Autoimmune Diseases and Charlatans

Beyond the Scale: Eating for Long-Term Health, Not Just Weight LossWeight 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.GLP-1 Medications Take the Lead; Your Diet Supports the ProcessWhen 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.The Mediterranean Diet: A Gold Standard for HealthWhen 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.Why the Mediterranean Diet WorksThe 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.The Science Behind Olive Oil and Omega-3sOlive 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.Don’t Get Stuck on ProteinProtein 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

Obesity: Not Just About Forks and WillpowerFor 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.The Myth of "Just Eat Less and Move More""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.The Hungry Brain: Why You Can’t Stop EatingOur 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).GLP-1: The Game-Changing HormoneHere’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).Why Obesity Is a Disease, Not a Lifestyle ChoiceThe idea that...

The Future of Diets: From Weight Loss to Nutrition, Thanks to GLP-1 DrugsFor 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.The GLP-1 Revolution: Shedding Pounds Without Shedding TearsGLP-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.Why This Changes EverythingGoodbye, 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.Hello, Health Goals: People can start focusing on nutrition instead of staring longingly at someone else’s fries.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.Citation: Clinical trials on GLP-1 drugs have shown sustained weight loss for a majority of participants (Wilding et al., 2021).From Weight Loss to Wellness: The New Role of DietsImagine 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.1. Nutrition Over NumbersThe 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.Fun Fact: Your brain is about 60% fat, so eating healthy fats can actually make you a better thinker. Finally, an excuse for avocado toast!2. Functional FoodsInstead 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...

From Starving to Stuffed: The Evolution of Obesity in AmericaThe 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.1970s: Setting the Stage for Ultra-Processed FoodsIn the 1970s, the food industry underwent dramatic changes that laid the groundwork for the proliferation of ultra-processed foods.Economic Shifts and Agricultural PoliciesIn 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.Rise of Convenient Snack Foods and Fast FoodAt 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.The “Diet” Food CrazeThe 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.1980s: Ultra-Processed Foods Take Center Stage, and Obesity Rates Start to ClimbBy the 1980s, ultra-processed foods had fully embedded themselves in American diets, creating a foundation for the obesity epidemic.Processed Food Production SurgesFood 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.Caloric Intake ClimbsAlongside 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).Obesity Rates Begin Their Upward TrajectoryDuring 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...

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.Understanding GLP-1 AgonistsGLP-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).How GLP-1 Agonists Affect the BrainRecent 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).GLP-1 Agonists and Food Noise“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).Implications for Other AddictionsInterestingly, 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.ConclusionGLP-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.ReferencesChaudhary, N., et al....

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.What is Atherosclerosis of the heart?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: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.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.The plaque can have no result.  Meaning, it isn't stopping blood flow to lead to angina, and it doesn't occlude the artery.What is in the plaque?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?The Process of Atherosclerotic Plaque FormationLipoprotein 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.Preventing Plaque FormationUnderstanding 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 particle sizeLDL particles can...

The Cyclical Nature of Autoimmune Diseases: A Huckster's PlaygroundAutoimmune 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.Why the Gut Isn’t the Root Cause of Autoimmune DiseaseIt'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. Myasthenia Gravis (MG) is an autoimmune disease where medical treatment significantly outperforms dietary interventions.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]Here’s why relying on gut health as the sole solution is like using a garden hose to fight a forest fire: A. The Complexity of Autoimmune DysregulationAutoimmune diseases involve dysregulation at multiple levels of the immune system. In...

Should I eat bread?The low carbohydrate movement has demonized bread.  But is bread fattening? Does it cause inflammation? And if so, why do we call bread the Staff of Life?The Staff of LifeImagine calling white bread the staff of life. And yet bread is more responsible for humans ending a nomadic existence. The cultivation of wheat and barley, both in the Nile and in the Euphrates/Tigris rivers, led to civilization.Calendars, Art, ReligionNot having to forage meant there was time to build a more permanent shelter. It also meant a steady supply of food.This also meant a calendar was needed because when is the optimal time to plant?The calendar helped predict when the rivers would swell and recede. The bottom land, with its rich topsoil, is ideal for growing crops.When you don't need to spend time looking for food, you have time to develop other things:Make a religion around grains - the god of the weather, of the earth of the riverGrain can become the first currency, facilitating tradeArt because you spend less time seeking foodStorage systems to overcome times of famine.Mathematics, weights, and measures are needed to buy and sell grainWriting to make contracts and facilitate trade of the grainA government is needed to settle disputesStorage SystemsHarvested grain can be stored. Storing grain in Egypt was easier because of the dry climate.  Joseph, of the Hebrew Bible, prophesied to the Pharoh of an upcoming famine. As a result, the Pharoh built silos and stored a portion of each harvest.  Seven years later, the harvest failed.  ButThe silo system was complex. Filling from the top and arranged in a way that winds would keep the grains cool.  Where did Egyptians get the idea for such an invention? From bees. You can see the bees' natural ventilation system here:Bees were the symbol of royalty in ancient Egypt. Their honey was tears from the sun god. Bee architecture was copied for the ventilation system for the silos storing grain.  Thus, the storage of grain allowed society to thrive during the time of famine.Bronze Age to Iron AgeBread was portable. Served as currency. Allowed armies to march. Facilitated trade between city states. The grain rich regions of the Nile produced grain traded with Mycennians for olive oil and wine.The Roman emperors gave bread to the poor as welfare. Part of the bread and circus program to keep Romans happy. Bread was imported to Rome, and ultimately, Roman citizens were given "their daily bread."Rome fell, but bread continued to be important.Bread until 1920Grains, including bread, were the major source of calories for most of Europe. From the fall of Rome through the Middle Ages, bread was the main source of calories, along with other grain products.Bread in the Industrial AgeWhite bread was considered pure, hygienic, the whiter the better. Brown bread could be contaminated. The ability of mills to separate wheat from chaff, and to make bread without a human hand touching it was irresistible. Industrial bread slicing resulted in "best thing since sliced bread."White bread became the preferred style of bread from the 1920s until 2009.Fortification of bread with vitamins in the 1940s made bread a health food.  Pellagra (vitamin B 3 deficiency) and beriberi  (thiamine deficiency) had sadly become common in the US and were eliminated by fortification. So it was indeed revolutionary, but calling it a health food? Even the Federal Trade Commission had issues with this "12 ways campaign" and sued Wonder Bread. The Feds lost.Age of Aquarius Beats BreadIn spite of the world loving white bread,

Seed Oils: Toxic or Not?Today, the low-carb/carnivore community has a new enemy. It is seed oils. Here is their argument:There were no seed oils in ancient landsSeed oils are highly inflammatorySeed oils are extracted with hexane, a cancer-causing agentThe rise of seed oils correlates with the rise of obesitySeed oils are high in omega-6 fatty acids, which are inflammatory That is the summary of their logic. Now, let's get to the science.What are Seed Oils?See those beautiful seeds, in them are bits of oil. This is the rapeseed plant, which we have covered before. From rapeseed came canola oil. And this has been used as a source of oil starting about 4000 years ago. A much misunderstood oil, please see our previous podcast.Seed OilsEvery seed has oil. Nuts are a type of seed, and their caloric density comes from oil. Oddly, low carb/keto types tend to eat nuts, the carnivore crowd avoids them.Seed oils are another name for vegetable oils, and they are used often in cooking because they have a neutral taste and high smoke point. The more common ones include corn, peanuts, sunflowers, grapes, and others.Seed Oils and Ancient Humans Besides the logical fallacy about what ancient humans ate, seed oils have been cultivated and used for the whole of written humanity. Ancient Egyptians used oils for cooking and perfume. Even the Bible talks about the use of oils, including the gifts sent to the birth of Jesus. To summarize, humans have recorded the use of oils from seeds through all recorded history.Components of Seed OilsThere is no one "oil" that can chemically be called a "seed oil." Rather, every seed contains different compositions of oils, and it is how the body uses those particular oils that makes us interested in them. Thus, seed oils as a term is silly. I wonder why the carnivore/keto crowd decided to use "seed oils" instead of vegetable oils? After all, they don't call beef tallow "meat oil."Oleic Acid: Olives to ButterOleic acid is the main fatty acid in olive oil (55-85% of the oil).  This is a mono-unsaturated fatty acid, which everyone seems to agree is heart healthy. Hence, the more oleic acid in something, the better.Peanut oil 48%Canola oil 65%Palm oil 39%Soybean oil 23%Coconut oil 7%Beef Tallow 47%Butter 24% But are Vegetable Oils Inflammatory?The short answer is no. To be inflammatory, they would have to elicit an inflammatory response. This means that inflammatory markers in the blood would be elevated for those who use vegetable oils over meat oils. In contrast, there is no increase in inflammatory markers of those who use vegetable oils.Want to see the data? Take a look at this paper where they look at foods, like vegetable oils, with high ratios of omega-6 fatty acids. What didn't they find? Higher levels of inflammatory markers. Thus, seed oils are not inflammatory.Atherosclerosis and Seed OilsDo vegetable oils increase your risk of atherosclerosis, or do they decrease it? If the carnivore crowd is correct, they have not been yet, then their view of the vegetable oils is that it would increase your risk of atherosclerosis REFERENCES: Courville AB, Majchrzak-Hong S, Yang S, Turner S, Wilhite B, Ness Shipley K, Horneffer Y, Domenichiello AF,

Ancestral Diets and Logical FallaciesThere is an appeal to ancient history: the idea that ancient beings were either "designed"—as from a creator—or "evolved" to eat in a certain way. Both are logical fallacies, but both are meant to be the "ex-cathedra" in a debate.You read these logical fallacies in communities that claim they understand this. Here are some comments you will get:Our ancestors ate xyz (fill in the blank) and never had the modern chronic diseasesOur teeth have (canines/molars), so we were designed to eat only (meat/plants)You won't see broccoli on the walls of cavesIf we ate like our ancestors, we would be in great health. Appealing arguments, but they are as flawed as they are simply incorrect.What Do We Know About Early Humans?Of the early human records, they are based on precious little data. Consider in the fossil record we have about our ancestors? And by the way, where do we start?If we begin with homo sapiens, we have been around as a species somewhere between 70,000 to 250,000 years.Often the "low-carb" community will conflate distant cousins of homo sapiens as direct ancestors. Most of them were not but were a branch on the tree of evolution that are only related to us.Homo ErectusPerhaps the best adapted was the homo erectus, which was around for two million years. It is doubtful that homo sapiens will make it that long, but we can hope.Most fossil finds come from Australia and Asia - where they not only foraged but also established some organized hunting.Fossil RecordsThere are about 6000 fossils of early man. That's it. Just 6,000. When we look for fossils of our particular, such as early homo sapiens, we have enough fossils that we might fill up a school bus.How long did they live? It turns out we know.  Many died around the age of 35 years.   So why do we want to eat like they did?At this point, someone in the audience will be bound to say - "They lived longer if you take into account infant mortality."When we date a fossil and see when it died, we don't average the infant mortality of the time.Recent DiscoveriesBones and teeth from seen people, and isolated teeth, were reported recently. These came from a cave in Morocco. As these teeth are from about 15,000 years ago. Hence, the diet was before the advent of agriculture.Evidence points to plants being a major part of these hunter-gatherer's menu.  As plants can be stored by hunter-gatherers all year round to protect against seasonal prey shortages. Thus, there is a regular food supply.Hunter-GatherersThe famous caveman diet- life wasn't so simple.When people of the carnivore tribe try to convince you about their diet, they invoke the mighty hunter.A better term was that our ancestors survived by being fishers, gatherers, and scavengers.