Cancer may be a systemic metabolic breakdown, not a genetic accident. Learn how restoring cellular energy, eliminating seed oils, and reducing stress may protect your health.
Great research report. It describes a fundamental concept in metabolic biochemistry known as the Randle Cycle (or glucose-fatty acid cycle). It is, essentially, a "fuel-saving" mechanism that allows the body to prioritize which energy source to burn based on availability.
The enzyme pyruvate dehydrogenase (PDH) acts as the main switch. Its function is to convert pyruvate (derived from glucose) into Acetyl-CoA so that it can enter the Krebs cycle within the mitochondria. When fatty acid oxidation is high, three things happen that block PDH:
----Excess Acetyl-CoA: The breakdown of fats produces large amounts of Acetyl-CoA, which directly inhibits PDH.
---Increased NADH: Beta-oxidation (fat burning) generates a lot of NADH. A high NADH/NAD ratio
----Citrate Accumulation: The first step of the Krebs cycle becomes saturated, and citrate is released into the cytosol, blocking phosphofructokinase (PFK), the enzyme that allows glycolysis to proceed.
When this mitochondrial "gate" closes, the cell finds itself in a paradoxical situation. Glucose is available, but it cannot be efficiently oxidized. Pyruvate Accumulation: Unable to enter the mitochondria, pyruvate accumulates in the cytoplasm. To prevent glycolysis from stopping completely (which would be fatal for the cell), pyruvate is diverted to lactate formation via the enzyme lactate dehydrogenase. While the complete oxidation of glucose in the mitochondria produces about 30-32 ATP, fermentation to lactate only produces 2 ATP.
Metabolic Flexibility: A healthy cell should be able to switch between fuels. If fat oxidation is permanently elevated (due to excess free fatty acids in the blood or chronic inflammation), the cell loses the ability to manage glucose, contributing to insulin resistance. In pathological contexts, such as cancer, this diversion of glucose to lactate, even in the presence of oxygen, is a central characteristic that allows for rapid tissue growth.
If the cell's powerhouse (the mitochondria) functions correctly and processes fuel cleanly, cell signaling stabilizes. Conversely, when the cell is forced to ferment glucose, a biological "emergency" state is activated, promoting uncontrolled growth. We need metabolic control mechanisms:
1. Fuel Control (Diet)
...Mitochondrial Efficiency: By reducing insulin spikes and maintaining glucose within stable ranges (such as levels of 70-75 mg/dL), we reduce the pressure on the fermentation system.
--Phytonutrients as Signaling Agents: Compounds like sulforaphane are not only "antioxidants"; they act on pathways like Nrf2, which improves detoxification and mitochondrial health, helping the cell decide to die (apoptosis) if it cannot be repaired.
2. Micronutrients: The Pieces of the Gear
As we saw with PDH, without the proper cofactors (B1, Magnesium, Lipoic Acid, Zinc), the machinery stops.
NAD+ and Repair: Maintaining optimal NAD+ levels allows PARP enzymes to repair damaged DNA, preventing the cell from shifting towards a tumor-like metabolism.
Vitamin D3: It acts more like a hormone than a vitamin, regulating the expression of hundreds of genes responsible for immune surveillance.
3. Light and Circadian Rhythms
Exposure to natural light (especially morning sunlight and avoiding blue light at night) regulates mitochondrial melatonin. Unlike the melatonin that enters the bloodstream to induce sleep, the melatonin produced within the mitochondria is the most potent antioxidant for protecting mitochondrial DNA from oxidative damage.
4. Hormonal Balance and Stress
High cortisol is a metabolic switch: it releases stored fatty acids and glucose, blocking the entry of glucose into the mitochondria (Randle Cycle).
Metabolic Environment: A state of hormonal calm sends "safety" signals to cells, allowing them to dedicate energy to repair and maintenance rather than defensive proliferation. 5. The Role of Senolytics and Mimetics
Substances like quercetin, fisetin, and berberine work by "cleaning" old or dysfunctional cells that no longer produce energy efficiently and that could induce inflammation in neighboring cells.
By managing these factors, you're not just attacking the disease; you're optimizing the ecosystem in which your healthy cells thrive and dysfunctional cells lose their competitive advantage. It's essentially about regaining control over your own biology.
Cortisol, the main stress hormone, acts as a master regulator of metabolism. In the context of cancer, chronically elevated cortisol can alter the cellular ecosystem, promoting tumor progression through several biochemical mechanisms. Chronic cortisol keeps the mitochondrial "door" closed by promoting fat oxidation and insulin resistance, forcing cells to ferment glucose in the cytoplasm (lactate), thus fueling the metabolic phenotype of cancer.
Cortisol raises blood glucose levels (hyperglycemia) and promotes insulin resistance. This provides a constant supply of "fuel" for cancer cells, which rely on glucose for rapid proliferation.
Chronic cortisol weakens the ability of T cells (of the immune system) to detect and destroy abnormal cells. This creates a microenvironment where the tumor can grow undisturbed.
Cortisol has been found to activate genes that help cancer cells survive as they travel through the bloodstream, protecting them from the oxidative stress that would normally kill them.
This study proposes that chronic stress (and the resulting cortisol) should be considered a fundamental cause in the initiation and promotion of cancer, just like genetics or diet.
HOW THE WRONG DIETARY COMPONENT CAN WRECK YOUR HEALTH
In this interview, Georgi Dinkov, an expert on linoleic acid (LA), details some of the health risks of this extremely common fat in the modern diet and how to safely eliminate it from the body.
Both Georgi and I are convinced that excessive linoleic acid consumption is one of the most important variables that can determine the success or failure of one's health, especially in the long term. It contributes far more to chronic and degenerative diseases, as well as mortality, than sugar, and is the main reason why processed foods are so harmful.
Historical incidence curves (from the last 50 to 75 years) of cancer, cardiovascular diseases (CVD), diabetes, and neurological diseases in the general population remarkably coincide with the ever-increasing consumption rates of PUFAs in developed countries, suggesting that PUFAs are an important factor in these diseases.
Being the typical American Diet loaded with Ultra- Processed Foods in turn loaded with sugar often hidden by using up to 60 different kinds, labels and then the icing on the cake - LA Oils. With this crippling the bodies ability to burn Both Sugar and Fat. With the Rockefeller heavy dominance on our medical system early insights about metabolic Dis-Ease's got swept under the rug. With a focus on weight, losing weight, a number on a scale multiple treadmill industries were born pushing us into never ending stories of different kinds of Chronic Dis-Ease's. My ear hears too much -especially refined sugars or too much fat, or in the Fast Food Grab and Gulps too much of both with an added insult both are too much of the wrong kinds of Sugars and Fat/Oil, has led us down a path destroying our once held status as about the healthiest people in the world, to todays majority of us Zombies, limping along with Chronic Dis-eases. Spending the most for the worst results to manage symptoms.
Before the expanded realized knowledge of our metabolic systems, Keto worked to lose weight and helped recover an ability to burn both sugars and fat, but there was a need to cycle between a fat heavy to healthy carb sources. This deeper understanding, and with likely more to come, we can ditch the LA Oils with our needs for such easily met with just healthy portions of good food and the same for sugars. Instead of the Machines keep us focused on weight loss - yoyo waist lines and feeding a Treadmill Profit Machine for the Chronic Dis-Ease to support it, the newer insights should help us find The Size that Fits Us Best by feeding our health with the right proportions of Healthy Carbs, Fats and Proteins. If having issues, feed your healthy body would want as if it were already healthy and need and eventually it should create an actual healthy body. If I understand correctly, reduced calories to initially lose weight to start the body to remember how to burn both sugar and oil. Then after a few days add just a few more calories so as to prevent the body from going into starvation mode. When you hit your best range, maintain it.
Obesity is a chronic, multifactorial metabolic disease that has become a global public health crisis. An estimated 2.6 billion people currently live with overweight or obesity, and this number is projected to exceed 4 billion by 2035. Its complex relationship with food production and consumption patterns demands sustainable solutions to reduce pressure on ecosystems and promote healthier lifestyles. Obesity affects more than one-third of Americans and increases the risk of cardiovascular disease and type 2 diabetes. Interventional trials have consistently shown that consuming plant-based diets reduces body fat in overweight and obese subjects, even while controlling for energy intake.
Combating obesity requires holistic strategies that address not only individual health but also the broader environmental impacts of food systems. A systematic review examined the relationship between plant-based diets and obesity, focusing on studies that assess body mass index (BMI) and body fat. Six main dietary mechanisms can lead to a reduction in body fat. These include (1) reduced calorie density, (2) improved gut microbiota symbiosis, (3) increased insulin sensitivity, (4) reduced trimethylamine N-oxide (TMAO), (5) activation of peroxisome proliferator-activated receptors (PPARs), and (6) overexpression of mitochondrial uncoupling proteins.
Excessive consumption of high-calorie, low-nutrient foods, particularly those high in saturated fat, sugar, and sodium, has led to a global obesity epidemic. This, in turn, increases the risk of chronic diseases such as heart disease, type 2 diabetes, and certain types of cancer.
Obesity and type 2 diabetes share a common characteristic: reduced gut microbial diversity. People who consume more dietary fiber from whole foods have a more diverse gut microbiota. Some of these monosaccharides can be fermented by the gut microbiota to form short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate.
A very important lesson I learned in 2000 when I was diagnosed with terminal lymphoma. All chemos, etc. failed, BUT ORGANIC, SUGAR FREE DID THE TRICK! MAIN PROBLEM IS, IT IS HARD, VERY HARD TO GIVE UP OREO COOKIES, CONVENIENCE OF GRAB AND GO FOOD! I WAS ADDICTED! To me this was harder then if I was addicted to heroin, cocaine! You do not need them to live, just do not take that first hit! You do need food to live and every processd food is full of sugar! It takes a lot of will power to give them up! BUT it is worth it to hear the doctor say "You are in complete remission".
No more cravings! Over 195 lbs lost! I felt better, could move better! They discovered type 2 diabetes in 2000 also, now thanks to Berberine I contol my blood sugar except when I get a pitty party, insulin brings it down to normal. At 85, still moving, driving, living by myself.
Yes, just. The evidence reported by Dr. Mercola reveals an essential foundation for health: the importance of an organic diet of fresh, non-ultra-processed foods (hydrogenated fats and carcinogenic compounds), low in omega-6 fatty acids, fish (EPA, DHA, vitamins D and E), saturated fats from coconut and grass-fed livestock, fasting, and exercise. These factors are crucial for preventing insulin resistance, obesity, and metabolic diseases. Obesity and aging predispose individuals to numerous overlapping chronic diseases. For example, metabolic abnormalities, including insulin resistance (IR) and type 2 diabetes (T2D), are major causes of morbidity and mortality. Chronic low-grade inflammation of tissues, such as the liver, visceral adipose tissue, and neurological tissues, is considered to contribute significantly to these chronic diseases. The intestinal barrier function is strongly implicated in the pathogenesis of obesity and age-related diseases.
The incidence of obesity and its related metabolic disorders has increased significantly over the past three decades, culminating in the current global epidemic of metabolic diseases and leading to the search for contributing factors. Exposure of the developing fetus/newborn to a typical Western diet increases the risk of obesity and metabolic disorders throughout life, creating an intergenerational cycle of metabolic diseases. In Western countries, this epidemic of metabolic diseases has coincided with a marked increase in the intake of omega-6 polyunsaturated fatty acids. Recent studies have emphasized the proadipogenic properties of omega-6 polyunsaturated fatty acids. Recent studies have shown that perinatal exposure to a diet rich in omega-6 polyunsaturated fatty acids results in a progressive accumulation of body fat across generations.
There is evidence supporting the hypothesis that omega-6 PUFAs have proadipogenic and prolipogenic properties, and exposure to a diet rich in omega-6 PUFAs during the first years of life has been shown to be sufficient to program an increase in body fat mass in offspring.
This review reports on the evidence of the real benefit of fish consumption in preventing sarcopenia and the positive effect of biological compounds present in fish on muscle mass. Fish improves glucose homeostasis, helping to prevent diabetes and metabolic syndrome, and has a positive impact on preserving muscle mass in the elderly, mediated by multiple mechanisms.
Experimental studies have suggested that omega-6 and omega-3 fatty acids have divergent effects on body fat gain through mechanisms of adipogenesis, adipose tissue darkening, lipid homeostasis, the brain-gut-adipose tissue axis, and, most importantly, systemic inflammation. Prospective studies clearly show an increased risk of obesity as omega-6 fatty acid levels and the omega-6/omega-3 ratio increase in red blood cell (RBC) membrane phospholipids, while red blood cell membrane phospholipids high in omega-3 decrease the risk of obesity. The omega-6/omega-3 ratio plays a significant role in the increased development of obesity through AA eicosanoid metabolites and hyperactivity of the endocannabinoid system, which can be reversed with increased intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).
Higher levels of dietary or circulating omega-3 PUFAs are associated with a lower risk of metabolic syndrome. Emerging findings in obesity indicate higher omega-6/omega-3 PUFA ratios. Omega-3 PUFAs may improve blood lipid profiles and glycemic outcomes in patients with type 2 diabetes mellitus and reduce liver fat in non-alcoholic fatty liver disease (NAFLD); findings from several recent meta-analyses support these effects. Genetic predisposition affects interindividual variability in insulin sensitivity response to omega-3 PUFA supplementation. Omega-3 PUFAs have prebiotic effects, altering the gut microbiota.
https://www.ingentaconnect.com/content/wk/cocnm/2022/00000025/00000006/art00012 (2022) Plasma levels of four omega-6 oxylipins were positively correlated with adiposity, metabolic syndrome prevalence, fatty liver index, and the homeostatic model assessment of the insulin resistance index and lipid parameters. Conversely, plasma levels of three omega-3 oxylipins were negatively correlated with adiposity, metabolic syndrome prevalence, fatty liver index, and the homeostatic model assessment of the insulin resistance index and lipid parameters. The seven-oxylipin panel predicted adiposity better than traditional inflammatory markers such as interferon-gamma or tumor necrosis factor-alpha. Pathway analyses revealed that obese individuals had higher plasma levels of omega-6 and lower plasma levels of omega-3 oxylipins than individuals of normal weight.
Great research report. It describes a fundamental concept in metabolic biochemistry known as the Randle Cycle (or glucose-fatty acid cycle). It is, essentially, a "fuel-saving" mechanism that allows the body to prioritize which energy source to burn based on availability.
The enzyme pyruvate dehydrogenase (PDH) acts as the main switch. Its function is to convert pyruvate (derived from glucose) into Acetyl-CoA so that it can enter the Krebs cycle within the mitochondria. When fatty acid oxidation is high, three things happen that block PDH:
----Excess Acetyl-CoA: The breakdown of fats produces large amounts of Acetyl-CoA, which directly inhibits PDH.
---Increased NADH: Beta-oxidation (fat burning) generates a lot of NADH. A high NADH/NAD ratio
----Citrate Accumulation: The first step of the Krebs cycle becomes saturated, and citrate is released into the cytosol, blocking phosphofructokinase (PFK), the enzyme that allows glycolysis to proceed.
When this mitochondrial "gate" closes, the cell finds itself in a paradoxical situation. Glucose is available, but it cannot be efficiently oxidized. Pyruvate Accumulation: Unable to enter the mitochondria, pyruvate accumulates in the cytoplasm. To prevent glycolysis from stopping completely (which would be fatal for the cell), pyruvate is diverted to lactate formation via the enzyme lactate dehydrogenase. While the complete oxidation of glucose in the mitochondria produces about 30-32 ATP, fermentation to lactate only produces 2 ATP.
https://pmc.ncbi.nlm.nih.gov/articles/PMC4580141/ (2015)
https://pmc.ncbi.nlm.nih.gov/articles/PMC4615232/ (2014)
Metabolic Flexibility: A healthy cell should be able to switch between fuels. If fat oxidation is permanently elevated (due to excess free fatty acids in the blood or chronic inflammation), the cell loses the ability to manage glucose, contributing to insulin resistance. In pathological contexts, such as cancer, this diversion of glucose to lactate, even in the presence of oxygen, is a central characteristic that allows for rapid tissue growth.
If the cell's powerhouse (the mitochondria) functions correctly and processes fuel cleanly, cell signaling stabilizes. Conversely, when the cell is forced to ferment glucose, a biological "emergency" state is activated, promoting uncontrolled growth. We need metabolic control mechanisms:
1. Fuel Control (Diet)
...Mitochondrial Efficiency: By reducing insulin spikes and maintaining glucose within stable ranges (such as levels of 70-75 mg/dL), we reduce the pressure on the fermentation system.
--Phytonutrients as Signaling Agents: Compounds like sulforaphane are not only "antioxidants"; they act on pathways like Nrf2, which improves detoxification and mitochondrial health, helping the cell decide to die (apoptosis) if it cannot be repaired.
2. Micronutrients: The Pieces of the Gear
As we saw with PDH, without the proper cofactors (B1, Magnesium, Lipoic Acid, Zinc), the machinery stops.
NAD+ and Repair: Maintaining optimal NAD+ levels allows PARP enzymes to repair damaged DNA, preventing the cell from shifting towards a tumor-like metabolism.
Vitamin D3: It acts more like a hormone than a vitamin, regulating the expression of hundreds of genes responsible for immune surveillance.
3. Light and Circadian Rhythms
Exposure to natural light (especially morning sunlight and avoiding blue light at night) regulates mitochondrial melatonin. Unlike the melatonin that enters the bloodstream to induce sleep, the melatonin produced within the mitochondria is the most potent antioxidant for protecting mitochondrial DNA from oxidative damage.
4. Hormonal Balance and Stress
High cortisol is a metabolic switch: it releases stored fatty acids and glucose, blocking the entry of glucose into the mitochondria (Randle Cycle).
Metabolic Environment: A state of hormonal calm sends "safety" signals to cells, allowing them to dedicate energy to repair and maintenance rather than defensive proliferation. 5. The Role of Senolytics and Mimetics
Substances like quercetin, fisetin, and berberine work by "cleaning" old or dysfunctional cells that no longer produce energy efficiently and that could induce inflammation in neighboring cells.
By managing these factors, you're not just attacking the disease; you're optimizing the ecosystem in which your healthy cells thrive and dysfunctional cells lose their competitive advantage. It's essentially about regaining control over your own biology.
https://pmc.ncbi.nlm.nih.gov/articles/PMC3609577/ (2013)
https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2022.989793/full (2022)
https://pmc.ncbi.nlm.nih.gov/articles/PMC11107735/ (2017)
https://pubmed.ncbi.nlm.nih.gov/31547055/ (2019)
-----------------------------------------
Cortisol, the main stress hormone, acts as a master regulator of metabolism. In the context of cancer, chronically elevated cortisol can alter the cellular ecosystem, promoting tumor progression through several biochemical mechanisms. Chronic cortisol keeps the mitochondrial "door" closed by promoting fat oxidation and insulin resistance, forcing cells to ferment glucose in the cytoplasm (lactate), thus fueling the metabolic phenotype of cancer.
Cortisol raises blood glucose levels (hyperglycemia) and promotes insulin resistance. This provides a constant supply of "fuel" for cancer cells, which rely on glucose for rapid proliferation.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8476513/ (2021)
Chronic cortisol weakens the ability of T cells (of the immune system) to detect and destroy abnormal cells. This creates a microenvironment where the tumor can grow undisturbed.
https://pmc.ncbi.nlm.nih.gov/articles/PMC8294471/ (2021)
Cortisol has been found to activate genes that help cancer cells survive as they travel through the bloodstream, protecting them from the oxidative stress that would normally kill them.
https://pubmed.ncbi.nlm.nih.gov/36766760/ (2023)
This study proposes that chronic stress (and the resulting cortisol) should be considered a fundamental cause in the initiation and promotion of cancer, just like genetics or diet.
https://pubmed.ncbi.nlm.nih.gov/36766760/ (2023) https://pmc.ncbi.nlm.nih.gov/articles/PMC12269309/ (2025)
-----------------------------------------------
HOW THE WRONG DIETARY COMPONENT CAN WRECK YOUR HEALTH
In this interview, Georgi Dinkov, an expert on linoleic acid (LA), details some of the health risks of this extremely common fat in the modern diet and how to safely eliminate it from the body.
Both Georgi and I are convinced that excessive linoleic acid consumption is one of the most important variables that can determine the success or failure of one's health, especially in the long term. It contributes far more to chronic and degenerative diseases, as well as mortality, than sugar, and is the main reason why processed foods are so harmful.
Historical incidence curves (from the last 50 to 75 years) of cancer, cardiovascular diseases (CVD), diabetes, and neurological diseases in the general population remarkably coincide with the ever-increasing consumption rates of PUFAs in developed countries, suggesting that PUFAs are an important factor in these diseases.
https://articles.mercola.com/sites/articles/archive/2023/01/01/omega-6-linoleic-acid.aspx?_gl=1*10m8j7b*_ga*NTAzNzg5OTMwLjE3NDg1MTk4NDI.*_ga_4MC0V1BXBK*czE3Nzc0NDUyODMkbzY3JGcxJHQxNzc3NDQ1NDA1JGo1OSRsMCRoMA.. (2023)
Being the typical American Diet loaded with Ultra- Processed Foods in turn loaded with sugar often hidden by using up to 60 different kinds, labels and then the icing on the cake - LA Oils. With this crippling the bodies ability to burn Both Sugar and Fat. With the Rockefeller heavy dominance on our medical system early insights about metabolic Dis-Ease's got swept under the rug. With a focus on weight, losing weight, a number on a scale multiple treadmill industries were born pushing us into never ending stories of different kinds of Chronic Dis-Ease's. My ear hears too much -especially refined sugars or too much fat, or in the Fast Food Grab and Gulps too much of both with an added insult both are too much of the wrong kinds of Sugars and Fat/Oil, has led us down a path destroying our once held status as about the healthiest people in the world, to todays majority of us Zombies, limping along with Chronic Dis-eases. Spending the most for the worst results to manage symptoms.
Before the expanded realized knowledge of our metabolic systems, Keto worked to lose weight and helped recover an ability to burn both sugars and fat, but there was a need to cycle between a fat heavy to healthy carb sources. This deeper understanding, and with likely more to come, we can ditch the LA Oils with our needs for such easily met with just healthy portions of good food and the same for sugars. Instead of the Machines keep us focused on weight loss - yoyo waist lines and feeding a Treadmill Profit Machine for the Chronic Dis-Ease to support it, the newer insights should help us find The Size that Fits Us Best by feeding our health with the right proportions of Healthy Carbs, Fats and Proteins. If having issues, feed your healthy body would want as if it were already healthy and need and eventually it should create an actual healthy body. If I understand correctly, reduced calories to initially lose weight to start the body to remember how to burn both sugar and oil. Then after a few days add just a few more calories so as to prevent the body from going into starvation mode. When you hit your best range, maintain it.
Should anyone have missed this. This expands why a different approach is needed to lose weight and renew proper functions.
https://articles.mercola.com/sites/articles/archive/2026/04/29/rapid-fat-loss.aspx?sd=20120104&utm_source=prnl&utm_medium=email&utm_content=art1HL&utm_campaign=20260429Z1&foDate=true&mid=DM1904245&rid=554704461
Obesity is a chronic, multifactorial metabolic disease that has become a global public health crisis. An estimated 2.6 billion people currently live with overweight or obesity, and this number is projected to exceed 4 billion by 2035. Its complex relationship with food production and consumption patterns demands sustainable solutions to reduce pressure on ecosystems and promote healthier lifestyles. Obesity affects more than one-third of Americans and increases the risk of cardiovascular disease and type 2 diabetes. Interventional trials have consistently shown that consuming plant-based diets reduces body fat in overweight and obese subjects, even while controlling for energy intake.
Combating obesity requires holistic strategies that address not only individual health but also the broader environmental impacts of food systems. A systematic review examined the relationship between plant-based diets and obesity, focusing on studies that assess body mass index (BMI) and body fat. Six main dietary mechanisms can lead to a reduction in body fat. These include (1) reduced calorie density, (2) improved gut microbiota symbiosis, (3) increased insulin sensitivity, (4) reduced trimethylamine N-oxide (TMAO), (5) activation of peroxisome proliferator-activated receptors (PPARs), and (6) overexpression of mitochondrial uncoupling proteins.
Excessive consumption of high-calorie, low-nutrient foods, particularly those high in saturated fat, sugar, and sodium, has led to a global obesity epidemic. This, in turn, increases the risk of chronic diseases such as heart disease, type 2 diabetes, and certain types of cancer.
Obesity and type 2 diabetes share a common characteristic: reduced gut microbial diversity. People who consume more dietary fiber from whole foods have a more diverse gut microbiota. Some of these monosaccharides can be fermented by the gut microbiota to form short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate.
https://www.mdpi.com/2072-6643/11/11/2712 (2019).--
https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2023.1108088/full (2023).--
https://link.springer.com/article/10.1186/s12944-023-01803-5 (2023).--
https://www.mdpi.com/2304-8158/12/5/1023 (2023).--
https://www.mdpi.com/2072-6643/16/14/2240 (2024).--
https://onlinelibrary.wiley.com/doi/full/10.1111/obr.13901 (2025)
https://lseee.net/index.php/ms/article/view/1041 (2025).--
https://www.mdpi.com/2072-6643/17/11/1753 (2025).--
https://www.mdpi.com/2227-9059/13/9/2173 (2025).---
A very important lesson I learned in 2000 when I was diagnosed with terminal lymphoma. All chemos, etc. failed, BUT ORGANIC, SUGAR FREE DID THE TRICK! MAIN PROBLEM IS, IT IS HARD, VERY HARD TO GIVE UP OREO COOKIES, CONVENIENCE OF GRAB AND GO FOOD! I WAS ADDICTED! To me this was harder then if I was addicted to heroin, cocaine! You do not need them to live, just do not take that first hit! You do need food to live and every processd food is full of sugar! It takes a lot of will power to give them up! BUT it is worth it to hear the doctor say "You are in complete remission".
No more cravings! Over 195 lbs lost! I felt better, could move better! They discovered type 2 diabetes in 2000 also, now thanks to Berberine I contol my blood sugar except when I get a pitty party, insulin brings it down to normal. At 85, still moving, driving, living by myself.
Yes, just. The evidence reported by Dr. Mercola reveals an essential foundation for health: the importance of an organic diet of fresh, non-ultra-processed foods (hydrogenated fats and carcinogenic compounds), low in omega-6 fatty acids, fish (EPA, DHA, vitamins D and E), saturated fats from coconut and grass-fed livestock, fasting, and exercise. These factors are crucial for preventing insulin resistance, obesity, and metabolic diseases. Obesity and aging predispose individuals to numerous overlapping chronic diseases. For example, metabolic abnormalities, including insulin resistance (IR) and type 2 diabetes (T2D), are major causes of morbidity and mortality. Chronic low-grade inflammation of tissues, such as the liver, visceral adipose tissue, and neurological tissues, is considered to contribute significantly to these chronic diseases. The intestinal barrier function is strongly implicated in the pathogenesis of obesity and age-related diseases.
https://febs.onlinelibrary.wiley.com/doi/full/10.1111/febs.16558 (2022)
The incidence of obesity and its related metabolic disorders has increased significantly over the past three decades, culminating in the current global epidemic of metabolic diseases and leading to the search for contributing factors. Exposure of the developing fetus/newborn to a typical Western diet increases the risk of obesity and metabolic disorders throughout life, creating an intergenerational cycle of metabolic diseases. In Western countries, this epidemic of metabolic diseases has coincided with a marked increase in the intake of omega-6 polyunsaturated fatty acids. Recent studies have emphasized the proadipogenic properties of omega-6 polyunsaturated fatty acids. Recent studies have shown that perinatal exposure to a diet rich in omega-6 polyunsaturated fatty acids results in a progressive accumulation of body fat across generations.
There is evidence supporting the hypothesis that omega-6 PUFAs have proadipogenic and prolipogenic properties, and exposure to a diet rich in omega-6 PUFAs during the first years of life has been shown to be sufficient to program an increase in body fat mass in offspring.
https://journals.lww.com/co-endocrinology/Fulltext/2013/02000/Omega_6_polyunsaturated_fatty_acids_and_the_early.12.aspx (2013)
This review reports on the evidence of the real benefit of fish consumption in preventing sarcopenia and the positive effect of biological compounds present in fish on muscle mass. Fish improves glucose homeostasis, helping to prevent diabetes and metabolic syndrome, and has a positive impact on preserving muscle mass in the elderly, mediated by multiple mechanisms.
https://www.mdpi.com/2072-6643/12/2/307 (2020)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8710756/ (2021)
https://journals.sagepub.com/doi/full/10.1177/11786388211022378 (2022)
Experimental studies have suggested that omega-6 and omega-3 fatty acids have divergent effects on body fat gain through mechanisms of adipogenesis, adipose tissue darkening, lipid homeostasis, the brain-gut-adipose tissue axis, and, most importantly, systemic inflammation. Prospective studies clearly show an increased risk of obesity as omega-6 fatty acid levels and the omega-6/omega-3 ratio increase in red blood cell (RBC) membrane phospholipids, while red blood cell membrane phospholipids high in omega-3 decrease the risk of obesity. The omega-6/omega-3 ratio plays a significant role in the increased development of obesity through AA eicosanoid metabolites and hyperactivity of the endocannabinoid system, which can be reversed with increased intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).
https://www.mdpi.com/2072-6643/8/3/128 (2016)
Higher levels of dietary or circulating omega-3 PUFAs are associated with a lower risk of metabolic syndrome. Emerging findings in obesity indicate higher omega-6/omega-3 PUFA ratios. Omega-3 PUFAs may improve blood lipid profiles and glycemic outcomes in patients with type 2 diabetes mellitus and reduce liver fat in non-alcoholic fatty liver disease (NAFLD); findings from several recent meta-analyses support these effects. Genetic predisposition affects interindividual variability in insulin sensitivity response to omega-3 PUFA supplementation. Omega-3 PUFAs have prebiotic effects, altering the gut microbiota.
https://www.ingentaconnect.com/content/wk/cocnm/2022/00000025/00000006/art00012 (2022) Plasma levels of four omega-6 oxylipins were positively correlated with adiposity, metabolic syndrome prevalence, fatty liver index, and the homeostatic model assessment of the insulin resistance index and lipid parameters. Conversely, plasma levels of three omega-3 oxylipins were negatively correlated with adiposity, metabolic syndrome prevalence, fatty liver index, and the homeostatic model assessment of the insulin resistance index and lipid parameters. The seven-oxylipin panel predicted adiposity better than traditional inflammatory markers such as interferon-gamma or tumor necrosis factor-alpha. Pathway analyses revealed that obese individuals had higher plasma levels of omega-6 and lower plasma levels of omega-3 oxylipins than individuals of normal weight.
https://onlinelibrary.wiley.com/doi/full/10.1002/oby.23282