I Have Both HPV Both 1 & 2, Is My Life Pretty Much Ruined?

dq139

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So, I had intercourse with this girl and it was only oral sex for the both of us. I didnt know she had herpes or was having a outbreak at the time..so long story short I get intense pain around my penis head and oral herpes with flu like symptoms within the 1st 15 hours after intercourse....it's been 2 days and I've been using colloidal silver 500ppm both oral and topical at max does and mega dosing lysine zinc vitamin c, echanacea and applying essential oils like tea tree clove oil, Apple cider vinegar ect. To the soars. And its not doing anything really..I'm still in alot of pain as of now....I have no insurance at the moment so I have to wait untill I get more money to go to the doctor & get medication & tested....I'm 28 now and I'm convinced I just ruined my life. I don't know how I can deal with these miserable outbreaks multiple times per year for life. And how can I tell a future partner that I have a std a common one or not??...also I hear having genital & oral herpes increase your chance of infertily, penile, testicular and mouth cancer. As if I didn't have enough problems working aganst me before right?...I haven't had too much sex before this, but I never thought it was so risky and destructive to hook up with a girl you meet at a bar. i hear people do it all the time...This really sucks big time!

So what I'm asking is what natural ways would ray peat recommend to ward off these oral and genital out breaks and protect against cancer and infertility. Also if anybody else has these types of herpes how are you coping with it and what are some pointers I could use to help this uncurable nightmare?? Thanks for the help.
 
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Herpes or HPV?
 

Inaut

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Methylene blue and other quinones found in pau d’arco could be helpful as well.
 
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you are very much over reacting. As I said, everyone has many forms of HPV. The key is maintaining a good immune system and then it goes away and stays away. "my life is ruined" is false unless you believe it, and this ain't so objectively.
 

Zpol

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Lysine supplement plus a low arginine diet will reduce future outbreaks. Also avoid vit D and vit C deficiency.
 
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I had horrible "crown" of HPV on penis all around the head. Got it after binging on MDMA and having sex all around for 3 days, no sleep, Viagra involved:)))) the doc I went to wanted ridiculous amount of money to remove it with laser. It went away completely just after one week on gluten free diet. I googled and found that anti-gliadin antibodies somehow block another antibodies body uses to fight HPV.
 

Inaut

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I’d go no more than 8mg daily. I’m sure higher doses are ok for a short time but less is more in medicine
 

S-VV

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Go to a doctor and get tested. If it is a herpesvirus Valtrex and Famvir are safe and effective.
 

Frankdee20

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From the research I've done I think it's Hpv. Like i said I can't go to the doctor right now for testing unless they can put me on a payment plan.

You didn’t wrap it up ?
 
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State your reasons

it's caused by a poor immune system. The things to bolster the immune system help put it into dormancy.

The drugs are known to cause kidney failure. There is no drug that is "anti virus" -- the drugs work by being cytotoxic to cells that are dividing. It is difficult to find studies on this of course because of how the system works but they are out there.

Acyclovir is what this review discusses, but it is really the same as the others mentioned as Valtrex is converted to it in vivo and the others probably work exactly the same:

Acute kidney injury due to acyclovir
Acyclovir is an important antiviral agent in the therapy of herpes simplex and varicella zoster virus infections [6]. Although the drug is well tolerated, severe nephrotoxicity, which often leads to acute renal failure, has been observed in patients [4, 7]. Acyclovir-induced renal failure occurs in approximately 12–48 % of cases [4]. The optimal usage of acyclovir is very important in order to avoid its potentially life-threatening complications. Acyclovir-induced nephrotoxicity is typically evident by an increase in the plasma creatinine level, abnormal urine sediment, or acute renal injury [8]. Acyclovir is rapidly excreted in the urine via glomerular filtration and tubular secretion, and reaches high concentrations in the tubular lumen. Renal excretion of unchanged drug reaches approximately 60–90 % [7, 9, 10]. Acyclovir is relatively insoluble in the urine, particularly in the distal tubular lumen [7, 912]. Rapid intravenous administration of high-dose acyclovir is associated with high luminal concentrations of this drug and the intratubular precipitation of crystals can cause renal injury [7, 9, 10]. Typically, crystalluria develops within 24–48 h of the initiation of acyclovir therapy. Severe intraparenchymal precipitation of crystals can cause interstitial congestion and hemorrhage, leading to a decrease of renal blood flow [7, 1012]. The serum creatinine levels of our patient also began to rise within 48 h of acyclovir treatment. Renal biopsy revealed no sign of precipitation of crystals. Clinical evidence of nephrotoxicity in the absence of crystalluria was suggested to be secondary to the direct cytotoxicity effect of the drug to tubular cells and acute interstitial nephritis in our patient, as mentioned in other studies [8, 13, 14]. Renal biopsy findings of patients with acyclovir toxicity include bulging of tubular cells, dilated tubular lumens, loss of proximal–distal tubular differentiation, flattening and vacuolization of epithelial cells, and epithelial cell mitoses [8, 14]. A moderate and patchy tubulointerstitial infiltration of inflammatory cells and focal necrosis of cortical proximal tubules with edema were noted in our patient.

The administration of high doses of acyclovir (≥1500 mg/m2 per day) with other nephrotoxic agents, pre-existing renal disease, and dehydration play important roles in acyclovir nephrotoxicity [15]. Acyclovir dose should be reduced in patients with underlying renal insufficiency. Furthermore, slow drug infusion, over 1–2 h, adequate fluid replacement, and induction of high urinary flow rates (100–150 ml/h) should be encouraged in order to prevent crystal precipitation and subsequent tubular obstruction [7, 911, 16]. Despite vomiting 4–5 times a day as a predisposing factor for prerenal failure in our patient, she was adequately hydrated and no clinical evidence of hypovolemia was observed. Furthermore, any drug that causes nephrotoxicity was not used with acyclovir therapy.
 
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Also they are very neurotoxic and they appear in the cerebrospinal fluid after administration.



Acyclovir Levels in Serum and Cerebrospinal Fluid after Oral Administration of Valacyclovir
The possible involvement of herpesviruses in the pathogenesis of multiple sclerosis (MS) was recently investigated in a clinical trial of valacyclovir in patients with MS. As an important part of that survey we performed an independent pharmacokinetic study in order to determine the concentration of acyclovir in cerebrospinal fluid (CSF). The concentrations of acyclovir in serum and CSF were measured at steady state after 6 days of oral treatment with 1,000 mg of valacyclovir three times a day. Samples were obtained from 10 patients with MS. All patients had normal renal function, and none had signs of a damaged blood-CSF barrier. The maximum concentration of acyclovir in serum was reached after 1 to 3 h (mean ± standard deviation [SD], 27.1 ± 5.6 μM), and the minimum concentration in serum was 3.1 ± 1.1 μM (mean ± SD). The acyclovir concentrations in CSF at 2 and 8 h were essentially stable, with the mean ± SD levels being 2.5 ± 0.9 and 2.3 ± 0.7 μM, respectively. Similar levels were recorded in serum and CSF samples from five other MS patients after 6 months of oral treatment with valacyclovir at identical dosages. The area under the concentration-time curve (AUC) for acyclovir in CSF to the AUC for acyclovir in serum (CSF/serum AUC ratio) was approximately 20%. We conclude that the improved bioavailability previously reported for valacyclovir in plasma results in higher concentrations in CSF, while the CSF/serum AUC ratio remains constant.
 
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