by Lloyd » Fri Jul 19, 2024 3:37 am
RESOLVING DIABETES, HEART DISEASE, LIVER DISEASE, DEMENTIA
Last April I transcribed a video about the danger of unsaturated fats at
https://naturalremedieswiki.substack.co ... rt-disease . Now I learned about a saturated fat that can replace the unsaturated fats in cell membranes to make them stronger. (There's a chemical formula for fats at
https://naturalremedieswiki.substack.co ... s-and-oils which shows that Saturated fats are stronger than Unsaturated fats.)
C15 IS A NEW-FOUND ESSENTIAL FAT IN DAIRY FOR HEALTH & LONGEVITY
C15 DEFICIENCY DISEASES. There is abundant evidence that C15 deficiency may accelerate the progression of aging-associated diseases, including dysmetabolic iron overload syndrome (DIOS), type 2 diabetes, cardiovascular disease, and NAFLD (Fatty Liver).
DAILY NEEDED AMOUNT. Historical and recent human data support a daily dietary C15 intake of around 100 to 200 mg to achieve optimal circulating C15 levels (over 0.2% of circulating fatty acids).
FOOD SOURCES. Get over 300 mg per 100 g from: Whipping Cream, Cream Cheese, Cheddar Cheese, American Cheese, Swiss Cheese (lesser amounts from other cheese and from some fish & meat). Too much dairy etc leads to constipation, so I avoid too much cheese and devour a lot of legumes and soaked chia seeds to prevent that.
A PINT OF MILK. Whole milk contains about 32.5 mg per 100 g, so a pint would provide c. 154 mg of C15.
(BRANDS. Several brands of milk are RBGH free, namely Organic Brands: Horizon Organic, Organic Valley, Stonyfield Organic; Other Brands: (Walmart's) Great Valu, Alta Dena, Brown Cow Farm.)
4 teaspoons of BUTTER (8mg/g) provides c. 160 mg of C15.
8 teaspoons of SOUR CREAM (30%) (3.5mg/g) has c. 140mg of C15.
9 teaspoons of CREAM CHEESE (3.4mg/g) has c. 153mg of C15.
2 slices of CHEDDAR CHEESE (3.2mg/g) has c. 179mg of C15 (c. 28g/slice).
3 slices of AMERICAN CHEESE (3.1mg/g) has c. 186mg of C15 (c. 20g/slice).
2 slices of SWISS CHEESE (3.1 mg/g) has c. 152mg of C15 (c.25g/slice).
C15. The new fat, or fatty acid, is called Pentadecanoic Acid. They call it C15, because it has 15 carbon atoms, but it seems like it should be called PDA, because other fatty acids are abbreviated that way, such as ALA, EPA, DHA etc. But I'll go with C15.
CANCER. I said before that casein in dairy is said to increase the risk of prostate cancer, but the body normally has enzymes to break down casein. So I assume it's only if the casein can't be broken down that it can be a problem.
ESSENTIAL FATTY ACID. Dairy is part of the Mediterranean Diet, and it's said to be one of the best diets, and since dairy is now shown to have an essential fatty acid, C15, I'm planning to resume milk and cream cheese or sour cream consumption.
REMINERALIZE TEETH? Milk contains calcium and phosphate which can remineralize teeth and it has a pH that doesn't harm the teeth, so I'm planning to start mouth rinsing with rBGH-free milk, i.e. Great Valu from Walmart, to see if that will heal my cavities. One lady dentist on Youtube recommends brushing with one of the Crest toothpastes designed for cavity fighting, as she said it's the only product proven to reduce cavities. She said the fluoride in it helps remineralize teeth, but she recommends spitting it out after brushing, because fluoride is toxic to the brain etc. However, I found that that toothpaste contains titanium oxide or dioxide, which is also toxic to the brain. And many companies now use nanoparticles of such ingredients, which is even worse than before. So I hope swishing with milk will heal my cavities.
PAPER TITLE. The Cellular Stability Hypothesis: Evidence of Ferroptosis and Accelerated Aging-Associated Diseases as Newly Identified Nutritional Pentadecanoic Acid (C15:0) Deficiency Syndrome
LINK.
https://www.mdpi.com/2218-1989/14/7/355
ABSTRACT. CELLULAR FRAGILITY SYNDROME
Ferroptosis is a newly discovered form of cell death caused by the peroxidation of fragile fatty acids in cell membranes, which combines with iron to increase reactive oxygen species and disable mitochondria. Ferroptosis has been linked to aging-related conditions, including type 2 diabetes, cardiovascular disease, and nonalcoholic fatty liver disease (NAFLD). Pentadecanoic acid (C15:0), an odd-chain saturated fat, is an essential fatty acid with the primary roles of stabilizing cell membranes and repairing mitochondrial function. By doing so, C15:0 reverses the underpinnings of ferroptosis. Under the proposed “Cellular Stability Hypothesis”, evidence is provided to show that cell membranes optimally need >0.4% to 0.64% C15:0 (of total circulating fatty acids) to support long-term health and longevity. A pathophysiology of a newly identified nutritional C15:0 deficiency syndrome (“Cellular Fragility Syndrome”) is provided that demonstrates how C15:0 deficiencies (≤0.2% total circulating fatty acids) can increase susceptibilities to ferroptosis, dysmetabolic iron overload syndrome, type 2 diabetes, cardiovascular disease, and NAFLD {Fatty Liver}. Further, evidence is provided that C15:0 supplementation can reverse the described C15:0 deficiency syndrome, including the key components of ferroptosis. Given the declining dietary intake of C15:0, especially among younger generations, there is a need for extensive studies to understand the potential breadth of Cellular Fragility Syndrome across populations.
CELL MEMBRANES DESTRUCTION. Based on A.J. Hulbert’s Cell Membrane Pacemaker Theory of Aging, mammalian longevity is determined by the stability of fatty acids in cell membranes, which protect against lipid peroxidation and slow the onset of diseases that eventually lead to mortality [1]. In support of this theory, Hulbert showed that cell membranes containing fatty acids with higher saturation had greater cellular stability. In turn, this stability resulted in lowered circulating lipid peroxidation and was associated with longer mammalian species’ lifespans. There is evidence that this association between cell membrane stability and lifespan is not limited to variations between species but also within species, including humans.
LIPID PEROXIDATION & IRON OVERLOAD. Ferroptosis requires two instigators: fragile polyunsaturated fatty acids in cell membranes that are susceptible to lipid peroxidation and excess intracellular iron [12,13]. Polyunsaturated fatty acids are particularly susceptible to lipid peroxidation because these lipids have multiple double bonds in their molecular structure that are more easily attacked by oxygen [14]. Lipid peroxidation, in and of itself, is a major contributor to numerous aging-related diseases, including metabolic syndrome, NAFLD, cardiovascular disease, and neurodegenerative diseases [15,16,17,18]. Further, dysregulated iron metabolism and direct tissue damage caused by iron overload are being increasingly recognized as drivers of type 2 diabetes, NAFLD, cardiovascular disease, and neurodegenerative diseases [19,20,21,22]. As described below, when lipid peroxidation combines with iron overload, the result is ferroptosis, which has wide-ranging effects that contribute to the onset and progression of metabolic and related diseases
TYPE 2 DIABETES. Studies support that ferroptosis is playing a role in the rising incidence of type 2 diabetes, in part due to a one–two punch that contributes to the onset and progression of disease [2]. First, pancreatic cells are more susceptible to ferroptosis relative to other cells due to naturally lower production of a key antioxidative enzyme called glutathione peroxidase; in turn, the ferroptosis of pancreatic cells results in lower insulin secretion [25]. Second, ferroptosis in the liver, another organ susceptible to lipid peroxidation and iron overload, can cause insulin resistance [26]. Together, these effects can impair glucose metabolism and support sustained hyperglycemia. It is well established that people with type 2 diabetes have a higher risk of co-morbidities, including cardiovascular disease, cancer, neurodegenerative diseases, and advanced NAFLD [27,28,29,30].
FATTY LIVER. NAFLD is a disease involving excessive fat deposition in the liver (i.e., steatosis) that can progress to inflammation, necrosis, cirrhosis {and liver failure}. ... Because the liver is a key organ responsible for lipid and iron metabolism, the vicious cycle of ferroptosis and liver injury may serve as the epicenter for ferroptosis throughout the body.
CARDIOVASCULAR DISEASE. Ferroptosis, due to both lipid peroxidation and iron accumulation in blood vessel walls, can cause or worsen inflammation and oxidized-LDL-associated atherosclerosis [37]. Ferroptosis has also been linked to coronary heart disease, multiple cardiomyopathies, and heart failure due to direct cardiac tissue injury [5]. Early studies in relevant animal models have demonstrated the potential to prevent or treat cardiovascular diseases by targeting ferroptosis [38].
NEURODEGENERATIVE DISEASE. The brain contains a substantial amount of lipids and, as such, is susceptible to lipid peroxidation. Further, iron deposition in the brain, which increases with age, can cause histologic changes consistent with Alzheimer’s disease [22]. Together, lipid peroxidation and iron accumulation from ferroptosis feed off each other, creating a destructive cycle that contributes to the onset and progression of neurodegenerative diseases [39].
[color=#FF0000]RESOLVING DIABETES, HEART DISEASE, LIVER DISEASE, DEMENTIA[/color]
Last April I transcribed a video about the danger of unsaturated fats at https://naturalremedieswiki.substack.com/p/heart-disease . Now I learned about a saturated fat that can replace the unsaturated fats in cell membranes to make them stronger. (There's a chemical formula for fats at https://naturalremedieswiki.substack.com/i/143243892/phytosterols-and-oils which shows that Saturated fats are stronger than Unsaturated fats.)
[color=#0000FF]C15 IS A NEW-FOUND ESSENTIAL FAT IN DAIRY FOR HEALTH & LONGEVITY[/color]
C15 DEFICIENCY DISEASES. There is abundant evidence that C15 deficiency may accelerate the progression of aging-associated diseases, including dysmetabolic iron overload syndrome (DIOS), type 2 diabetes, cardiovascular disease, and NAFLD (Fatty Liver).
DAILY NEEDED AMOUNT. Historical and recent human data support a daily dietary C15 intake of around 100 to 200 mg to achieve optimal circulating C15 levels (over 0.2% of circulating fatty acids).
FOOD SOURCES. Get over 300 mg per 100 g from: Whipping Cream, Cream Cheese, Cheddar Cheese, American Cheese, Swiss Cheese (lesser amounts from other cheese and from some fish & meat). Too much dairy etc leads to constipation, so I avoid too much cheese and devour a lot of legumes and soaked chia seeds to prevent that.
A PINT OF MILK. Whole milk contains about 32.5 mg per 100 g, so a pint would provide c. 154 mg of C15.
(BRANDS. Several brands of milk are RBGH free, namely Organic Brands: Horizon Organic, Organic Valley, Stonyfield Organic; Other Brands: (Walmart's) Great Valu, Alta Dena, Brown Cow Farm.)
4 teaspoons of BUTTER (8mg/g) provides c. 160 mg of C15.
8 teaspoons of SOUR CREAM (30%) (3.5mg/g) has c. 140mg of C15.
9 teaspoons of CREAM CHEESE (3.4mg/g) has c. 153mg of C15.
2 slices of CHEDDAR CHEESE (3.2mg/g) has c. 179mg of C15 (c. 28g/slice).
3 slices of AMERICAN CHEESE (3.1mg/g) has c. 186mg of C15 (c. 20g/slice).
2 slices of SWISS CHEESE (3.1 mg/g) has c. 152mg of C15 (c.25g/slice).
C15. The new fat, or fatty acid, is called Pentadecanoic Acid. They call it C15, because it has 15 carbon atoms, but it seems like it should be called PDA, because other fatty acids are abbreviated that way, such as ALA, EPA, DHA etc. But I'll go with C15.
CANCER. I said before that casein in dairy is said to increase the risk of prostate cancer, but the body normally has enzymes to break down casein. So I assume it's only if the casein can't be broken down that it can be a problem.
ESSENTIAL FATTY ACID. Dairy is part of the Mediterranean Diet, and it's said to be one of the best diets, and since dairy is now shown to have an essential fatty acid, C15, I'm planning to resume milk and cream cheese or sour cream consumption.
REMINERALIZE TEETH? Milk contains calcium and phosphate which can remineralize teeth and it has a pH that doesn't harm the teeth, so I'm planning to start mouth rinsing with rBGH-free milk, i.e. Great Valu from Walmart, to see if that will heal my cavities. One lady dentist on Youtube recommends brushing with one of the Crest toothpastes designed for cavity fighting, as she said it's the only product proven to reduce cavities. She said the fluoride in it helps remineralize teeth, but she recommends spitting it out after brushing, because fluoride is toxic to the brain etc. However, I found that that toothpaste contains titanium oxide or dioxide, which is also toxic to the brain. And many companies now use nanoparticles of such ingredients, which is even worse than before. So I hope swishing with milk will heal my cavities.
PAPER TITLE. The Cellular Stability Hypothesis: Evidence of Ferroptosis and Accelerated Aging-Associated Diseases as Newly Identified Nutritional Pentadecanoic Acid (C15:0) Deficiency Syndrome
LINK. https://www.mdpi.com/2218-1989/14/7/355
[color=#0000FF]ABSTRACT. CELLULAR FRAGILITY SYNDROME[/color]
Ferroptosis is a newly discovered form of cell death caused by the peroxidation of fragile fatty acids in cell membranes, which combines with iron to increase reactive oxygen species and disable mitochondria. Ferroptosis has been linked to aging-related conditions, including type 2 diabetes, cardiovascular disease, and nonalcoholic fatty liver disease (NAFLD). Pentadecanoic acid (C15:0), an odd-chain saturated fat, is an essential fatty acid with the primary roles of stabilizing cell membranes and repairing mitochondrial function. By doing so, C15:0 reverses the underpinnings of ferroptosis. Under the proposed “Cellular Stability Hypothesis”, evidence is provided to show that cell membranes optimally need >0.4% to 0.64% C15:0 (of total circulating fatty acids) to support long-term health and longevity. A pathophysiology of a newly identified nutritional C15:0 deficiency syndrome (“Cellular Fragility Syndrome”) is provided that demonstrates how C15:0 deficiencies (≤0.2% total circulating fatty acids) can increase susceptibilities to ferroptosis, dysmetabolic iron overload syndrome, type 2 diabetes, cardiovascular disease, and NAFLD {Fatty Liver}. Further, evidence is provided that C15:0 supplementation can reverse the described C15:0 deficiency syndrome, including the key components of ferroptosis. Given the declining dietary intake of C15:0, especially among younger generations, there is a need for extensive studies to understand the potential breadth of Cellular Fragility Syndrome across populations.
[color=#0000FF]CELL MEMBRANES DESTRUCTION.[/color] Based on A.J. Hulbert’s Cell Membrane Pacemaker Theory of Aging, mammalian longevity is determined by the stability of fatty acids in cell membranes, which protect against lipid peroxidation and slow the onset of diseases that eventually lead to mortality [1]. In support of this theory, Hulbert showed that cell membranes containing fatty acids with higher saturation had greater cellular stability. In turn, this stability resulted in lowered circulating lipid peroxidation and was associated with longer mammalian species’ lifespans. There is evidence that this association between cell membrane stability and lifespan is not limited to variations between species but also within species, including humans.
[color=#0000FF]LIPID PEROXIDATION & IRON OVERLOAD.[/color] Ferroptosis requires two instigators: fragile polyunsaturated fatty acids in cell membranes that are susceptible to lipid peroxidation and excess intracellular iron [12,13]. Polyunsaturated fatty acids are particularly susceptible to lipid peroxidation because these lipids have multiple double bonds in their molecular structure that are more easily attacked by oxygen [14]. Lipid peroxidation, in and of itself, is a major contributor to numerous aging-related diseases, including metabolic syndrome, NAFLD, cardiovascular disease, and neurodegenerative diseases [15,16,17,18]. Further, dysregulated iron metabolism and direct tissue damage caused by iron overload are being increasingly recognized as drivers of type 2 diabetes, NAFLD, cardiovascular disease, and neurodegenerative diseases [19,20,21,22]. As described below, when lipid peroxidation combines with iron overload, the result is ferroptosis, which has wide-ranging effects that contribute to the onset and progression of metabolic and related diseases
[color=#0000FF]TYPE 2 DIABETES.[/color] Studies support that ferroptosis is playing a role in the rising incidence of type 2 diabetes, in part due to a one–two punch that contributes to the onset and progression of disease [2]. First, pancreatic cells are more susceptible to ferroptosis relative to other cells due to naturally lower production of a key antioxidative enzyme called glutathione peroxidase; in turn, the ferroptosis of pancreatic cells results in lower insulin secretion [25]. Second, ferroptosis in the liver, another organ susceptible to lipid peroxidation and iron overload, can cause insulin resistance [26]. Together, these effects can impair glucose metabolism and support sustained hyperglycemia. It is well established that people with type 2 diabetes have a higher risk of co-morbidities, including cardiovascular disease, cancer, neurodegenerative diseases, and advanced NAFLD [27,28,29,30].
[color=#0000FF]FATTY LIVER.[/color] NAFLD is a disease involving excessive fat deposition in the liver (i.e., steatosis) that can progress to inflammation, necrosis, cirrhosis {and liver failure}. ... Because the liver is a key organ responsible for lipid and iron metabolism, the vicious cycle of ferroptosis and liver injury may serve as the epicenter for ferroptosis throughout the body.
[color=#0000FF]CARDIOVASCULAR DISEASE.[/color] Ferroptosis, due to both lipid peroxidation and iron accumulation in blood vessel walls, can cause or worsen inflammation and oxidized-LDL-associated atherosclerosis [37]. Ferroptosis has also been linked to coronary heart disease, multiple cardiomyopathies, and heart failure due to direct cardiac tissue injury [5]. Early studies in relevant animal models have demonstrated the potential to prevent or treat cardiovascular diseases by targeting ferroptosis [38].
[color=#0000FF]NEURODEGENERATIVE DISEASE.[/color] The brain contains a substantial amount of lipids and, as such, is susceptible to lipid peroxidation. Further, iron deposition in the brain, which increases with age, can cause histologic changes consistent with Alzheimer’s disease [22]. Together, lipid peroxidation and iron accumulation from ferroptosis feed off each other, creating a destructive cycle that contributes to the onset and progression of neurodegenerative diseases [39].