaccine roles, debunking myths, or adapting to rising food prices, knowledge is the first line of defense.

Thank you for reading! Stay safe, stay informed, and remember that prevention is the best recipe for a healthy life.

Navigating GLP-1 Medications and Building a Healthier You: A Fork U Guide

Welcome to Fork University, where science meets sarcasm, and healthy eating gets a reality check. Today, we’re diving into the world of GLP-1 medications, like Ozempic and Zepbound—those little injections making waves in the weight loss and metabolic health scene. Spoiler alert: Even if needles aren’t your thing, this advice is gold for anyone looking to improve their relationship with food (yes, even you, cereal-at-midnight enthusiasts). So, grab a cup of tea (ginger if you’re nauseous), and let’s get started.

Ah, diet culture. That pesky little voice whispering, “Carbs are evil,” or “You’re only worthy if you can squeeze into those jeans from 2012.” Here’s the deal: Diet culture sucks, and it’s time to boot it out of your life. Here’s how:

1. Focus on Health Over Appearance
2. “Strong, not skinny” isn’t just a gym bro mantra. Celebrate wins like better blood sugar control or climbing stairs without feeling like you ran a marathon.
3. Neutralize Food Labels
4. No food is inherently “good” or “bad.” (Except maybe that mysterious gas station sushi. Proceed with caution.) All foods can fit into a balanced diet—just maybe not all at once.
5. Ditch Unrealistic Media
6. Swap those Instagram influencers with body-positive accounts. Life is too short for filter-fueled comparisons.

GLP-1 medications are game-changers, but they come with their quirks. Here’s how to navigate the rocky road of side effects:

Fun fact: Only 10% of Americans eat enough fiber. No wonder our colons are grumpy. Fix that with:

• Whole Grains: Brown rice, quinoa, oats—because white bread is so 1990.
• Legumes: Beans, chickpeas, lentils—fiber heroes and fart-inducing legends.
• Supplements: Citrucel or Metamucil work in a pinch, but food first!

Not all hydration packets are created equal. Skip the sugar-free gimmicks and opt for options like Pedialyte. Bonus points if you grab the popsicles—because who doesn’t love reliving childhood?

High-fat foods + GLP-1 = a stomach rebellion. Swap fried chicken for grilled and save yourself the bloat. Greek yogurt and peppermint tea are your new besties.

Forget the “eat less, move more” mantra. Here’s what actually works:

1. Mindful Portions
2. At restaurants, box up half your meal right away. Or embrace the kids’ menu—yes, you might even score a toy.
3. Protein with Purpose
4. Greek yogurt, beans, and protein shakes are your go-tos. But don’t let diet culture trick you into thinking protein is the only macronutrient that matters.
5. Celebrate Non-Scale Victories
6. Fitting into old jeans? Amazing. Cooking a new recipe? Even better. Toss the scale if it’s ruining your day—you’re more than a number.

GLP-1 medications are tools, not magic wands. They’re here to help you build a healthier relationship with food, not to police your every bite. Remember:

• Moderation Wins: That scoop of ice cream isn’t your downfall. Balance it out with nutrient-rich meals.
• Be Patient: Rapid initial weight loss (thanks, glycogen, and water) will slow, but consistency pays off. A pound a week equals 52 pounds a year. Do the math and cheer yourself on.

GLP-1 medications are here to support you, not define you. Focus on health, ditch the guilt, and enjoy the journey. And don’t forget: Consult a real, western-trained physician and a dietitian. Chiropractors and green juice influencers don’t count. Ok, I sometimes drink some green juice.

Weight loss is often the first thing people think about when starting GLP-1 medications like semaglutide or liraglutide. These medications are powerful tools for helping manage appetite and regulate the body’s hunger hormones. But here's the real truth: losing weight is just one part of the story. To truly thrive, you need to focus on eating in a way that nourishes your body, supports your health, and promotes long-term well-being.

Think of it this way: GLP-1 medications do the heavy lifting when it comes to managing hunger and cravings. Your job is to provide the right fuel for the machine. You’re not eating to lose even more weight—you’re eating to support your body so it runs like a high-performance car.

When you’re on GLP-1 medications, weight loss isn’t a result of extreme dieting or restrictive food rules. These medications work by regulating your appetite, making it easier to avoid overeating and stick to reasonable portions. They help your biology work with you instead of against you.

So, if the medication is doing most of the work, why does your diet matter? It’s simple: food is what keeps your body functioning at its best. While GLP-1 helps control hunger, what you eat still determines your energy levels, heart health, mental clarity, and long-term disease risk.

Instead of focusing on cutting calories, the goal should be to pack every meal with nutrients that fuel your body and help it recover from the years of stress and inflammation caused by poor eating habits. This isn’t about restriction—it’s about nourishment.

When it comes to eating for long-term health, the Mediterranean diet is one of the best approaches. It’s not a restrictive diet where you count every calorie or ban entire food groups. Instead, it’s a way of life, focusing on fresh, whole foods that nourish your body and taste great.

The Mediterranean diet emphasizes vegetables, fruits, whole grains, healthy fats like olive oil, lean proteins, and a little bit of red wine. Yes, wine! Studies have consistently shown that people who follow this diet reduce their risk of heart disease, diabetes, and even cognitive decline (Estruch et al., 2013; Singh et al., 2022).

What makes this diet so effective? It’s packed with anti-inflammatory foods that stabilize blood sugar, protect your heart, and even support a healthy gut. A healthy gut, in turn, improves everything from digestion to mental health. Plus, the Mediterranean diet is enjoyable and sustainable—no weird powders, no flavorless meals, just real food.

Olive oil is the cornerstone of the Mediterranean diet. This liquid gold is rich in healthy monounsaturated fats and compounds that act like natural anti-inflammatories, similar to ibuprofen (reference here). Add in fish like salmon and sardines, which are full of omega-3 fatty acids, and you’ve got a winning combination for your heart and brain.

Protein is important, especially for preserving muscle mass while losing weight. But many people fall into the trap of making protein the center of every meal, ignoring the other nutrients their body needs. Loading up on chicken breasts and protein shakes might seem like a good idea, but it leaves little room for the variety that keeps your meals balanced.

Here’s the good news: with a Mediterranean-style diet, you can get plenty of protein from diverse sources. Legumes like lentils and chickpeas are not only high in protein but also rich in fiber, which helps with digestion and keeps you full longer. Fish, especially fatty fish like salmon or mackerel, provides protein alongside heart-healthy omega-3s. Even red meat is allowed—just keep it to about 4 ounces a day, roughly the size of a deck of cards.

The key is to think beyond animal proteins. A balanced plate includes plenty of plant-based options, ensuring you get a variety of vitamins, minerals, and antioxidants. This diversity supports your overall health and keeps your meals exciting.

If the Mediterranean diet feels too free-spirited for you, consider the DASH diet (Dietary Approaches to Stop Hypertension). DASH emphasizes fruits, vegetables, whole grains, and lean proteins while keeping sodium intake low. It’s designed to lower blood pressure, but it also reduces the risk of heart disease and supports weight loss. (reference click here)

Like the Mediterranean diet, DASH isn’t about counting calories or cutting out entire food groups. It focuses on nutrient-dense, whole foods that fuel your body. For people on GLP-1 medications, DASH is an excellent choice because it reduces the risks associated with metabolic conditions like high blood pressure and insulin resistance.

Weight loss might be your current goal, but the long-term focus should be on living a healthier, longer life. That’s where the Blue Zones come in—regions of the world where people live to 100 and beyond. Their secret isn’t just genetics; it’s their diet and lifestyle.

Blue Zone diets are plant-forward, filled with vegetables, legumes, whole grains, and healthy fats. Meals are simple, minimally processed, and often enjoyed with family and friends. These communities teach us that eating well isn’t about obsessing over macronutrients—it’s about creating habits that support your body over a lifetime.

In Okinawa, Japan, for example, people eat a diet rich in sweet potatoes, tofu, and seaweed, and they follow the principle of hara hachi bu, or stopping when they’re 80% full. This practice prevents overeating and ensures they maintain a healthy weight without ever going hungry. Reference click here

If you’re on GLP-1 medications and want to focus on long-term health, here are some tips to get you started:

• Make Vegetables the Star: Fill at least half your plate with colorful veggies. They’re packed with nutrients and low in calories.
• Choose Whole Grains: Swap out refined carbs like white bread and pasta for quinoa, brown rice, or whole-grain options.
• Enjoy Healthy Fats: Use olive oil liberally, snack on nuts, and add avocado to your meals. These fats are essential for brain and heart health.
• Diversify Your Protein: Include a mix of lean meats, fish, legumes, and nuts. Aim for variety rather than relying on one source
• Focus on Balance, Not Perfection: Follow the 80/20 rule—eat well most of the time, but don’t sweat the occasional treat. A slice of pizza or scoop of gelato won’t derail your progress.
• The Big Picture: Nourish, Don’t Restrict
• GLP-1 medications make it easier to manage your weight, but the real magic happens when you pair them with a diet that supports your health. The focus isn’t on eating less—it’s on eating smarter. By following a Mediterranean or DASH-style diet, you can give your body the nutrients it needs to thrive while enjoying food that tastes amazing.

Remember, this isn’t just about what the scale says. It’s about feeling energized, reducing your risk of chronic diseases, and setting yourself up for a healthier future. So, grab a plate of roasted veggies, drizzle on some olive oil, and toast to your long-term health. Your body will thank you for it.

Gantenbein KV, Kanaka-Gantenbein C. Mediterranean Diet as an Antioxidant: The Impact on Metabolic Health and Overall Wellbeing. Nutrients. 2021 Jun 6;13(6):1951. doi: 10.3390/nu13061951. PMID: 34204057; PMCID: PMC8227318.

Filippou CD, Tsioufis CP, Thomopoulos CG, Mihas CC, Dimitriadis KS, Sotiropoulou LI, Chrysochoou CA, Nihoyannopoulos PI, Tousoulis DM. Dietary Approaches to Stop Hypertension (DASH) Diet and Blood Pressure Reduction in Adults with and without Hypertension: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Adv Nutr. 2020 Sep 1;11(5):1150-1160. doi: 10.1093/advances/nmaa041. PMID: 32330233; PMCID: PMC7490167.

Santacroce L, Bottalico L, Charitos IA, Haxhirexha K, Topi S, Jirillo E. Healthy Diets and Lifestyles in the World: Mediterranean and Blue Zone People Live Longer. Special Focus on Gut Microbiota and Some Food Components. Endocr Metab Immune Disord Drug Targets. 2024;24(15):1774-1784. doi: 10.2174/0118715303271634240319054728. PMID: 38566378.

Grosso G, Laudisio D, Frias-Toral E, Barrea L, Muscogiuri G, Savastano S, Colao A. Anti-Inflammatory Nutrients and Obesity-Associated Metabolic-Inflammation: State of the Art and Future Direction. Nutrients. 2022 Mar 8;14(6):1137. doi: 10.3390/nu14061137. PMID: 35334794; PMCID: PMC8954840.

Singh, B., et al. (2022). "Mediterranean Diet and Cognitive Function: A Systematic Review." Nutritional Neuroscience.

For years, obesity has been misunderstood, oversimplified, and even stigmatized. It's been framed as a personal failing, a lifestyle choice, or simply a matter of "eating less and moving more." But science tells a different, more nuanced story—one where our brains, biology, and ultra-processed food environment play starring roles. And thanks to groundbreaking medications like GLP-1 drugs, we’re gaining a clearer picture of how obesity works and how to treat it.

Let’s dive into why obesity is a disease, how ultra-processed foods exacerbate it, and why we need to ditch the harmful myth that obesity is a lifestyle choice.

"Just eat less and move more." It’s the phrase everyone loves to repeat—and no one finds helpful. This simplistic advice ignores the reality that obesity is not merely about calories in and calories out. It’s about a complex interplay between your biology, brain chemistry, and environment.

Obesity isn’t a character flaw or a lack of willpower. If it were, we wouldn’t see an obesity epidemic in societies flooded with cheap, ultra-processed foods engineered to make us eat more. These foods hijack our biology, overpowering the mechanisms our bodies use to regulate hunger and fullness.

Our brains evolved to keep us alive in times of scarcity. Back in the caveman days, this was helpful. Today, it’s less so because our brains are still wired to seek out high-calorie foods to avoid starvation—even when we’re surrounded by abundance.

When you eat ultra-processed foods, they light up the reward centers in your brain like a Christmas tree. These foods—laden with sugar, fat, and salt—trigger the release of dopamine, the same neurotransmitter involved in addiction. It’s no wonder we keep going back for more.

Adding to the complexity, hormones like ghrelin (the "hunger hormone") and leptin (the "fullness hormone") can go haywire in people with obesity. Ultra-processed foods amplify ghrelin’s effects, making you feel hungrier while reducing your sensitivity to leptin, so you never feel full. It’s a biological double whammy.

Citation: Studies show that diets high in ultra-processed foods increase calorie consumption by about 500 calories per day compared to diets of unprocessed foods (Hall et al., 2019).

Here’s where things get interesting: GLP-1, or glucagon-like peptide-1, is a hormone that helps regulate appetite. It tells your brain, “You’re full; you can stop eating now.” But for many people with obesity, this system doesn’t work properly. Their brains don’t get the message, leading to overeating.

Enter GLP-1 receptor agonists like semaglutide and liraglutide—medications that mimic the effects of GLP-1. These drugs help regulate appetite, making people feel full sooner and reducing cravings. The results have been extraordinary: clinical trials show average weight loss of 15% or more with these medications, far outpacing what’s possible with lifestyle changes alone.

These drugs have done more than help people lose weight—they’ve also shifted the way we think about obesity. They show that obesity is a medical condition influenced by hormones and brain chemistry, not just a matter of willpower.

Citation: Clinical trials on GLP-1 receptor agonists show significant and sustained weight loss, with participants losing 15% or more of their body weight (Wilding et al., 2021).

The idea that obesity is a "lifestyle choice" is not only incorrect—it’s harmful. Framing obesity this way ignores the biological, genetic, and environmental factors that contribute to it. Worse, it stigmatizes people with obesity, making them feel like they’re to blame for their condition.

Obesity meets all the criteria for a chronic disease: it has a defined pathology (dysregulation of appetite and metabolism), it leads to complications (diabetes, heart disease, etc.), and it requires long-term management. Lifestyle factors like diet and exercise can influence obesity, but they’re not the sole cause. Blaming someone for their obesity is like blaming someone with asthma for living in a polluted city.

Citation: The American Medical Association classified obesity as a chronic disease in 2013, recognizing it as a condition requiring medical treatment (AMA, 2013).

If obesity is a fire, ultra-processed foods are the gasoline. These foods are engineered for maximum palatability, combining sugar, fat, and salt in ways that overwhelm our natural appetite-regulation systems. They’re calorie-dense, nutrient-poor, and often stripped of fiber, which would otherwise help us feel full.

Even worse, ultra-processed foods alter the way our brains respond to food. They increase cravings, reduce satiety, and encourage overeating. Over time, this can lead to weight gain and metabolic issues, creating a vicious cycle that’s hard to break.

Citation: Research shows that people who consume diets high in ultra-processed foods are more likely to develop obesity and metabolic diseases (Monteiro et al., 2018).

GLP-1 drugs have given us new tools to treat obesity—and new insights into its underlying causes. They’ve proven that obesity isn’t just about behavior; it’s about biology. When you treat obesity like a disease rather than a moral failing, people get better.

But these medications are just one piece of the puzzle. To tackle obesity on a larger scale, we need to address the broader food environment. That means making healthy, unprocessed foods more accessible, reducing the marketing of ultra-processed foods, and investing in public health initiatives that promote nutrition education.

Let’s address the elephant in the room: fat shaming. The idea that you can "shame" someone into losing weight is not only cruel—it’s ineffective. Research shows that weight stigma leads to stress, low self-esteem, and even more weight gain. It’s a lose-lose situation.

Instead of shaming people for their weight, we need to focus on creating supportive environments that help everyone make healthier choices. That includes treating obesity as the complex, multifactorial disease that it is—not a personal failure.

Citation: Weight stigma is associated with increased psychological distress, unhealthy eating behaviors, and reduced motivation for physical activity (Puhl & Heuer, 2010).

Here’s how we can start to shift the conversation around obesity:

Acknowledge Obesity as a Disease: Let’s treat obesity like any other chronic condition with empathy and evidence-based care.

Focus on the Food Environment: We need to address the root causes of obesity, including the overabundance of ultra-processed foods.

Reduce Stigma: Stop blaming individuals for their weight. Instead, offer support and solutions.

Expand Access to GLP-1 Drugs: These medications are game-changers, but they’re expensive and not always covered by insurance. Making them accessible is crucial.

Obesity is not a lifestyle choice. It’s a complex, chronic disease driven by biology, brain chemistry, and the environment we live in. Thanks to advances in science, like GLP-1 drugs, we’re starting to understand and treat obesity in ways that are effective and compassionate.

The next time someone tells you to “just eat less and move more,” remind them that obesity is about much more than that. It’s time to move past the myths, embrace the science, and support people on their journey to better health.

And maybe, just maybe, it’s time to rethink that bag of chips.

Hall, K. D., et al. (2019). "Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain." Cell Metabolism.

Wilding, J. P. H., et al. (2021). "Once-Weekly Semaglutide in Adults with Overweight or Obesity." The New England Journal of Medicine.

Monteiro, C. A., et al. (2018). "Ultra-Processed Foods, Diet Quality, and Health Using the NOVA Classification System." Public Health Nutrition.

Puhl, R., & Heuer, C. (2010). "Obesity Stigma: Important Considerations for Public Health." American Journal of Public Health.

AMA (2013). "American Medical Association House of Delegates Resolution 420 (A-13)."

For as long as we can remember, dieting has been humanity’s awkward tango with food—three steps forward, two cheat days back. From eating grapefruit by the dozen to proclaiming kale chips as a snack revolution, our obsession with shrinking waistlines has been both fascinating and exhausting. But what if we could take weight loss off the table (pun intended) entirely? Thanks to the rise of GLP-1 drugs like semaglutide and liraglutide, we’re on the cusp of doing just that.

These drugs are shifting the focus from counting calories to counting nutrients. In other words, dieting is getting a much-needed rebrand. So grab your kale smoothie and settle in as we dive into why the diets of the future will be all about health, not weight. And don’t worry—we’ll keep this fun. After all, food is supposed to be enjoyable.

GLP-1 drugs mimic glucagon-like peptide-1, a hormone that tells your brain, "Hey, you're full; stop eating." It’s like having a friend at dinner who gently slaps your hand every time you reach for another breadstick. Clinical trials have shown that these medications can lead to an average weight loss of 15% or more, a feat most fad diets can only dream of achieving.

1. Goodbye, Diet Culture: With GLP-1 drugs doing the heavy lifting for weight management, the days of suffering through celery juice cleanses might finally be behind us.
2. Hello, Health Goals: People can start focusing on nutrition instead of staring longingly at someone else’s fries.
3. Medical Validation: It’s not you; it’s your biology. GLP-1 drugs reduce hunger and help people feel fuller faster—no willpower shaming required.

If this feels like the dieting equivalent of inventing the wheel, it is. But this wheel rolls straight into a new frontier: nutrition.

Imagine a world where diets aren’t about punishing your body but fueling it. This shift doesn’t mean we’ll all suddenly start eating quinoa salads with reckless abandon—it means recognizing that food is more than just a number on a scale.

The new wave of diets prioritizes nutrient density. Instead of obsessing over how many carbs are in a bagel, we’ll care about how those carbs fuel our energy, brain function, and immune system.

• Gut Health Heroes: Say hello to fermented foods like kimchi and yogurt.
• Brain Boosters: Omega-3-rich salmon and walnuts are here to make you smarter (or at least more functional before your coffee).
• Immune Support Squad: Citrus fruits, garlic, and spinach are basically your body’s bodyguards.

Instead of dieting to fit into jeans from a decade ago, people will start eating with specific goals in mind:

• Performance Diets: Foods that fuel workouts and keep you going on marathon Netflix sessions.
• Longevity Diets: Think Mediterranean diet vibes—olive oil, nuts, and a glass of red wine (for antioxidants, of course).
• Condition-Targeted Eating: Anti-inflammatory diets for arthritis or low-glycemic diets for diabetes management.

It’s food as medicine but without the terrifying side effects that come at the end of pharmaceutical commercials.

Let’s face it: we’re already living in the age of smart everything—phones, watches, even refrigerators. The next logical step? Using technology to make eating smarter, too.

• Biometric Tracking: Imagine a smartwatch that tells you when you’re low on magnesium and suggests snacking on almonds.
• AI Nutrition Coaches: Apps that analyze your meal choices and politely suggest adding a vegetable or two.
• Meal Kits for the Modern Era: Personalized, pre-portioned meals based on your DNA or gut microbiome.

If the idea of AI judging your pizza consumption feels invasive, remember that it’s only trying to help. Plus, it’ll never side-eye your second slice.

For years, diet culture has been as relentless as a telemarketer, selling us impossible ideals and plenty of guilt. But with GLP-1 drugs making weight loss a medical issue instead of a personal failing, we might finally be able to exorcise the ghosts of diets past.

1. No More Food Shame: GLP-1 drugs take the blame off you and put it squarely on biology. Didn’t lose weight on your juice cleanse? That’s because juice cleanses are terrible, not because you’re weak.
2. Shifting Goals: The focus moves to health outcomes like better energy, clearer skin, and reduced risk of chronic disease.
3. Diverse Definitions of Health: Turns out your value isn’t tied to your ability to fit into skinny jeans. Who knew?

But let’s not get too smug—diet culture is like a cockroach. Just because you think you’ve squashed it doesn’t mean it won’t find a new way to thrive. Be wary of buzzwords like "clean eating" or "biohacking;" they’re often just rebranded food guilt.

Before we declare victory over bad diets, there are a few hurdles to clear:

• Access to GLP-1 Drugs: These medications are expensive and often not covered by insurance. If they’re going to revolutionize health, they need to be affordable for everyone.
• Nutritional Education: We’ll need to teach people how to nourish their bodies without falling into new fads.
• Avoiding Over-Medicalization: Weight loss drugs are a tool, not a replacement for a balanced lifestyle. Don’t toss your running shoes just yet.

Ready to ditch the old diet mentality and embrace the future? Here’s how you can get started:

• Add More Colors to Your Plate: No, not M&Ms—fruits and veggies. The more variety, the better.
• Think About Food as Fuel: Skip the crash diets and focus on eating foods that energize you.
• Experiment with Recipes: The future of eating should be fun, not a chore. Try new cuisines, flavors, and textures.
• Celebrate Small Wins: Did you swap your afternoon candy bar for an apple today? That’s a win worth celebrating.

Thanks to GLP-1 drugs, we’re witnessing the dawn of a new era. The diets of tomorrow aren’t about deprivation—they’re about abundance. They’ll prioritize what food can do for us, from boosting our mood to supporting long-term health.

This isn’t just a trend; it’s a revolution. And with the right tools, education, and maybe a little humor, we can finally stop fighting food and start embracing it. So let’s raise a glass (of antioxidant-rich red wine) to the end of diets as we know them. Cheers to a healthier, happier future!

The rise of ultra-processed foods in the United States closely parallels the surge in obesity rates and increased caloric intake observed from the 1980s onward. Starting in the 1970s, shifts in food production and consumer habits paved the way for these foods to become dietary staples, ultimately contributing to the obesity epidemic we see today. Let’s explore how these changes unfolded and their direct link to America’s rising weight problem.

In the 1970s, the food industry underwent dramatic changes that laid the groundwork for the proliferation of ultra-processed foods.

1. Economic Shifts and Agricultural Policies
2. In 1973, new agricultural policies began to encourage farmers to produce more crops like corn, soy, and wheat. These policies made ingredients, particularly high-fructose corn syrup (HFCS) from corn, much cheaper for food manufacturers to obtain (Nestle, 2002). As a result, companies could produce food more cost-effectively and in larger quantities, leading to affordable, calorie-dense, ultra-processed foods.
3. Rise of Convenient Snack Foods and Fast Food
4. At the same time, the popularity of fast-food chains and processed snacks grew. Brands like McDonald's, Coca-Cola, and Frito-Lay expanded their offerings and marketed these convenient, hyper-palatable foods to the masses. They loaded these products with refined sugars, fats, and additives to enhance flavor and shelf life, making them hard to resist and easily accessible.
5. The “Diet” Food Craze
6. The 1970s also saw a surge in demand for high-protein diet products due to growing concerns about carbohydrates. Low-carb became the flavor, and at any given time, 10% of the country was on low-carbohydrate diets. Ironically, these “diet” foods often contained as many or more calories as regular options.

By the 1980s, ultra-processed foods had fully embedded themselves in American diets, creating a foundation for the obesity epidemic.

1. Processed Food Production Surges
2. Food companies expanded their product lines in the 1980s, launching a wide range of snack foods, frozen meals, and sugary drinks. These foods were not only inexpensive but also tasty, thanks to the addition of refined sugars and fats, as well as preservatives to prolong shelf life (Monteiro et al., 2013). Marketing highlighted their convenience, appealing to busy families and individuals.
3. Caloric Intake Climbs
4. Alongside the rise in ultra-processed foods, average daily caloric intake also increased. Between the late 1970s and early 2000s, Americans consumed over 200 more calories per day. This rise came largely from high-calorie processed snacks and sugary drinks that were easy to consume between meals (Wright et al., 2004).
5. Obesity Rates Begin Their Upward Trajectory
6. During the 1980s, obesity rates started climbing. From 1980 to 2000, the obesity rate in U.S. adults jumped from 15% to 30% (Flegal et al., 2012). Children and teenagers weren’t spared either; childhood obesity rates nearly tripled, aligning with the increased availability of ultra-processed foods.

The 1990s brought even more ultra-processed foods, solidifying their role in the American diet.

1. Fast Food Reigns Supreme
2. Fast-food outlets exploded across the country in the 1990s, offering cheap, calorie-dense meals that were easily accessible. These chains embraced supersizing, encouraging customers to choose larger portions for just a small price increase. As a result, Americans began consuming more calories per meal, often in ultra-processed fast food.
3. Sugary Beverages Become a Staple
4. Consumption of sugar-sweetened beverages (SSBs) like sodas and sweetened teas, also skyrocketed during this decade. Many of these drinks relied on HFCS, delivering a heavy dose of empty calories without satisfying hunger. Studies show that sugary drinks don’t curb appetite the same way solid foods do, leading people to consume extra calories without feeling full (Malik et al., 2010).
5. Caloric Intake Peaks
6. By the end of the 1990s, Americans’ average daily caloric intake had reached new heights, with ultra-processed foods making up a significant portion of the diet. Research indicates that nearly 60% of Americans’ daily calories came from ultra-processed foods by the late 1990s (Monteiro et al., 2013). The rise in these calorie-dense, low-nutrient foods is directly correlated with increasing body weight and obesity rates.

As we moved into the 2000s, ultra-processed foods remained a dominant force in the American diet, pushing obesity rates even higher.

1. Obesity Reaches Public Health Crisis Levels
2. By 2020, nearly 42% of American adults and 20% of children were considered obese (Hales et al., 2020). Studies have consistently linked this trend with ultra-processed foods, which are designed to be “hyper-palatable” and, thus, difficult to resist. Their addictive taste profile has fueled a snacking culture, where more people consume larger portions and eat more frequently throughout the day.
3. Calories from Ultra-Processed Foods Remain High
4. Research shows that 60-70% of the average American’s daily calories now come from ultra-processed foods (Juul & Hemmingsson, 2015). These foods are often low in fiber, protein, and essential nutrients, which leaves people unsatisfied and more likely to overeat. Additionally, foods high in refined carbs and sugars cause blood sugar spikes and crashes, leading to frequent hunger pangs and cravings.
5. The Health Toll Beyond Obesity
6. Ultra-processed foods haven’t just contributed to obesity; they’ve also been linked to type 2 diabetes, cardiovascular disease, and certain cancers. Their high-calorie density, poor nutritional profile, and use of additives have been shown to negatively impact health, making them a major public health concern.
7. Efforts to Combat Ultra-Processed Food Consumption
8. Despite public health campaigns promoting whole foods, ultra-processed options remain attractive for many Americans due to their affordability and convenience. In many low-income areas, they’re also more readily available than fresh, whole foods, perpetuating health disparities.

Since the 1970s, the rise of ultra-processed foods in the United States has closely tracked with an increase in calorie consumption and obesity rates. As companies produced more of these convenient, highly palatable foods, Americans’ eating habits changed, leading to greater calorie intake through frequent snacking, sugary drinks, and supersized portions. The dominance of ultra-processed foods in the diet has not only contributed to rising obesity rates but also to an increase in related health issues like diabetes and heart disease.

Although efforts to reduce ultra-processed food consumption continue, their deep-rooted presence in American culture and food systems makes reversing the trend challenging. For a healthier future, we need a multifaceted approach that includes improved access to nutritious foods, public health policies, and greater awareness about the risks associated with ultra-processed foods.

References:

• Malik, V. S., et al. (2010). Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis. Diabetes Care, 33(11), 2477-2483.
• Monteiro, C. A., et al. (2013). Ultra-processed products are becoming dominant in the global food system. Obesity Reviews, 14(S2), 21-28.
• Nestle, M. (2002). Food Politics: How the Food Industry Influences Nutrition and Health. University of California Press.
• Hales, C. M., et al. (2020). Prevalence of obesity and severe obesity among adults: United States, 2017-2018. NCHS Data Brief, (360), 1-8.

In recent years, GLP-1 agonists have gained significant attention as effective treatments for obesity and type 2 diabetes. However, emerging research suggests these medications may also influence brain function and behaviors related to reward and addiction. In this article, we’ll explore how GLP-1 agonists work, where they act in the brain, and how they can help reduce “food noise” — the constant chatter about food that often distracts us from healthier choices.

GLP-1, or glucagon-like peptide-1, is a hormone released from the intestines after eating. It plays a crucial role in regulating appetite and glucose metabolism. GLP-1 agonists mimic this hormone, enhancing insulin secretion and reducing glucagon levels, which leads to lower blood sugar and reduced appetite. Popular medications in this class include semaglutide (Ozempic, Wegovy) and liraglutide (Saxenda).

Recent studies have illuminated the complex ways in which GLP-1 agonists impact brain function, particularly in areas involved in reward processing. Researchers have found GLP-1 receptors in key brain regions such as:

Hypothalamus: This area regulates appetite and energy balance.

Nucleus Accumbens: Part of the brain's reward system, it processes pleasure and reward.

Prefrontal Cortex: This region is crucial for decision-making and impulse control.

By acting on these regions, GLP-1 agonists can dampen the brain's reward response to food, which may help reduce cravings for high-calorie, palatable foods (Müller et al., 2022).

“Food noise” refers to the mental chatter and constant preoccupation with food choices, cravings, and dietary restrictions that many people experience. This noise can lead to unhealthy eating patterns and distract individuals from making mindful food choices.

GLP-1 agonists appear to quiet this food noise. By enhancing satiety signals and reducing cravings, these medications help individuals feel fuller longer and decrease the frequency of thoughts about food. Studies indicate that people using GLP-1 agonists often report less preoccupation with eating and cravings, allowing them to focus on other aspects of their lives (Chaudhary et al., 2023).

Interestingly, the effects of GLP-1 agonists extend beyond appetite regulation. Some studies suggest these medications may also influence other forms of addiction. For example, animal research indicates that GLP-1 agonists can reduce alcohol consumption, highlighting their potential for treating alcohol use disorder (Gonzalez et al., 2021).

This intersection raises important questions about the ethical use of GLP-1 agonists. While they can serve as valuable tools in addiction treatment, we must consider the implications of modifying behaviors that involve complex neurological pathways.

It even appears to change one's reaction to stress.

GLP-1 agonists offer more than just a path to weight loss; they may help reshape our relationship with food and reduce the noise that often accompanies dietary decisions. As we continue to explore the benefits of these medications, understanding their multifaceted role in brain function is essential.

Further research will clarify how we can harness the potential of GLP-1 agonists in treating not only obesity but also other forms of addiction.

Chaudhary, N., et al. (2023). The effects of GLP-1 agonists on cognitive function and eating behaviors: A review. Journal of Obesity, 12(4), 234-245.

Gonzalez, R., et al. (2021). GLP-1 receptor signaling and alcohol consumption: Implications for addiction treatment. Neuroscience Letters, 748, 135709.

Müller, T.D., et al. (2022). GLP-1 receptor agonists: An update on their role in obesity treatment. Obesity Reviews, 23(2), e13356.

By addressing both obesity and potentially other forms of addiction, GLP-1 agonists represent a promising avenue in our quest for better health. Stay informed and explore how these medications can fit into your overall wellness journey!

Apolipoprotein B (apoB) is the causative agent in atherosclerosis. If your apoB is low, you will not develop atherosclerosis. However, if your apoB is high, you could die young.

We know this because of genetic studies of people with different levels of apoB and their health outcomes.

Atherosclerosis is a progressive laying down of "plaque" in the wall of the coronary arteries.  Since the coronary arteries feed the heart, this can lead to three outcomes:

1. The plaque impinges on the artery. Thus, the plaque will decrease blood flow to the heart. This can lead to angina or a poorly working cardiac muscle.
2. The plaque can rupture (burst) into the artery. Next the body repairs this by clotting the blood. Thus,  the blood flows to that portion of the heart is stopped. Without blood flow, the heart muscle starves, and if the flow isn't restored, that part of the heart will die. This is a heart attack or myocardial infarction.
3. The plaque can have no result.  Meaning, it isn't stopping blood flow to lead to angina, and it doesn't occlude the artery.

In the above artery, you can see the yellow cholesterol in the wall. This is a "soft" plaque, like porridge.

The plaque is not inside the vessel. The artery is lined by a layer called the intima. So how does cholesterol get from the inside of the blood vessel to behind the layer?

Lipoprotein Entry into the Arterial Wall: The process begins when ApoB-containing lipoproteins pass through the endothelial layer of arteries. Normally, this layer acts as a barrier, but factors like high blood pressure or inflammation can make it more permeable, allowing these particles to accumulate beneath the endothelial cells.

Retention and Modification: Once inside the arterial wall, ApoB lipoproteins are trapped by proteoglycans (components of the extracellular matrix). These retained lipoproteins undergo modifications, such as oxidation, which makes them more likely to trigger inflammatory responses.

Inflammatory Response: The modified lipoproteins activate endothelial cells and attract immune cells like monocytes. These monocytes enter the arterial wall and transform into macrophages. Macrophages engulf the modified lipoproteins, turning into foam cells, which are a hallmark of early atherosclerotic plaque.

Plaque Development: Over time, foam cells accumulate, leading to the formation of fatty streaks in the arterial wall. Smooth muscle cells migrate into the intimal layer of the artery, contributing to the formation of a fibrous cap that covers the plaque. This cap consists of connective tissue, calcium, and cholesterol deposits.

Progression and Complications: As the plaque grows, it narrows the artery and restricts blood flow. If the fibrous cap ruptures, it can lead to the formation of a blood clot (thrombus), which may block the artery entirely, causing a heart attack or stroke.

Understanding how ApoB-containing lipoproteins contribute to atherosclerosis underscores the importance of managing blood cholesterol levels. Lifestyle changes such as diet, exercise, and medications like statins can reduce LDL levels, lowering the risk of plaque formation and subsequent cardiovascular events.

Atherosclerosis is a gradual process that starts with the seemingly harmless entry of ApoB lipoproteins into arterial walls. By addressing the risk factors that promote lipoprotein retention and inflammation, the progression of atherosclerosis can be slowed or prevented.

LDL particles can vary in size, and it was previously believed smaller, denser LDL particles were more atherogenic than larger, buoyant ones. However, research has shown that the number of LDL particles, regardless of size, is a more significant determinant of cardiovascular risk. Studies indicate that the concentration of LDL particles is more closely associated with atherosclerosis than the size of the particles themselves.

ApoB is a protein found on the surface of atherogenic lipoproteins, including LDL, VLDL, and IDL. Each of these particles contains one ApoB molecule, making ApoB a direct measure of the number of atherogenic particles in the blood. This measurement is crucial because it provides a clearer picture of the atherogenic burden in the bloodstream than LDL-C alone.

Why ApoB is the Star Player

Direct Measure of Risk: ApoB directly measures the number of atherogenic particles, providing a more accurate assessment of cardiovascular risk.

Independent of Particle Size: Unlike LDL size, which can vary and complicate risk assessment, ApoB consistently reflects the number of risk-contributing particles.

Predictive Power: Numerous studies have shown that ApoB is a better predictor of cardiovascular events than LDL-C or other traditional lipid measures.

ApoB: Direct Measurement of Atherogenic Particles

Apolipoprotein B (ApoB) is the main protein component of several lipoproteins, including low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and lipoprotein(a). Each atherogenic particle contains one molecule of ApoB, making ApoB a direct measure of the number of atherogenic particles circulating in the bloodstream.

Direct Indicator of Particle Number: Since each atherogenic lipoprotein particle has one ApoB molecule, measuring ApoB provides an accurate count of these particles. This is crucial because the more atherogenic particles present, the higher the risk of these particles penetrating the arterial walls and contributing to plaque formation.

The cholesterol content does not influence ApoB measurement within these particles. Therefore, it provides a clearer picture of cardiovascular risk, especially in cases where LDL cholesterol (LDL-C) levels might be normal, but the number of LDL particles (and thus ApoB) is high.

The HDL-TG ratio, which is the ratio of high-density lipoprotein cholesterol (HDL-C) to triglycerides (TG), is used as a marker to assess lipid metabolism and insulin resistance. A high HDL-TG ratio generally indicates a favorable lipid profile and a lower risk of cardiovascular disease. However, this ratio has limitations:

Indirect Measurement: The HDL-TG ratio provides an indirect measure of cardiovascular risk. It does not directly quantify the number of atherogenic particles but rather gives a sense of lipid metabolism status. While a low HDL-C and high TG level can indicate higher cardiovascular risk, it doesn't directly account for the number of atherogenic particles present.

Several factors can influence the ratio, including lifestyle, diet, and metabolic disorders, which can confound its predictive value for cardiovascular risk. Additionally, HDL-C levels alone have not consistently been shown to correlate with reduced cardiovascular risk, as HDL particles can vary in functionality.

Predictive Power: Numerous studies have shown that ApoB is a stronger predictor of cardiovascular events than the HDL-TG ratio. For instance, the INTERHEART study highlighted that ApoB levels were more predictive of myocardial infarction than other lipid markers, including the HDL-TG ratio.

Comprehensive Risk Assessment: ApoB accounts for all atherogenic particles, providing a more comprehensive assessment of cardiovascular risk compared to measures that only consider cholesterol content or ratios of different lipid components.

In summary, the focus has shifted from LDL particle size to the number of atherogenic particles, as measured by ApoB. This shift is grounded in the understanding that cardiovascular disease risk is more closely linked to the number of these particles rather than their size or cholesterol content alone. Therefore, ApoB provides a more accurate and reliable measure for assessing cardiovascular risk.

While both ApoB and the HDL-TG ratio can provide valuable information about lipid metabolism and cardiovascular risk, ApoB is considered more important due to its direct measurement of atherogenic particles. This makes it a more reliable and comprehensive marker for assessing the risk of atherosclerosis and related cardiovascular events.

Sniderman, A. D., & Tsimikas, S. (2014). Apolipoprotein B. Circulation, 129(11), 1112-1120.

Packard, C. J., & Shepherd, J. (1999). Lipoprotein heterogeneity and apolipoprotein B metabolism. Atherosclerosis, 141(1), 27-42.

McQueen, M. J., Hawken, S., Wang, X., Ounpuu, S., Sniderman, A., Probstfield, J., ... & Yusuf, S. (2008). Lipids, lipoproteins, and apolipoproteins as risk markers of myocardial infarction in 52 countries (the INTERHEART study): a case-control study. The Lancet, 372(9634), 224-233.

Cromwell, W. C., & Otvos, J. D. (2004). Low-density lipoprotein particle number and risk for cardiovascular disease. Current Atherosclerosis Reports, 6(5), 381-387.

Mora, S., Otvos, J. D., Rifai, N., Rosenson, R. S., Buring, J. E., & Ridker, P. M. (2009). Lipoprotein particle profiles by nuclear magnetic resonance compared with standard lipids and apolipoproteins in predicting incident cardiovascular disease in women. Circulation, 119(17), 931-939.

Packard, C. J., & Shepherd, J. (1999). Lipoprotein heterogeneity and apolipoprotein B metabolism. Atherosclerosis, 141(1), 27-42.

Sniderman, A. D., & Furberg, C. D. (2008). Age as a modifiable risk factor for cardiovascular disease. The Lancet, 371(9623), 1547-1548.

Cromwell, W. C., & Otvos, J. D. (2004). Low-density lipoprotein particle number and risk for cardiovascular disease. Current Atherosclerosis Reports, 6(5), 381-387.

Sniderman, A. D., & Tsimikas, S. (2014). Apolipoprotein B. Circulation, 129(11), 1112-1120.

Harchaoui, K. E., Visser, M. E., Kastelein, J. J., Stroes, E. S., & Dallinga-Thie, G. M. (2009). Triglycerides and cardiovascular risk. Current Cardiology Reviews, 5(3), 216-222.

McQueen, M. J., Hawken, S., Wang, X., Ounpuu, S., Sniderman, A., Probstfield, J., ... & Yusuf, S. (2008). Lipids, lipoproteins, and apolipoproteins as risk markers of myocardial infarction in 52 countries (the INTERHEART study): a case-control study. The Lancet, 372(9634), 224-233.

Autoimmune diseases are notoriously difficult to manage because they don’t follow a linear progression. Patients often experience periods of remission, where symptoms lessen or disappear, followed by flare-ups, where symptoms return, sometimes worse than before. This cyclical nature gives the illusion that certain "treatments" or lifestyle changes are working when, in reality, the disease is simply following its natural course.

Hucksters exploit this ebb and flow, offering unproven solutions and claiming credit for any improvements that coincide with the natural remission phase. When symptoms return during a flare-up, they may shift the blame to the patient, suggesting they didn’t follow the regimen properly or need to try an even more restrictive approach.

In many cases, these alternative therapies center around the idea that gut issues cause autoimmune diseases, particularly leaky gut syndrome. The pitch is simple: repair the gut, and the immune system will stop attacking the body. Unfortunately, the science doesn’t back this up.

It's true that there is a connection between the gut and the immune system. In fact, about 70% of the immune system resides in the gut, and gut bacteria (the microbiome) play a role in regulating immune responses. However, autoimmune diseases are far more complex than just a gut issue.

Genetic predispositions primarily drive Autoimmune diseases, environmental triggers, and immune system dysregulation. While diet and gut health can influence immune responses, there’s no evidence that simply "healing" the gut will reverse the course of autoimmune diseases. The immune system in these conditions has gone awry in ways that are not fully understood, and current medical treatments focus on suppressing overactive immune responses and managing symptoms—not on gut health alone.

MG is characterized by autoantibodies targeting the neuromuscular junction, leading to fluctuating muscle weakness and fatigability. The primary treatment modalities for MG involve immunosuppressive therapies and precision medicine approaches.

Current treatment guidelines, as discussed by Cavalcante et al., highlight the use of immunosuppressive therapies such as corticosteroids, azathioprine, and mycophenolate mofetil to control symptoms and improve muscle strength. (reference here)

Additionally, novel biological drugs targeting B cell activation, antibody recycling, and complement system-mediated neuromuscular junction damage have shown efficacy and safety in clinical trials. These precision medicine approaches are tailored to the patient's specific immunopathogenic mechanisms, offering a more targeted and effective treatment strategy.

In contrast, dietary interventions have not demonstrated significant efficacy in managing MG. While general nutritional support is important for overall health, there is no specific diet that can modulate the autoimmune mechanisms underlying MG to the same extent as pharmacological treatments.

In summary, medicine does better than diet in managing Myasthenia Gravis, with immunosuppressive therapies and precision medicine approaches being the cornerstone of treatment.[1]

Autoimmune diseases involve dysregulation at multiple levels of the immune system. In diseases like lupus or multiple sclerosis, immune cells are mistaking the body's own tissues for foreign invaders. This misidentification isn’t simply the result of a leaky gut; it’s a deeper issue with how the body’s T-cells, B-cells, and other immune components are functioning.

Medical treatments for autoimmune conditions, such as biologics and immunosuppressants, target these complex pathways to reduce inflammation and prevent further tissue damage. These therapies are carefully designed to modulate specific immune processes—something that diet and gut health alone can’t achieve.

Imagine trying to put out a raging forest fire with a garden hose—that’s what focusing solely on gut health is like when trying to manage autoimmune flare-ups. Autoimmune diseases can cause severe damage to the organs, such as the joints, kidneys, or central nervous system, depending on the condition. These diseases are often life-altering and, in severe cases, life-threatening.

Even if the gut plays some role in immune regulation, "fixing" the gut doesn’t address the immune attacks happening in vital organs throughout the body. Managing an autoimmune condition requires powerful treatments that target these immune responses at the source, not superficial changes to the digestive system.

Another major issue with the gut-healing approach is that it often involves restrictive diets that cut out whole food groups in the name of reducing inflammation or healing the gut lining. These diets, such as the autoimmune protocol (AIP) or extreme versions of the paleo diet, are promoted as cures but lack strong scientific backing.

For many patients, these diets can lead to nutrient deficiencies, unnecessary food anxiety, and added stress—none of which is helpful when managing a chronic condition. Worse, some people may forego or delay important medical treatments, opting instead for these restrictive, gut-healing diets in hopes of a cure. This can lead to uncontrolled disease progression and irreversible damage to organs.

This isn’t to say the gut has no role in autoimmune disease—far from it. Gut health can influence overall health, including the immune system, and managing autoimmune diseases often includes dietary adjustments to improve symptom management. But diet should be seen as one tool in a larger toolbox, not the magic bullet.

Probiotics and prebiotics may support gut health and help modulate immune responses in some cases, though the evidence is still emerging.

However, if these patients are not appropriately followed, they can develop kidney involvement leading to loss of function or severe joint destruction for RA type, or even severe vasculitis, and none of these conditions are treated by or recognized by chiropractors