medhelp.org/posts/Epstein-Ba … wer_header
This guy thinks EBV shrunk his penis, caused him to lose his morning wood and now he feels as if he doesnt even have a penis between his legs much like us.
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A note about this guy
peaktestosterone.com/forum/i … ic=12331.0
Before taking the antibiotics he took Chinese herbs to gain weight. This is when his libido went down and he got dandruff and some other problems. He does not know which herbs he was given.
Breast implant illness can seem to cause
Muscle twitches
Loss of libido
Bad fatigue
and many other things
Others report bad anxiety, depression etc etc
you are wrong his libido was already down before taking chinese herb and his Vit D was low too.
He took herbs before the antibiotics to gain weight. He is not sure which herbs. This is when his troubles started. He then got much worse after getting sick and taking an antibiotic. He is now stuck in this state for a long time.
abstract
Lipopolysaccharide (LPS) is frequently used experimentally to mimic acute infection. Through activation of the host’s immune response, an LPS injection has profound effects on the adrenocortical response to stress and on behaviors including reduction in activity, water and food intake, and libido. These behavioral changes occurring during infection are collectively called “sickness behavior.” It is thought that adoption of sickness behavior reallocates energy from other fitness-enhancing activities, such as reproduction, for use in the immune response. Although the behavioral effects of LPS treatment are well-known, less information is available regarding the effects of LPS on the brain in terms of controlling reproductive behavior, specifically concerning a newly discovered neuropeptide, gonadotropin-inhibitory hormone (GnIH). This study investigated the effects of an LPS injection on the behavior and the hypothalamic neuropeptides controlling reproduction [GnIH and gonadotropin-releasing hormone (GnRH)] of zebra finches (Taeniopygia guttata). Overall, there was a decrease in activity in birds injected with LPS. The number of GnRH-immunoreactive neurons was significantly reduced in birds injected with LPS when compared to controls, while the number of GnIH-releasing neurons remained unchanged. At the level of gene expression, a similar pattern was found: there was reduced expression of GnRH mRNA in LPS-injected animals, whereas GnIH expression remained unchanged. Plasma testosterone did not change significantly in LPS-injected animals, nor did plasma corticosterone. Taken together, these results indicate a rapid (within 3h) inhibition of the reproductive axis during an immune challenge mimicking an infection, specifically acting on the GnRH system. The present study expands our knowledge on the interaction between the immune system and the reproductive system.
It has also been shown that peripherally injection of LPS in doses, higher than doses which were used in the present study, induced sickness behavior including reduction in appetite and body weight, suppresses exploratory and social activity, fatigue and malaise, impairment in cognitive abilities, reduced libido and sexual behavior and anhedonia as well as depression like behaviors.
Infections are associated with a specific behavioral pattern that includes hypomotility, hypophagia, increased sleep, decreased libido, and decreased exploration. This behavioral response is considered adaptive and important for the survival of the animal. A similar behavioral pattern was observed following treatment with endotoxin (lipopolysaccharide [LPS]) and cytokines, such as interleukin-1 (IL-1). Because the secretion of these cytokines is induced by LPS and infections, it is possible that they mediate the behavioral responses to infection
In the present study, administration of LPS was found to induce several sickness behavior symptoms. These findings replicate the results of many previous studies, which demonstrated that activation of the immune system by LPS, as well as other immune challenges, induces a reduction in appetite and body weight, suppression of locomotor, exploratory, and social activity, fatigue and malaise, impairment in cognitive abilities, reduced libido and sexual behavior, and anhedonia (Anisman and Merali 1999; Dantzer et al. 1999; Maier and Watkins 1998; Yirmiya 1996; Yirmiya et al. 1994, 1999)
May of us got gum recession after crashing.
People with poor oral hygiene or gum disease may be at a greater risk of developing Alzheimer’s disease, according to a study published online in the Journal of Alzheimer’s Disease on May 10.
Researchers at The University of Central Lancashire (UCLan) School of Medicine and Dentistry in England led by Drs. StJohn Crean and Sim K. Singhrao examined brain tissue samples donated by 10 patients without dementia and 10 patients with dementia.They found gum disease bacteria lipopolysaccharides (the surface of the bacterium) in the sample from four of the people with dementia and none of the people who did not have dementia. Bacteria can enter the bloodstream through everyday activities such as eating, chewing and toothbrushing. Once in the bloodstream, the bacteria can be carried to other parts of the body.
The researchers hypothesized that when the bacteria reach the brain, they may trigger an immune system response (like they do in the mouth), killing brain cells.This immune response could be one mechanism that leads to changes in the brain, which is typical in Alzheimer’s disease. It could play a role in causing symptoms such as confusion and deteriorating memory.
“This new research indicates a possible association between gum disease and individuals who may be susceptible to developing Alzheimer’s disease, if exposed to the appropriate trigger,” said Dr. Crean, who is the dean at the School of Medicine and Dentistry. “Research currently underway at UCLan is playing an active role in exploring this link, but it remains to be proven whether poor dental hygiene can lead to dementia in healthy people, which obviously could have significant implications for the population as a whole. It is also likely that these bacteria could make the existing disease condition worse.”
This was a small study examining only brain tissue samples from only 20 people. Because of that, the association between Alzheimer’s disease and gum disease in this study could have occurred by chance. It is also possible that people with Alzheimer’s disease have worse oral hygiene than do people without dementia. Therefore, the bacteria in the brain tissue may be the result of Alzheimer’s disease, not the cause. More research is needed to determine whether or not having gum disease increases the risk of developing Alzheimer’s disease.
Lipopolysaccharide-induced sickness behaviour evaluated in different models of anxiety and innate fear in rats.
Bassi GS1, Kanashiro A, Santin FM, de Souza GE, Nobre MJ, Coimbra NC.
Author information
Abstract
The fact that there is a complex and bidirectional communication between the immune and nervous systems has been well demonstrated. Lipopolysaccharide (LPS), a component of gram-negative bacteria, is widely used to systematically stimulate the immune system and generate profound physiological and behavioural changes, also known as ‘sickness behaviour’ (e.g. anhedonia, lethargy, loss of appetite, anxiety, sleepiness). Different ethological tools have been used to analyse the behavioural modifications induced by LPS; however, many researchers analysed only individual tests, a single LPS dose or a unique ethological parameter, thus leading to disagreements regarding the data. In the present study, we investigated the effects of different doses of LPS (10, 50, 200 and 500 μg/kg, i.p.) in young male Wistar rats (weighing 180-200 g; 8-9 weeks old) on the ethological and spatiotemporal parameters of the elevated plus maze, light-dark box, elevated T maze, open-field tests and emission of ultrasound vocalizations. There was a dose-dependent increase in anxiety-like behaviours caused by LPS, forming an inverted U curve peaked at LPS 200 μg/kg dose. However, these anxiety-like behaviours were detected only by complementary ethological analysis (stretching, grooming, immobility responses and alarm calls), and these reactions seem to be a very sensitive tool in assessing the first signs of sickness behaviour. In summary, the present work clearly showed that there are resting and alertness reactions induced by opposite neuroimmune mechanisms (neuroimmune bias) that could lead to anxiety behaviours, suggesting that misunderstanding data could occur when only few ethological variables or single doses of LPS are analysed. Finally, it is hypothesized that this bias is an evolutionary tool that increases animals’ security while the body recovers from a systemic infection.
Why doesn’t he go back to the place he got them and ask or a similar specialist? Herbs for putting on weight instead of protein-rich food? So they made him estrogen-dominant so he gets fat? Was it Saw Palmetto or something like that?
Was in a different country. But regardless I think we have not had much luck focusing on the “causative agent” in doing this we have not focused enough on our current state.
Knobil and Neill’s Physiology of Reproduction
www.google.com.pg/patents/US8343488
Lots of talk about bad rt3 to t3 ratios in what he calls " human dormancy syndrome-related sequellae"
Many here have noted we have a high ratio of t3 to rt3 here.
"Human Dormancy Syndrome
Diagnosis of human dormancy syndrome can be accomplished using clinical history, physical findings, and chemical tests of urine, blood, cerebrospinal fluid (CSF) and/or tissues. Pertinent historical features include symptoms of persistent fatigue, cognitive impairment, weight gain, depression, alopecia, constipation, insomnia, sleep apnea, loss of libido, cold intolerance, exercise intolerance, addiction to stimulants, history of Raynaud’s syndrome, dyslipidemia, atherosclerosis, syndrome X, peripheral vascular disease, type II diabetes, Alzheimer’s disease (and other dementias), demyelinating disease, (muscle tension headache, migraine), fibrocystic breast disease, breast cancer, prostate cancer, ovarian cancer, other cancers, cholelithiasis, pulmonary artery hypertension, pulmonary fibrosis, COPD, asthma, systemic hypertension, infertility, fibromyalgia, chronic fatigue syndrome, chronic wide spread pain and other chronic pain states, and obesity. (autoimmune conditions such as lupus, scleroderma, rheumatoid arthritis, sarcoidosis, vasculitis, myositis, ankylosising spondylitis, psoriatic arthritis, reactive arthritis, Reiter’s syndrome, Becet’s and polymyalgia rheumatica, viral, bacterial and fungal infections, septic shock, pneumonia and other serous infections, narcolepsy, hypertension, liver disease, esophageal dysmotility, inflammatory bowel disease, renal disease, Parkinson’s disease, coma, impaired stage 4 sleep, irritable bowel syndrome, elevated CRH, elevated sympathetic nervous system activity, dysregulated HPA, low serotonin, altered nitric oxide metabolism and NOS activity, low oxytocin levels, mitochondrial impairment and structural changes with decreased membrane permeability, compulsivity, hypervigilance, dissociation, impaired natural killer cell activity, elevated CSF substance P levels, blunted growth hormone response during provocation testing, orthostatic hypotension, altered cerebral blood flow."
We all originally had some sort of infection. This left our immune systems a bit overactive, or crazy overactive in some of us who weren’t well. The overactive immune systems then went after something when we stopped the pill. The AR, 5ar enzymes, the brain (GABA-a).
I honestly feel like something is eating at the gaba part of my brain. Sounds crazy but knowing what I know about the body, it just feels like it.
Cure for us would be rebuilding immune system with monthly IVIG infusions, plasmapheresis as well.
Google “brain on fire.” We have a similar issue to this girl and she recovered 100% with the above treatments.
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chronicsorethroat.wordpress.com/
This guy named hip swears he got CFS from a virus. Read all his symptoms you will find so many are similar to PFS even low libido, anhedonia, anxiety etc etc.
My biggest clue seems to be my eoisnihils and ige which went high around the time i crashed on fin.
Unfortunately high eosiniphils an ige can indicate almost every kind of infection fungal, parasitic, bacterial and viral so it is not that much help.
We have no idea how taking fin depleated our immune system allowing something in which may have never got in if we were not taking fin. Also 5ar is found in the spine how can we be sure that fin did not cause an infection which may have already been confined in our body to move to another area such as the brain? Viruses can live in us for a life time and when the body becomes weak they can reactive like shingles does.
bruschi11 you have huge mycoplasma levels that in itself would probably make one feel like garbage. But why is your body not taking care of the mycoplasma?
I had sinus ssurgery for the cyst. The DR said it did not look infected. He a biopsy of the inflamation and it found high levels of eosiniphils. My eosiniphils had been high ever since I got PFS. Strange that there is no obvious infection.
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Low vitamin D and elevated immunoreactivity against Epstein-Barr virus before first clinical manifestation of multiple sclerosis.
Décard BF1, von Ahsen N, Grunwald T, Streit F, Stroet A, Niggemeier P, Schottstedt V, Riggert J, Gold R, Chan A.
Author information
Abstract
OBJECTIVE:
Vitamin D deficiency and Epstein-Barr virus (EBV) infection may be associated with the development of multiple sclerosis (MS). We investigated serum 25-hydroxyvitamin D (25-OH-D) levels and anti-EBV immunoreactivity in 25 individuals before the first clinical manifestation of MS.
PATIENTS AND METHODS:
56 serum samples of 25 individuals who had donated blood prior to the first clinical MS manifestation (clinically isolated syndrome (CIS)) (four male subjects, 21 female subjects, mean age 31.5 years at time of pre-CIS blood sampling; mean age at disease onset 33.4 years) were available, covering an interval of 7.3 years-2 months (mean 31.5 months) before CIS. In 18 of 25 patients serum samples were also obtained after established diagnosis of MS. Longitudinal age- and gender-matched healthy blood donors (four male subjects, 21 female subjects, 39 samples, mean age 32.5 years) served as controls. Serum 25-OH-D was measured by isotope dilution-liquid chromatography-tandem mass spectrometry. 25-OH-D levels were deconvoluted using published seasonal coefficients from a German population. Immunoglobulin G (IgG) against Epstein-Barr virus nuclear antigen-1 (EBNA1) were assessed using commercially available ELISA.
RESULTS:
Low 25-OH-D levels were observed during the 24-month pre-CIS interval (47.8 (32.5-77.2) nmol/l, median (IQR); healthy controls: 81.6 (57.7-98.5), p=0.004, however, still higher than after established diagnosis (24.5 (13.7-47.7), p<0.0001 compared with controls). IgG against EBNA1 during the 36-month pre-CIS interval was increased (185.9 (91.2-460.0) IU/ml, median (IQR); healthy controls 63.7 (29.5-121.6), p=0.002).
CONCLUSIONS:
Low vitamin D and remote EBV infection may be associated with clinical MS breakthrough within 2-3 years.
You may be right. I’m almost positive that I developed some type of infection while swimming in a river three months prior to crashing for my first time from a DHT inhibitor. I remember going to the river on a really hot day while on creatine. I was drinking heavy and spent almost the whole day swimming in a river with tons of other people in it close by. Anyway the next day I had a strange pain in my right side and was urinating frequently even though small amounts of urine would only come out at a time. I may have just been dehydrated because a couple of days later the urinary symptoms went away. The strange thing though was that the pain in my right side did not go away and I still get it on and off to this day seven years later.
Three months later I took a DHT inhibitor and was never the same. I always suspected that maybe I had bowel disease like crohns or something and that symptoms started that day after drinking heavy. I suspected this because lower right side pain is a common location for crohns to develop in the large intestines. Pain in this area with the fact that most doctors suspect crohns disease is a autoimmune disease caused by the immune system attacking the lining of the intestines and the possible PFS autoimmune connection, I was always concerned about autoimmune bowel disease and that maybe taking the DHT inhibitor caused it to get much worse really fast.
Well I recently ruled this out by having a colonoscopy. No evidence of bowel disease such as crohns or inflammation was found. This leads me to believe that the symptoms that I developed right after swimming in that river was from some type of infection. Three months later I took the DHT inhibitor and started suffering from this syndrome…
I don’t think that you have to be “sick” to have this abnormal reaction from a DHT inhibitor but your body needs to.be already stressed which sets you up for PFS. When we see things like low vitamin D and low blood sugar after our crash it seems like our body is burning more of these things trying to correct what’s wrong.
I’m not sure thought that it’s autoimmune or chronic infection. If it was I think more of us would see more evidence of this in our labs. I think that what ever was stressing our bodies in the first place resulted in 5ar not being able to recover right away and that low 5ar enzymes through out the body resulted in neurosteriods that require 5ar to be reduced into their metabolites not getting reduced properly. I believe it’s hormonal and 5ar related but that it has nothing to do with plasma testosterone or DHT. We just see testosterone being off in our initial labs after crashing and assume this is what needs to be corrected. I think testosterone being off initially is the endocrine systems most logical reaction after it sees it’s metabolites further down the pathway not getting converted properly. It’s like a giant negative feed back loop being all messed up. Seeing that the neurosteriod studies find increased T in the CSF of PFS patients kinda of hints towards this.