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Low test and immune function?
- Thread starter tfuray
- Start date
Yes Low T levels and added High E levels can be quite detrimental
Easiest way to avoid this off cycle is the use of a low dose steroidal AI with Glutamine Peptides, Vitamin C, Multi V etc.
G-covery Glutamine Peptides may be worth a shot:
www.AGXsports.com
http://agxsports.com/gcovery.html
Easiest way to avoid this off cycle is the use of a low dose steroidal AI with Glutamine Peptides, Vitamin C, Multi V etc.
G-covery Glutamine Peptides may be worth a shot:
www.AGXsports.com
http://agxsports.com/gcovery.html
Last edited:
Thanks
Off cycle can be a good and normal experience as long as you supplement with certain things.
When you lower E do a degree ( not zero) you shift endogenous levels to favor T
Then you add supps that increase Cellular Energy ( Creatines, Carnitines etc) and add pro immune system compounds such as G-covery and a good Vitamin, your pretty much set.
Off cycle can be a good and normal experience as long as you supplement with certain things.
When you lower E do a degree ( not zero) you shift endogenous levels to favor T
Then you add supps that increase Cellular Energy ( Creatines, Carnitines etc) and add pro immune system compounds such as G-covery and a good Vitamin, your pretty much set.
Yes G-5 agreed
but I suspect there are toxins, phyto and synthetic estrogens in our water supplies do to industrial and medical pollution that are hindering male Test Production and levels and elevating E to an undo degree.
Very disturbing especially considered the study that just came out stating that male T rates have decreased by a measurable rate in only the last 20 years for no particular reason:
new study has found a "substantial" drop in U.S. men's testosterone levels since the 1980s, but the reasons for the decline remain unclear. This trend also does not appear to be related to age.
The average levels of the male hormone dropped by 1 percent a year, Dr. Thomas Travison and colleagues from the New England Research Institutes in Watertown, Massachusetts, found. This means that, for example, a 65-year-old man in 2002 would have testosterone levels 15 percent lower than those of a 65-year-old in 1987. This also means that a greater proportion of men in 2002 would have had below-normal testosterone levels than in 1987.
"The entire population is shifting somewhat downward we think," Travison told Reuters Health. "We're counting on other studies to confirm this."
Travison and his team analyzed data from the Massachusetts Male Aging Study, a long-term investigation of aging in about 1,700 Boston-area men. Data from the men were collected for three time intervals: 1987-1989, 1995-1997, and 2002-2004.
While a man's testosterone level will fall steadily as he ages, the researchers observed a speedier decline in average testosterone levels than would have been expected with aging alone.
They hypothesized that the rising prevalence of obesity as well as the sharp decline in cigarette smoking might help explain their findings, given that testosterone levels are lower among overweight people and smoking increases testosterone levels. But these factors accounted for only a small percentage of the observed difference.
It's likely that some sort of environmental exposure is responsible for the testosterone decline, Travison said, although he said attempting to explain what this might be based on the current findings would be "pure conjecture."
The researchers used body mass index, the ratio of height to weight, to estimate obesity levels, he noted, but this is not a very accurate way to gauge the real adiposity, or fat content of the body, so it's possible that obesity might be more of a factor than it appears in this analysis.
"I think like most things that are complex, it's likely that there is no one cause," he said.
SOURCE: Journal of Clinical Endocrinology and Metabolism, January 2007.
but I suspect there are toxins, phyto and synthetic estrogens in our water supplies do to industrial and medical pollution that are hindering male Test Production and levels and elevating E to an undo degree.
Very disturbing especially considered the study that just came out stating that male T rates have decreased by a measurable rate in only the last 20 years for no particular reason:
new study has found a "substantial" drop in U.S. men's testosterone levels since the 1980s, but the reasons for the decline remain unclear. This trend also does not appear to be related to age.
The average levels of the male hormone dropped by 1 percent a year, Dr. Thomas Travison and colleagues from the New England Research Institutes in Watertown, Massachusetts, found. This means that, for example, a 65-year-old man in 2002 would have testosterone levels 15 percent lower than those of a 65-year-old in 1987. This also means that a greater proportion of men in 2002 would have had below-normal testosterone levels than in 1987.
"The entire population is shifting somewhat downward we think," Travison told Reuters Health. "We're counting on other studies to confirm this."
Travison and his team analyzed data from the Massachusetts Male Aging Study, a long-term investigation of aging in about 1,700 Boston-area men. Data from the men were collected for three time intervals: 1987-1989, 1995-1997, and 2002-2004.
While a man's testosterone level will fall steadily as he ages, the researchers observed a speedier decline in average testosterone levels than would have been expected with aging alone.
They hypothesized that the rising prevalence of obesity as well as the sharp decline in cigarette smoking might help explain their findings, given that testosterone levels are lower among overweight people and smoking increases testosterone levels. But these factors accounted for only a small percentage of the observed difference.
It's likely that some sort of environmental exposure is responsible for the testosterone decline, Travison said, although he said attempting to explain what this might be based on the current findings would be "pure conjecture."
The researchers used body mass index, the ratio of height to weight, to estimate obesity levels, he noted, but this is not a very accurate way to gauge the real adiposity, or fat content of the body, so it's possible that obesity might be more of a factor than it appears in this analysis.
"I think like most things that are complex, it's likely that there is no one cause," he said.
SOURCE: Journal of Clinical Endocrinology and Metabolism, January 2007.
OMEGA said:
Right on Omega,
from an article I read plastics (like plastic containers we all keep food in) if heated it releases some chemicals which mimics estrogen or the production of estrogen. Troubling stuff!
I'm personally replacing most of my lunch containers with ceramic ones.
A also agree that obesity plays an imortant role in test production as well.
gjohnson5
New member
Yes , chemicals which mimic estrogen are present in plastic containers and have been linked to certain cancers...
http://www.mindfully.org/Plastic/Monomers/BPA-Prostate-Cancer3jan05.htm
PHILADELPHIA — An estrogen-like chemical commonly used to synthesize plastic food containers has been shown to encourage the growth of a specific category of prostate cancer cell, potentially affecting the treatment efficacy for a subset of prostate cancers.
According to a study published in the January 1 issue of Cancer Research, such prostate cancer cells proved to be vulnerable to exposure to the chemical BPA (bisphenol A), an industrial chemical and nonsteroidal environmental estrogen used in the manufacture of food cans, milk container linings, food storage containers and water supply pipes. About 2.5 billion pounds of the chemical are produced each year.
In particular, the study showed that the affected class of prostate cancer cell, characterized by mutated receptors for androgens, the male hormone, can proliferate in response to BPA.
“The results may have implications for men who develop BPA-susceptible mutations in their androgen receptor genes during the course of prostate cancer treatment, although these concepts will need to be verified in animal systems,” according to Karen Knudsen, Ph.D., an assistant professor in the University of Cincinnati’s Department of Cell Biology and Center for Environmental Genetics. Scientists estimate that anywhere from eight to 25 percent of all prostate cancer patients may fall into this category.
In the United States alone this year, almost 220,000 men will be diagnosed with prostate cancer. The disease is the second most common type of cancer found in American men, and approximately 29,000 men will die from prostate cancer this year.
Many cases of prostate cancer depend on androgens like testosterone for tumor growth and cancer cell proliferation, said Dr. Knudsen, the study’s senior author. A common treatment for prostate cancer includes limiting testosterone synthesis. Patients with mutated androgen receptors may not respond to this therapy and according to this new study, exposure to BPA among these patients could potentially put them at higher risk for increased cancer cell growth.
“The results we see in cell culture in response to BPA are ready to be moved to appropriate animal models next,” said Dr. Knudsen. The effect of the environmental non-steroidal BPA on human prostate cancer tumor implants in laboratory animal models will shed additional light on whether the synthetic pseudo-estrogen encourages tumor growth in whole animal systems.
“We’ll know more about the ‘hormone sensitizing’ ability of BPA in prostate cancer cells from studies on animals. It is also important to note that our study demonstrates that the actual dose of BPA exposure may change the biological response,” Dr. Knudsen said.
The safety of BPA has been under intense debate for several years, with some arguing that exposure to the chemical among humans is safe, with others contending that it may promote the growth of human tumor cells and alter the growth and development of animals.
Also participating in the study were Yelena Wetherill, Ph.D., Nicola Fisher, B.S., and Ann Staubach, B.S., all with the University of Cincinnati; Mark Danielsen, Ph.D., Georgetown University, Washington, D.C.; and Ralph De Vere White, M.D., the University of California, Davis.
Contact: Russell Vanderboom, Ph.D. Phone: 215/440-9300 Ext. 120 E-mail: [email protected]
source: http://www.aacr.org/2005pressjan1.asp 30jan2005
http://www.mindfully.org/Plastic/Monomers/BPA-Prostate-Cancer3jan05.htm
PHILADELPHIA — An estrogen-like chemical commonly used to synthesize plastic food containers has been shown to encourage the growth of a specific category of prostate cancer cell, potentially affecting the treatment efficacy for a subset of prostate cancers.
According to a study published in the January 1 issue of Cancer Research, such prostate cancer cells proved to be vulnerable to exposure to the chemical BPA (bisphenol A), an industrial chemical and nonsteroidal environmental estrogen used in the manufacture of food cans, milk container linings, food storage containers and water supply pipes. About 2.5 billion pounds of the chemical are produced each year.
In particular, the study showed that the affected class of prostate cancer cell, characterized by mutated receptors for androgens, the male hormone, can proliferate in response to BPA.
“The results may have implications for men who develop BPA-susceptible mutations in their androgen receptor genes during the course of prostate cancer treatment, although these concepts will need to be verified in animal systems,” according to Karen Knudsen, Ph.D., an assistant professor in the University of Cincinnati’s Department of Cell Biology and Center for Environmental Genetics. Scientists estimate that anywhere from eight to 25 percent of all prostate cancer patients may fall into this category.
In the United States alone this year, almost 220,000 men will be diagnosed with prostate cancer. The disease is the second most common type of cancer found in American men, and approximately 29,000 men will die from prostate cancer this year.
Many cases of prostate cancer depend on androgens like testosterone for tumor growth and cancer cell proliferation, said Dr. Knudsen, the study’s senior author. A common treatment for prostate cancer includes limiting testosterone synthesis. Patients with mutated androgen receptors may not respond to this therapy and according to this new study, exposure to BPA among these patients could potentially put them at higher risk for increased cancer cell growth.
“The results we see in cell culture in response to BPA are ready to be moved to appropriate animal models next,” said Dr. Knudsen. The effect of the environmental non-steroidal BPA on human prostate cancer tumor implants in laboratory animal models will shed additional light on whether the synthetic pseudo-estrogen encourages tumor growth in whole animal systems.
“We’ll know more about the ‘hormone sensitizing’ ability of BPA in prostate cancer cells from studies on animals. It is also important to note that our study demonstrates that the actual dose of BPA exposure may change the biological response,” Dr. Knudsen said.
The safety of BPA has been under intense debate for several years, with some arguing that exposure to the chemical among humans is safe, with others contending that it may promote the growth of human tumor cells and alter the growth and development of animals.
Also participating in the study were Yelena Wetherill, Ph.D., Nicola Fisher, B.S., and Ann Staubach, B.S., all with the University of Cincinnati; Mark Danielsen, Ph.D., Georgetown University, Washington, D.C.; and Ralph De Vere White, M.D., the University of California, Davis.
Contact: Russell Vanderboom, Ph.D. Phone: 215/440-9300 Ext. 120 E-mail: [email protected]
source: http://www.aacr.org/2005pressjan1.asp 30jan2005
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