Xeno-estrogens (plastics in masks, test swabs, water bottles ... and oh, yea, straws) are also endocrine (sex hormone) disruptors.
ESTROGEN, COPPER, STRESS, HYPOXIA, METABOLIC DYSFUNCTION ... and the genes of iron, copper, zinc, B vitamins
A functional.genomic analysis looks at enzymes (genes/proteins) involved in movement of these compounds in and out of the cell. For example, there is a gene that makes a compound that transports iron out of the cell; when variated and downregulated, iron gets stuck in cell and the iron buildup can be damaging. When you also have issues with the removal of superoxide from variants in superoxide dismutase (SOD), that iron can combine with superoxide to make hydroxyl radicals. That is called the Fenton reaction and is quite harmful to the cell.
A functional.genomic analysis looks at enzymes (genes/proteins) involved in movement of these compounds in and out of the cell. For example, there is a gene that makes a compound that transports iron out of the cell; when variated and downregulated, iron gets stuck in cell and the iron buildup can be damaging. When you also have issues with the removal of superoxide from variants in superoxide dismutase (SOD), that iron can combine with superoxide to make hydroxyl radicals. That is called the Fenton reaction and is quite harmful to the cell.
Forwarded from Danny Roddy
Ceruloplasmin: The Emergency "Acute Phase Reactant" Liver Protein Increased by Estrogen, Stress, and Infection
In general, acute phase reactants rise in response to injury. I think the chronic elevation of these substances (e.g., ferritin, CRP, TNF-a, etc.), while defensive, would indicate a pathological process.
"...Despite gallant efforts by numerous laboratories and investigators, no single factor has emerged as indispensable for mediating copper passage into cells in vivo. This apparent failure allows one to question whether delivery of an essential nutrient would be expected to depend on a single component. Thus, it is more likely that cells have evolved numerous ways for absorbing copper from their immediate surroundings. This would imply that numerous carriers, including ceruloplasmin and albumin, have the potential to behave as copper transporters."
— Harris E. Cellular copper transport and metabolism. Annu Rev Nutr. 2000;20:291-310.
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"Plasma ceruloplasmin, a copper-containing protein, belongs to a class called acute phase proteins...."
"Stress was known to increase Ceruloplasmin."
"We found lowest ceruloplasmin level after stress in overiectomised animals, while on substitution of estradiol the trend appeared to be reversed. The result suggested a direct effect of estrogen on hepatic ceruloplasmin production/release..."
— Ganaraja B., et al. Effect of estrogen on plasma ceruloplasmin level in rats exposed to acute stress. (2004)
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"In conclusion, serum ceruloplasmin level is elevated in the subjects with metabolic syndrome, as well as in subjects with impaired glucose regulation or diabetes mellitus. In addition, serum ceruloplasmin level is associated with various cardiovascular risk factors. These results suggest that elevated serum ceruloplasmin level can be a marker for metabolic stresses associated with metabolic syndrome."
— Kim C., et al. Elevated serum ceruloplasmin levels in subjects with metabolic syndrome: a population-based study. (2002)
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"...Plasma caeruloplasmin values were similar in the kindergarten and Health Centre children with infection, but those with chronic infection had significantly higher values than the others..."
— Ismadi S., et al. Usefulness of plasma ceruloplasmin and transferrin levels in the assessment of protein calorie malnutrition among pre-school children. (1971)
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"Ceruloplasmin level, a marker of hepatic estrogen metabolism, was significantly elevated in patient groups receiving both dosages of oral estrogen..."
— Alkjaersig N., et al. Blood coagulation in postmenopausal women given estrogen treatment: comparison of transdermal and oral administration. (1988)
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"We studied the presence of a different responsiveness of the human liver to the estrogens in two groups of post-menopausal women by evaluating the changes in ceruloplasmin serum level. Conjugated equine estrogens were administered at different times (A: 8 a.m. and B: 8 p.m.). The replacement therapy increased ceruloplasmin serum levels both in group A and B, but the increase was higher in group B than in group A."
— Clemente C., et al. Ceruloplasmin serum level in post-menopausal women treated with oral estrogens administered at different times. (1992)
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Q: When estrogen increases ceruloplasmin do you see that as a defensive reaction to hypoxia?
A: "I think so, helping to keep iron in an oxidized state." Ray Peat, PhD (2022)
In general, acute phase reactants rise in response to injury. I think the chronic elevation of these substances (e.g., ferritin, CRP, TNF-a, etc.), while defensive, would indicate a pathological process.
"...Despite gallant efforts by numerous laboratories and investigators, no single factor has emerged as indispensable for mediating copper passage into cells in vivo. This apparent failure allows one to question whether delivery of an essential nutrient would be expected to depend on a single component. Thus, it is more likely that cells have evolved numerous ways for absorbing copper from their immediate surroundings. This would imply that numerous carriers, including ceruloplasmin and albumin, have the potential to behave as copper transporters."
— Harris E. Cellular copper transport and metabolism. Annu Rev Nutr. 2000;20:291-310.
-------
"Plasma ceruloplasmin, a copper-containing protein, belongs to a class called acute phase proteins...."
"Stress was known to increase Ceruloplasmin."
"We found lowest ceruloplasmin level after stress in overiectomised animals, while on substitution of estradiol the trend appeared to be reversed. The result suggested a direct effect of estrogen on hepatic ceruloplasmin production/release..."
— Ganaraja B., et al. Effect of estrogen on plasma ceruloplasmin level in rats exposed to acute stress. (2004)
-------
"In conclusion, serum ceruloplasmin level is elevated in the subjects with metabolic syndrome, as well as in subjects with impaired glucose regulation or diabetes mellitus. In addition, serum ceruloplasmin level is associated with various cardiovascular risk factors. These results suggest that elevated serum ceruloplasmin level can be a marker for metabolic stresses associated with metabolic syndrome."
— Kim C., et al. Elevated serum ceruloplasmin levels in subjects with metabolic syndrome: a population-based study. (2002)
-------
"...Plasma caeruloplasmin values were similar in the kindergarten and Health Centre children with infection, but those with chronic infection had significantly higher values than the others..."
— Ismadi S., et al. Usefulness of plasma ceruloplasmin and transferrin levels in the assessment of protein calorie malnutrition among pre-school children. (1971)
-------
"Ceruloplasmin level, a marker of hepatic estrogen metabolism, was significantly elevated in patient groups receiving both dosages of oral estrogen..."
— Alkjaersig N., et al. Blood coagulation in postmenopausal women given estrogen treatment: comparison of transdermal and oral administration. (1988)
-------
"We studied the presence of a different responsiveness of the human liver to the estrogens in two groups of post-menopausal women by evaluating the changes in ceruloplasmin serum level. Conjugated equine estrogens were administered at different times (A: 8 a.m. and B: 8 p.m.). The replacement therapy increased ceruloplasmin serum levels both in group A and B, but the increase was higher in group B than in group A."
— Clemente C., et al. Ceruloplasmin serum level in post-menopausal women treated with oral estrogens administered at different times. (1992)
-------
Q: When estrogen increases ceruloplasmin do you see that as a defensive reaction to hypoxia?
A: "I think so, helping to keep iron in an oxidized state." Ray Peat, PhD (2022)
Forwarded from Heather Rae
Watch "#37: Harmful Meditation? | Intermittent Fasting is Dangerous | Obesity Paradox | Current Events" on YouTube
https://youtube.com/clip/Ugkx2OV-ux1C2EeMt8PuLBOzVP9sh_nk9ONK
https://youtube.com/clip/Ugkx2OV-ux1C2EeMt8PuLBOzVP9sh_nk9ONK
YouTube
✂️ DUTCH, an excretion (urine) test for hormones should be done in combination with blood test
41 seconds · Clipped by Heather Rae, INHC · Original video "#37: Harmful Meditation? | Intermittent Fasting is Dangerous | Obesity Paradox | Current Events" ...
CRH & NEURODEGERATION ...CRH is implicated in ALS, MS, PD and can be blocked by pregnelalone. (You may want to first assess why it is being released in the first place and consider reducing toxins (stress!), improving nutrients/pH and electromagnetic (non-chemical) therapies.
ANOTHER OPTION FOR BLOCKING IRON WHEN YOU HAVE HFE &/OR TF GENE VARIANTS ... there is another version (no carnitine) for people with thyroid dysregulation.
Low Lipids, Low Cholesterol and Choline Deficiency | Beyond MTHFR
https://drrostenberg.wordpress.com/2013/12/05/low-lipids-low-cholesterol-and-choline-deficiency/
https://drrostenberg.wordpress.com/2013/12/05/low-lipids-low-cholesterol-and-choline-deficiency/
Beyond MTHFR
Low Lipids, Low Cholesterol and Choline Deficiency
Low Lipids as a Common Cause of Choline Deficiency Choline is an amazing molecule and one that is very important for optimum health. It has often been said that our health depends first and foremo…
👆👆👆👆 INTERMITTENT FASTING & VARIANTS IN PEMT, BHMT and methylation (FOLATE) GENES ... & NEURODEGENERATION
If you have a compromised ability to make choline/PC due to variants in these genes, fasting is probably not a good idea. Statins (derived originally from a fungus, btw) which block the body's ability to create choline/PC will also contribute to problems (like AD).
"The solution to low cholesterol and [triglyderides] resides in frequent eating, eating fatty and cholesterol-rich foods, and by avoiding excess HPA-axis activation"
"Meal skipping, poor digestion and improper food selection are the main causes of low lipids. Taking nutritional supplements with choline without fixing the dietary habits will create frustration and lackluster results."
If you have a compromised ability to make choline/PC due to variants in these genes, fasting is probably not a good idea. Statins (derived originally from a fungus, btw) which block the body's ability to create choline/PC will also contribute to problems (like AD).
"The solution to low cholesterol and [triglyderides] resides in frequent eating, eating fatty and cholesterol-rich foods, and by avoiding excess HPA-axis activation"
"Meal skipping, poor digestion and improper food selection are the main causes of low lipids. Taking nutritional supplements with choline without fixing the dietary habits will create frustration and lackluster results."
Forwarded from Heather Rae, Functional Health Practitioner
Fatty Acid Assist™ – Professional Health Products®
https://professional-health-products.com/product/fatty-acid-assist/
This blend includes fennel, dandelion and B2 ... which gives you a good idea on how to support fat/lipid metabolism via diet!.
https://professional-health-products.com/product/fatty-acid-assist/
This blend includes fennel, dandelion and B2 ... which gives you a good idea on how to support fat/lipid metabolism via diet!.
Professional-Health-Products
Fatty Acid Assist™ – Professional Health Products®
Forwarded from Heather Rae, Functional Health Practitioner
VACCINE INJURY & YOUR GENETICS (a close up) In the past few years, I've participated in genomic analysis of over 100 case studies of people struggling with complex chronic health conditions. Then came "COVID" I knew the 'SARS COV2 'virus' had never been found in a human being, so it wasn't clear, not at all, what "COVID" meant. When my mentor said, "COVID" or "virus" my brain exploded a little, and I made mental holding place for 'whatever that is." Then came the "COVID injections" and spike proteins, I got really deep into the inflammation (genes/enzymes) of spike proteins and those angiotensin enzymes that kick up histamine and mast cells and RANTES. Now these genomic analyses have shifted to looking at inflammatory NF-kB and TNF (mentioned a couple posts above). "COVID" so goes the narrative, activates inflammatory NF-kB and TNF-a. The ovals in the diagram above are genes/enyzmes. In the next post, I'll list the names of the natural compounds and pharma drugs that suppress TNF-a.
Forwarded from Heather Rae, Functional Health Practitioner