Koveras
Member
- Joined
- Dec 17, 2015
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It is well known that fertility tends to decline with age in both men and women. Still popular is the notion that women have a limited number of eggs and the idea that this is strongly determined by genetics and mostly unchangeable (see wikipedia quotes below). New research shows that inflammation and fibrosis are strongly involved in the age related decline in fertility and with the implication that lifestyle factors that influence these factors could accelerate or delay these changes.
As anyone familiar with Peat may know - serotonin, estrogen, histamine, nitric oxide, lactic acid, free fatty acids, stress, etc are all involved in fibrotic processes to varying degrees
Age and female fertility - Wikipedia, the free encyclopedia
"Female fertility is affected by age. Age is thus a major fertility factor for women. After puberty, female fertility increases and then decreases, with advanced maternal age causing an increased risk of female infertility. In humans, a woman's fertility peaks in the early and mid-20s, after which it starts to decline slowly, with a more dramatic drop at around 35.[1] At age 45, a woman starting to try to conceive will have no live birth in 50-80 percent of cases."
Ovarian reserve - Wikipedia, the free encyclopedia
"The ovary is generally thought of as an egg bank from which the woman draws during her reproductive life. The human ovary contains a population of primordial follicles. At 18–22 weeks post-conception, the female ovary contains its peak number of follicles (about 300,000 in the average case, but individual peak populations range from 35,000 to 2.5 million[3]). The size of the initial ovarian reserve is strongly influenced by genetics."
https://www.sciencedaily.com/releases/2016/08/160805230054.htm
"Our work establishes fibrosis and inflammation as hallmarks of the aging ovary and lays the foundation for considering the use of anti-fibrotic or anti-inflammatory treatments to delay or counteract the impact of reproductive aging,"
Peat-related quotes:
"To reverse this process, it’s necessary to avoid doing the things that caused the problem to develop. The accumulation of heavy metals and of the unstable unsaturated fats (linoleic, linolenic, and arachidonic acids) can be slowed or reversed by careful dietary choices. The calorie restricted diets that slow the aging process reduce the accumulation of the unstable fats and the heavy metals. Vitamin E reduces the vascular leakiness and the free radical peroxidation that are so closely involved in fibrosis. Since serotonin and nitric oxide are involved in these processes, they should be minimized by keeping carbon dioxide production high (by optimizing thyroid function), and by eating protein that have a safe balance of the amino acids. Too much arginine increases nitric oxide formation, and too much tryptophan increases serotonin production. Too much glutamic acid, aspartic acid, and cysteine can be directly excitotoxic, and the metabolites of cysteine include proinfiammatory homocysteine, which can disrupt collagen structure."
"Ray has said numerous times that serotonin is intimately involved in fibrotic conditions of the lungs, and my own research shows that it is involved in many other fibrotic conditions including cirrhosis, cystic fibrosis, and of course carcinoid syndrome. This study now adds the condition known as systemic sclerosis or scleroderma to the list of conditions where serotonin plays a causative role. This suggests that lowering serotonin may be therapeutic in this condition for which officially there is no cure and it is eventually fatal."
"Serotonin is one of the primary mediators of fibrosis in the human body, antiserotonin drugs are currently actually getting approved and pretty quickly so could be treating things like cystic fibrosis, heart failure, liver cirrhosis (which is actually a fibrosis of the liver); it shows that serotonin has a very quick and detrimental effect on many organs and tissues, and endotoxins raise serotonin tremendously in people who eat a decent amount of PUFA."
"Lactic acid does lead first to water-logging, inflammation and eventually the fibrosis."
"When you aren't able to oxidize your sugar all the way to carbon dioxide you produce lactic acid very easily. Even at rest, a person will keep producing lactic acid as if they were under strenuous exercise. And the lactic acid turns on a lot of inflammatory mediators which have systemic effects on your bone and skin, hair growth, everything. Lactic acid itself acts as a toxin. Gradually if you are experiencing that year after year it leads to a tendency of fibrosis, arthritis, and so called connective tissue diseases in general from an imbalance of the inflammatory mediators (histamine and serotonin especially) and a tendency of the soft tissues to calcify, so it contributes to hardening of the arteries and heart failure."
"The only mistake that I think Hans Selye made in his work in stress. In some places he talks about a limited ability to adapt to stress, because we are born with a certain amount of ‘adaptive energy’ or stress resistant energy, but I don’t think there is such a thing as ‘adaptive energy’. I think of such things as sugar, sucrose and fructose, which let us deal with these menacing things such as serotonin, starches, indigestible fibers, various plant irritants. The sugars are directly oxidised to energy, and inhibit the interfering substances, such as oxidising unsaturated fats. I think what the equivalent of a lack adaptive energy that Selye proposed, I think what it is, is that we have such a bad environment to adapt to that we get worse as we adapt to bad things, such as polyunsaturated fats and chronic excess of serotonin defending us against those irritants. So I think these immediate adaptive substances that in the short range protect us when we have to keep adapting with these short range measure, for example, serotonin increases collagen production, leads progressively to fibrosis of blood vessels, liver, kidney, even the brain develops collagen under excessive stress and serotonin. So too much adaptation to a bad environment, I think is what causes ageing and degeneration, rather than the lack of this hypothetical ‘adaptive energy’."
""Mast cells express the high-affinity estrogen receptor and studies have shown that estrogens augment their activities: in the presence of high levels of estrogens, mast cell responses to compound 48/80 are increased, leading to more substantial degranulation and release of histamine and serotonin.” "Mast cells are found in a diverse range of tissues and have the ability to adapt their function to the microenvironment.” "Interestingly, however, there is an increase in testicular mast cells in infertile men through mast cell activation of fibroblasts and promotion of collagen synthesis, could contribute to testicular fibrosis.” "Progesterone is necessary for the maintenance of pregnancy and plays a key role in maintaining cervical integrity prior to labour induction. Progesterone can prevent the migration of mast cells in response to chemokines and down-regulate surface chemokine receptor expression. In addition, mast cell function can be altered by the presence of high concentrations of progesterone. For example, progesterone inhibits the secretion of histamine from mast cells. Notably, these observations would suggest that mast cells present within the uterus during pregnancy are quiescent and inhibited by high levels of progesterone, and also that recruitment of mast cell progenitors from the circulation may be limited.”
As anyone familiar with Peat may know - serotonin, estrogen, histamine, nitric oxide, lactic acid, free fatty acids, stress, etc are all involved in fibrotic processes to varying degrees
Age and female fertility - Wikipedia, the free encyclopedia
"Female fertility is affected by age. Age is thus a major fertility factor for women. After puberty, female fertility increases and then decreases, with advanced maternal age causing an increased risk of female infertility. In humans, a woman's fertility peaks in the early and mid-20s, after which it starts to decline slowly, with a more dramatic drop at around 35.[1] At age 45, a woman starting to try to conceive will have no live birth in 50-80 percent of cases."
Ovarian reserve - Wikipedia, the free encyclopedia
"The ovary is generally thought of as an egg bank from which the woman draws during her reproductive life. The human ovary contains a population of primordial follicles. At 18–22 weeks post-conception, the female ovary contains its peak number of follicles (about 300,000 in the average case, but individual peak populations range from 35,000 to 2.5 million[3]). The size of the initial ovarian reserve is strongly influenced by genetics."
https://www.sciencedaily.com/releases/2016/08/160805230054.htm
"Our work establishes fibrosis and inflammation as hallmarks of the aging ovary and lays the foundation for considering the use of anti-fibrotic or anti-inflammatory treatments to delay or counteract the impact of reproductive aging,"
Peat-related quotes:
"To reverse this process, it’s necessary to avoid doing the things that caused the problem to develop. The accumulation of heavy metals and of the unstable unsaturated fats (linoleic, linolenic, and arachidonic acids) can be slowed or reversed by careful dietary choices. The calorie restricted diets that slow the aging process reduce the accumulation of the unstable fats and the heavy metals. Vitamin E reduces the vascular leakiness and the free radical peroxidation that are so closely involved in fibrosis. Since serotonin and nitric oxide are involved in these processes, they should be minimized by keeping carbon dioxide production high (by optimizing thyroid function), and by eating protein that have a safe balance of the amino acids. Too much arginine increases nitric oxide formation, and too much tryptophan increases serotonin production. Too much glutamic acid, aspartic acid, and cysteine can be directly excitotoxic, and the metabolites of cysteine include proinfiammatory homocysteine, which can disrupt collagen structure."
"Ray has said numerous times that serotonin is intimately involved in fibrotic conditions of the lungs, and my own research shows that it is involved in many other fibrotic conditions including cirrhosis, cystic fibrosis, and of course carcinoid syndrome. This study now adds the condition known as systemic sclerosis or scleroderma to the list of conditions where serotonin plays a causative role. This suggests that lowering serotonin may be therapeutic in this condition for which officially there is no cure and it is eventually fatal."
"Serotonin is one of the primary mediators of fibrosis in the human body, antiserotonin drugs are currently actually getting approved and pretty quickly so could be treating things like cystic fibrosis, heart failure, liver cirrhosis (which is actually a fibrosis of the liver); it shows that serotonin has a very quick and detrimental effect on many organs and tissues, and endotoxins raise serotonin tremendously in people who eat a decent amount of PUFA."
"Lactic acid does lead first to water-logging, inflammation and eventually the fibrosis."
"When you aren't able to oxidize your sugar all the way to carbon dioxide you produce lactic acid very easily. Even at rest, a person will keep producing lactic acid as if they were under strenuous exercise. And the lactic acid turns on a lot of inflammatory mediators which have systemic effects on your bone and skin, hair growth, everything. Lactic acid itself acts as a toxin. Gradually if you are experiencing that year after year it leads to a tendency of fibrosis, arthritis, and so called connective tissue diseases in general from an imbalance of the inflammatory mediators (histamine and serotonin especially) and a tendency of the soft tissues to calcify, so it contributes to hardening of the arteries and heart failure."
"The only mistake that I think Hans Selye made in his work in stress. In some places he talks about a limited ability to adapt to stress, because we are born with a certain amount of ‘adaptive energy’ or stress resistant energy, but I don’t think there is such a thing as ‘adaptive energy’. I think of such things as sugar, sucrose and fructose, which let us deal with these menacing things such as serotonin, starches, indigestible fibers, various plant irritants. The sugars are directly oxidised to energy, and inhibit the interfering substances, such as oxidising unsaturated fats. I think what the equivalent of a lack adaptive energy that Selye proposed, I think what it is, is that we have such a bad environment to adapt to that we get worse as we adapt to bad things, such as polyunsaturated fats and chronic excess of serotonin defending us against those irritants. So I think these immediate adaptive substances that in the short range protect us when we have to keep adapting with these short range measure, for example, serotonin increases collagen production, leads progressively to fibrosis of blood vessels, liver, kidney, even the brain develops collagen under excessive stress and serotonin. So too much adaptation to a bad environment, I think is what causes ageing and degeneration, rather than the lack of this hypothetical ‘adaptive energy’."
""Mast cells express the high-affinity estrogen receptor and studies have shown that estrogens augment their activities: in the presence of high levels of estrogens, mast cell responses to compound 48/80 are increased, leading to more substantial degranulation and release of histamine and serotonin.” "Mast cells are found in a diverse range of tissues and have the ability to adapt their function to the microenvironment.” "Interestingly, however, there is an increase in testicular mast cells in infertile men through mast cell activation of fibroblasts and promotion of collagen synthesis, could contribute to testicular fibrosis.” "Progesterone is necessary for the maintenance of pregnancy and plays a key role in maintaining cervical integrity prior to labour induction. Progesterone can prevent the migration of mast cells in response to chemokines and down-regulate surface chemokine receptor expression. In addition, mast cell function can be altered by the presence of high concentrations of progesterone. For example, progesterone inhibits the secretion of histamine from mast cells. Notably, these observations would suggest that mast cells present within the uterus during pregnancy are quiescent and inhibited by high levels of progesterone, and also that recruitment of mast cell progenitors from the circulation may be limited.”
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