Fork U with Dr. Terry Simpson

From Starving to Stuffed: The Evolution of Obesity in America

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.

1970s: Setting the Stage for Ultra-Processed Foods

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.

1980s: Ultra-Processed Foods Take Center Stage, and Obesity Rates Start to Climb

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.

1990s: Fast Food and Convenience Foods Dominate the American Diet

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.

2000s to Present: Ultra-Processed Foods and the Obesity Epidemic

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.

Conclusion: Ultra-Processed Foods and America’s Obesity Epidemic

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.

Understanding GLP-1 Agonists

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).

How GLP-1 Agonists Affect the Brain

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).

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 Addictions

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.

Conclusion

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.

References

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.

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:

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.

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 Formation

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.

Preventing Plaque Formation

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 particle size

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.

The ApoB Factor: Why It's a Big Deal

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.

Key Points:

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.

Independent of Cholesterol Content:

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.

HDL-TG Ratio: A Marker of Lipid Metabolism

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 vs direct measure:

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.

Variability and Confounding Factors:

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.

Why ApoB is More Important

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.

 Focusing on the Right Metric

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.

Conclusion

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.

 

Citations:

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.

The Cyclical Nature of Autoimmune Diseases: A Huckster's Playground

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.

Why the Gut Isn’t the Root Cause of Autoimmune Disease

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.

 

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 Dysregulation

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.

B. Gut Health Cannot Reverse Severe Immune Attacks

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.

C. Gut-Focused Diets Can Be Restrictive and Harmful

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.

What We Do Know: The Gut’s Role in Autoimmune Disease Management

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.

For example:

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

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 Life

Imagine 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, Religion

Not 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 river
• Grain can become the first currency, facilitating trade
• Art because you spend less time seeking food
• Storage systems to overcome times of famine.
• Mathematics, weights, and measures are needed to buy and sell grain
• Writing to make contracts and facilitate trade of the grain
• A government is needed to settle disputes

Storage Systems

Harvested 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.  But

The 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 Age

Bread 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 1920

Grains, 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 Age

White 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 Bread

In spite of the world loving white bread, with baby boomers and Gen X growing up on it, there was rebellion.  Health guru Adele Davis, who sold millions of health books, decried bread for its lack of fiber and urged people to make whole wheat bread at home.

But then came the hippies and the summer of love.  Hundreds of kids were flocking to San Francisco without jobs, without money, and hungry. Feeding these young adults became a group priority.

In 1967, Walt Reynolds came, brought 400 pounds of flour, and baked bread twice a week to feed these kids. They didn't have enough bread trays, so they used coffee cans.

Walt insisted on using whole wheat bread, something rare in those days. But this became part of the counter-culture. Make your own bread. Make it healthy. It became their own bread, their own symbol.

We don't know what happened to Walt Reynolds after this - he lives, changed the way a generation looked at bread, and then disappeared.

Atkins and Bread

The low carb movement of the 1970's meant bread sales went declined. They recovered a bit, but in the second Atkins revolution, bread sales were down in some bakeries by 40%. Today Atkins Corporation sells bread.

But How to Make It

While there were lots of recipes to make bread from Digger Bread, as seen above, home cooks wondered. Then came along another baker who made the bread everyone dreamed of. From the baker of the Zen Retreat - we have this book.

In 2009 whole wheat bread surpassed white bread as the major bread sold over time. With fiber at the core all whole wheat products have increased.

And we can say for certain—yes, you can buy bread—but buy or make your own. Today, I can walk to a local baker who makes whole-grain sourdough 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 lands
• Seed oils are highly inflammatory
• Seed oils are extracted with hexane, a cancer-causing agent
• The rise of seed oils correlates with the rise of obesity
• Seed 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 Oils

Every 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 Oils

There 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 Butter

Oleic 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 Oils

Do 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, Schwandt M, Cutler RG, Chen KY, Hibbeln JR, Ramsden CE. Dietary linoleic acid lowering alone does not lower arachidonic acid or endocannabinoids among women with overweight and obesity: A randomized, controlled trial. Lipids. 2023 Nov;58(6):271-284. doi: 10.1002/lipd.12382. PMID: 38100748; PMCID: PMC10767670.

 

Innes JK, Calder PC. Omega-6 fatty acids and inflammation. Prostaglandins Leukot Essent Fatty Acids. 2018 May;132:41-48. doi: 10.1016/j.plefa.2018.03.004. Epub 2018 Mar 22. PMID: 29610056.

 

Fava M, De Dominicis N, Forte G, Bari M, Leuti A, Maccarrone M. Cellular and Molecular Effects of Microgravity on the Immune System: A Focus on Bioactive Lipids. Biomolecules. 2024 Apr 5;14(4):446. doi: 10.3390/biom14040446. PMID: 38672462; PMCID: PMC11048039.

 

Ooi EM, Watts GF, Ng TW, Barrett PH. Effect of dietary Fatty acids on human lipoprotein metabolism: a comprehensive update. Nutrients. 2015 Jun 2;7(6):4416-25. doi: 10.3390/nu7064416. PMID: 26043038; PMCID: PMC4488792.

 

Prater MC, Scheurell AR, Paton CM, Cooper JA. Blood Lipid Responses to Diets Enriched with Cottonseed Oil Compared With Olive Oil in Adults with High Cholesterol in a Randomized Trial. J Nutr. 2022 Sep 6;152(9):2060-2071. doi: 10.1093/jn/nxac099. PMID: 35511204; PMCID: PMC9449680.

 

Isaakidis A, Maghariki JE, Carvalho-Barros S, Gomes AM, Correia M. Is There More to Olive Oil than Healthy Lipids? Nutrients. 2023 Aug 18;15(16):3625. doi: 10.3390/nu15163625. PMID: 37630815; PMCID: PMC10459315.

Schwingshackl L, Bogensberger B, Benčič A, Knüppel S, Boeing H, Hoffmann G. Effects of oils and solid fats on blood lipids: a systematic review and network meta-analysis. J Lipid Res. 2018 Sep;59(9):1771-1782. doi: 10.1194/jlr.P085522. Epub 2018 Jul 13. PMID: 30006369; PMCID: PMC6121943.

 

Neuenschwander M, Stadelmaier J, Eble J, Grummich K, Szczerba E, Kiesswetter E, Schlesinger S, Schwingshackl L. Substitution of animal-based with plant-based foods on cardiometabolic health and all-cause mortality: a systematic review and meta-analysis of prospective studies. BMC Med. 2023 Nov 16;21(1):404. doi: 10.1186/s12916-023-03093-1. PMID: 37968628; PMCID: PMC10652524.

Ancestral Diets and Logical Fallacies

There 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 diseases
• Our teeth have (canines/molars), so we were designed to eat only (meat/plants)
• You won't see broccoli on the walls of caves
• If 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 Erectus

Perhaps 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 Records

There 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 Discoveries

Bones 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-Gatherers

The 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.

Rice and Fruit or Carnivore

The rice diet successfully treated malignant hypertension. Today, we have medications that treat malignant hypertension. Before the 1940s, there were no drugs available to treat this disease, resulting in death from untreated malignant hypertension within six months.  Despite the best medical care available, President Franklin Delano Roosevelt died from this disease.

History of the Rice Diet

Walter Kempner developed the rice diet to treat malignant hypertension. For example, failing kidneys would be given a reprieve with a diet low in sodium and protein. Then removal of saturated fat would allow some recovery of the heart.

In a disease that had 100 percent death in six months, Kempner's results were amazing. For example, in Kempner’s original cohort of 192 people, only 25 patients died.  In addition, 107 patients showed significant improvement (from 200/112 mm Hg to 149/96 mm Hg) with the diet. Equally important, heart size decreased in 66 of 72 patients. Moreover, cholesterol was reduced in 73 of 82 patients. Finally, retinopathy improved or disappeared completely in 21 of 33 patients.

"Therapeutic results are little short of miraculous," noted an editorial in the New England Journal of Medicine.

The Rice Diet

Patients were first hospitalized. The diet consisted of white rice, sugar, fruit, fruit juices, vitamins and iron. Total calories were 2,000 with 20 grams of protein and 150 mg of sodium.

Kempner kept careful records of his patients. Reporting success and failure is a key to academic transparency. Finally, the ability to reproduce the data in other centers provided the final key to Kempner's work.

Contrast the Carnivore Diet

The carnivore diet is popular among young, buff men whose living is made by promoting and coaching this diet. They sell the diet based on classic marketing techniques used for overweight patients.

• Lose weight without trying
• No need to log your food
• Eat as much as you want
• Hunger isn't an issue

Marketing phrases used by hucksters for years to trap people unhappy about their weight.

No Science in the Carnivore Diet

The carnivore diet relies on anecdotes, not evidence. Testimonials rule Facebook and YouTube sites. There are no publications about the diet. Finally, many in the carnivore community push against medicine. Conspiratorial thinking is strong, with phrases like this:

• Doctors want you to be sick
• The Medical Community wants to push pills
• Vegetables have anti-nutrients

Try to raise a concern about how this diet would increase the risk of heart disease, and they double down with misinformation. They will deny the evidence showing that high cholesterol leads to heart attacks and strokes. Or make the claim that if you are "metabolically healthy," you don't need to worry about cholesterol.

No Academic Researchers

There are no academic research scientists following people trying the carnivore diet.

That means there is no transparency about the results. In addition, there is no accountability for any bad results.

Those who promote the diet include Paul Saladino, a physician who doesn't see patients and makes his income selling supplements.

The Liver King, who doesn't follow the diet, was caught using performance-enhancing drugs.

Shawn Baker is an orthopedic-trained surgeon who lost his medical license and makes his money promoting the carnivore diet. The New Mexico Medical Board ordered the "voluntary and permanent surrender" of Baker's medical license in 2017. "This action was based on failure to report adverse action taken by a healthcare entity and incompetence to practice as a licensee." He had his license reinstated but is not seeing patients for anything more than coaching for $150 for half an hour.

Ken Berry also lost his medical license for inadequate infection prevention in his offices. He has regained his license.

Concerning Comments

Some comments left on a recent YouTube video by Shawn Baker include:

• A patient developed painful neuropathy from vitamin B6 toxic levels. He quit the carnivore diet and vows never to return
• Another patient developed high oxylate levels. More kidney stones come from eating red meat than spinach - sorry, Paul Saladino.
• One noted fasting glucose increased to 126, which we call diabetes. Saturated fat is not a friend of the pancreas and increases insulin resistance.
• Another noted worsening kidney function with his filtration rate decreasing by 23 percent.
• Multiple complaints about LDL, including one that went from 148 to 353
• Psoriasis is often touted as being healed with this diet, but one noted their psoriasis spreading and getting worse. Red meat is highly inflammatory and not the optimal diet for people with psoriasis. Although psoriasis will come and go spontaneously, a carnivore diet is the worst diet for these patients.
• Gynecomastia was noted by one male, and if you look at many carnivore shirtless salesmen of scams, you will see they also suffer from gynecomastia - those aren't pectoral muscles, those are breasts. Red meat can increase estrogen levels greatly.

Not once did Shawn Baker instruct these people to see their regular doctor for appropriate treatment and follow-up. Hopefully, this will change.

University Studies

Do a research study with human subjects in a university, and there will be an independent board looking over the results. If there are any adverse results, those are reported to the research board, and sometimes studies are stopped because of too many adverse events. When results are published, both the good and the bad - like Kempner's work - are reported.

Don't Do The Rice Diet

The rice diet is for historical purposes only. The Mediterranean Diet is a far superior and more balanced diet. With over 13,000 peer reviewed publications, the Mediterranean Diet is the current pattern of eating that we recommend.

The Benefits of Whole Grains in Your Diet

I want to take you back in time. While we talk about the Mediterranean diet not being a diet of culture but a pattern of eating – it still had its origins in the Mediterranean.

The original Mediterranean diet was described as far back as 500 BC in the Ilead. The ancient Greeks ate whole grains, fruits, vegetables, pulses, and a bit of fish. Red meat was rare.

While red meat may not have been a dietary staple for the Ancient Greeks, it was consumed during feasts, festivals, and special occasions.

Cows were considered sacred gods, like Zeus, and their slaughter was for religious ceremonies and consumed during feasts

The majority of the population received protein from fish, poultry, legumes, and whole grains.

The First Olympics

This was the diet of the first Olympians, as well as the Romans. Ancient Greeks worshiped the body, as you can see from the statues, as well as our language.

We get the word gym from the Greek word “gymnasion," which translates to a place to exercise naked. But those gyms not only had a place to train but also schools, where literature, philosophy, math, and music were taught, as well as a social gathering place.

We also get Diet from the Greeks, which originates from “diaita,” meaning the “way of life” or a manner of living. The Greeks had a balanced approach to health and well-being, emphasizing diet, exercise, and the mind.

Gym bros and bro science were yet to be invented.

Ancient Grains

Could those Olympians of old who ate diets filled with whole-grain cereals have been wrong? Or could it be that those grains of the past were different from today’s grains?

If you’ve ever been on a “low carb” diet, one of the first food groups you eliminate are grains.

As you dutifully got rid of the last bit of joy in your life, you feel it was the cost to have your weight drop.

You might have thought – "Grains are evil."

Low Carb Life Without Grains

Eating burgers without the bun, breakfast without toast, no pastries, no bread, no pasta, no rice, and you were losing weight. Lots of confirmation bias.

Oh those heady early days of a low carb diet, losing weight, feeling better, maybe even noticing cholesterol improved. Hard to sustain though, and did you ever get tired of steak?

Finding Joy in the Mediterranean Diet

Now you come here and find the best diet is the Mediterranean diet. Lots of peer reviewed literature to support it.

Then you wondered what in grains was evil. The first easy thought was that it all breaks down to glucose, and glucose is evil.

Unless you know biochemistry and realize no, that’s not it. Your body runs on glucose.

It's the Gluten

And maybe you read about celiac disease and gluten as its trigger. Maybe some blogger convinced you that wheat in America is filled with gluten, and this is the problem.

Unable to sustain a low-carb diet, you return to the joy of the morning pastry or dessert, all the while thinking grains are what caused the weight to return.

Now you come to the Mediterranean Diet, and whole grains, not refined grains, are on the menu.

Still, you are suspicious, and you think – maybe it was the gluten.

Celiac Disease

Or what happens if you come to the Mediterranean diet and have Celiac disease and gluten causes horrific issues?

But should we all avoid gluten? And can we have a Mediterranean diet if we must be gluten-free?

Should the ancient Greeks become Carnivores instead of those grizzly men who are on a diet now associated with the healthiest people on planet Earth?

Clearly not. Eating too much red meat is associated with increasing heart disease and cancer, while the Mediterranean diet is associated with less heart disease and cancer.

Carnivore's Take

Carnivores like pointing to the ancient wrestler Milo of Croton, who ate twenty pounds of meat a day. They fail to mention that he also ate twenty pounds of bread and drank 18 pints of wine while training. Funny, they all talk about the meat. –There are always outliers, and Milo was one.

When Milo trained, he carried a calf, and as the creature grew, he kept carrying it. He won about six Olympic medals (560 BC).

While we don’t know details, it is odd he ate meat, since his mentor Pythagoras – of the theorem – thought eating meat was unhealthy and made people wage war.

Grains are Evil - "They" Say

And despite what the low-carb and carnivore community tells you, Whole grains have been associated with decreased risk of diabetes, less obesity, and lower rates of cancer and heart disease.

Whole grains have a lot of fiber. In fact, whole grains are one of the fiber rich portions of the foods you eat.

Gluten is a protein found in many grains, like wheat, but not all grains.  Do you know how to stretch dough? Like pizza, the reason you can do it is gluten.

For most of us, gluten isn’t an issue. But for about one percent of the population, gluten can exacerbate an auto-immune response against your small bowel.

If you have celiac disease...

If you have celiac disease and have gluten in your diet, your bowel will be harmed. Thus, you will not effectively absorb nutrients. Many with celiac disease have anemia from an inability to absorb iron.

Most patients with celiac disease will feel bloated with gas, sometimes diarrhea, or even constipation. They might have chronic fatigue or weakness due to a lack of nutrients. In children, it often leads to weight loss. In adults, it can manifest in weight gain.

The symptoms are vague and not specific, but they are part of a history that we see with our patients.

Gluten-free for Everyone

Since the symptoms are so general, many people advocate a gluten-free diet. Some have written books about how gluten causes issues in everyone, and we should avoid it. This is incorrect, but it does sell a lot of books.

Incorporating Gluten-Free Whole Grains

Here are some easy ways to add gluten-free whole grains to your Mediterranean-inspired meals:

1. Quinoa: Swap traditional grains like couscous with quinoa in salads, pilafs, or stuffed vegetables. Quinoa is a complete protein and offers a nutty flavor that complements Mediterranean ingredients well.
2. Brown Rice: Use brown rice instead of traditional pasta in dishes like risotto, stir-fries, or alongside grilled fish or chicken. Brown rice provides a hearty texture and adds a dose of fiber to your meal.
3. Millet: Experiment with millet in place of bulgur wheat in tabbouleh salads or use it as a base for grain bowls topped with roasted vegetables and a drizzle of olive oil.
4. Buckwheat: Incorporate buckwheat flour into your baking for gluten-free bread, pancakes, or crepes. You can also use cooked buckwheat groats as a nutritious alternative to traditional grains in salads or as a side dish.
5. Amaranth: Add amaranth to soups, stews, or porridge for a nutrient-packed boost. Its slightly nutty flavor pairs well with Mediterranean spices and herbs.

My favorite is oatmeal. But make sure you get oats that were ground away from wheat. Bob’s Red Mill has a gluten free oat that you can use. Since oats are a staple of my morning breakfast you might find these a great choice.

 

Finally, corn is a whole grain. Good to add to salads, and my favorite cowboy caviar dish.

By incorporating gluten-free whole grains into your Mediterranean diet, you can enjoy a diverse range of flavors and textures while reaping the nutritional benefits of these wholesome ingredients. Whether you're looking to support digestive health, manage blood sugar levels, or simply explore new culinary horizons, there's a gluten-free whole grain waiting to elevate your next meal.

 

Whole grains are a powerhouse of nutrition, offering a range of health benefits that make them an essential part of a balanced diet.

Why Gluten-Free Whole Grains?

But what if you have celiac disease and cannot tolerate gluten?

Gluten is a protein found in many grains. It is responsible for stretching dough, like pizza.

If you do not have a problem with gluten, there is no reason to avoid gluten.  But if you have celiac disease, gluten must be avoided.

The Mediterranean Diet

The Mediterranean diet is renowned for its focus on fresh fruits and vegetables, lean proteins, healthy fats, and whole grains. By incorporating gluten-free whole grains into this already nutritious diet, you can further enhance its health benefits while catering to dietary restrictions or preferences.

Conclusion

By incorporating gluten-free whole grains into your Mediterranean diet, you can enjoy a diverse range of flavors and textures while reaping the nutritional benefits of these wholesome ingredients. Whether you're looking to support digestive health, manage blood sugar levels, or simply explore new culinary horizons, there's a gluten-free whole grain waiting to elevate your next meal.

Learn to Cook Fish

Fish is not only a healthy option but also a versatile ingredient that can be transformed into a myriad of mouthwatering dishes. Whether you're a seafood aficionado or looking to expand your culinary repertoire, mastering the art of cooking fish can elevate your cooking skills to new heights. In this article, we'll explore the techniques and recipes to create delicious fish dishes that will impress even the most discerning palates.

Cooking Methods:

1. Grilling: Grilling fish over an open flame adds a smoky flavor and beautiful charred marks. Brush the fish with oil to prevent sticking, and cook for a few minutes on each side until opaque and flaky.
2. Baking: Baking fish in the oven is a simple and foolproof method. Place seasoned fish fillets on a baking sheet lined with parchment paper and bake at 375°F (190°C) for 10-15 minutes, depending on the thickness of the fish.
3. Pan-Searing: Pan-searing fish in a hot skillet creates a crispy exterior while keeping the inside moist and tender. Heat oil in a skillet over medium-high heat, then add the fish and cook for 3-4 minutes per side until golden brown.
4. Steaming: Steaming fish is a healthy cooking method that preserves its delicate flavor and texture. Place seasoned fish fillets in a steamer basket over boiling water and steam for 6-8 minutes until cooked through.

Delicious Fish Recipes:

Now that you're familiar with the basics of preparing and cooking fish let's explore some mouthwatering recipes to try at home:

1. Lemon Herb Grilled Salmon: Marinate salmon fillets in a mixture of lemon juice, olive oil, garlic, and fresh herbs. Grill over medium heat for 4-5 minutes per side until charred and cooked through. Serve with a squeeze of fresh lemon juice.
2. Baked Cod with Garlic Butter: Place cod fillets in a baking dish and top with a mixture of melted butter, minced garlic, lemon zest, and chopped parsley. Bake in the oven for 15-20 minutes until flaky and tender.
3. Pan-Seared Sea Bass with Mango Salsa: Season sea bass fillets with salt, pepper, and paprika. Sear in a hot skillet for 3-4 minutes per side until golden brown. Serve with a refreshing mango salsa made with diced mango, red onion, jalapeno, cilantro, and lime juice.

For more great recipes, see terrysimpson.com.