Re: Utis Caused By Super Bugs
26 days agoHi Wendy,
I had a gut test and found that I had citrobacter freundii, terrible diarrhea etc. I took Bactrim because the stool test (from Doctor's Data) indicated that it was the only antibiotic that would work. But it didn't because almost none work for me as I have had too many over the years. I took chlorine dioxide for 10 days to get rid of it. Did the Master Mineral route of 1 drop to 1 drop, sodium chlorite to HCL. Took a bath in it also, 30-60 drops in a hot tub; can add salt to enhance (not epsom, only himalayan or celtic, etc). I used 60.
Mine was not a UTI but I used to have chronic UTIs. I did everything when I had one, an antibiotic, colloidal silver, lemon and cranberry juice (no sugar), rife machine, Hydrogen peroxide drops for 10 days. Way too much, as I had gastritis afterward, but no UTI, lol and it didn't come back. But chlorine dioxide is much better, no gut pain and no yeast side effects. Will get some detox diarrhea but you can control the dose.
I am 68 years old but have had UTI's since my 20s. I do have autoimmune and I know that is a factor because of heavy metals and yeast; don't know about GLP's, but would suspect them as all meds have side effects.
If you end up taking another antibiotic definitely take colloidal silver as it enhances any antibiotic, even old and outdated ones, from a 10% to 100% boost. My usual dose of silver was 7 teaspoons a day, but I had to keep increasing over the years because of constant infections. My usual dose then was 4 TBSPs a day when I was sick. I only took it when I was sick; one time getting up to 14 TBSPs because I wasn't getting better. Now, I don't take it, because my body got used to it and it doesn't work anymore. It could be a biofilm issue, and that is one of the issues with UTIs, chlorine dioxide is good for that.
Ascorbic Acid Vitamin C for Peptic Ulcers
26 days agoASCORBIC ACID (PURE VITAMIN C): PEPTIC ULCER
From the Book: Healing Factor Vitamin C Against Disease – by Irwin Stone, Linus Pauling, Albert Szent-Gyorgyi 1972.
Source on-line: https://vitamincfoundation.org/stone/
Source download book: https://welib.org/md5/35609ae8abf6e1dcb1cc701374943358
Peptic ulcers may be the butt of many jokes, but as any ulcer sufferer can testify, having one is not funny. Ulcers are a painful, chronic disease affecting about 14 million Americans during their productive years. Every day some 4,000 individuals develop an ulcer and each year about 10,000 people die of complications from peptic ulcer. The drain on the economy is estimated to be 500 million dollars in lost man-hours and cost of medical treatment. A simple, inexpensive, successful preventive and therapeutic regime is needed.
Our stomach is the second stop in the processing of food for digestion and absorption. It is a tough, strong, muscular, spheroidal-shaped bag with an opening at the top (inlet) and at the side (outlet). Each opening is surrounded by a circular muscle, the sphincter, controlled by nerve impulses for opening and closing. The top opening is connected to the esophagus, which carries the food from the mouth; the side opening is connected to the duodenum, the first section of the intestines. The lining of the stomach secrets strong hydrochloric acid and a powerful enzyme, pepsin, which dissolves and digests proteins.
The stomach contents are normally highly irritating, corrosive, and erosive. This can be seen when the stomach contents sometimes back up into the esophagus producing the distressing sensations of "heartburn" and in the sour, irritating taste of vomit. Since the stomach walls are themselves made of protein, they must in some way be protected against the corrosive action of their own secretions. Sometimes this equilibrium is disrupted and open sores and lesions in the lining result. If they are in the stomach, they are called gastric ulcers; if in the adjacent intestine, duodenal ulcers. In the United States, duodenal ulcers are about eight times more common than gastric ulcers.
The secretion of hydrochloric acid and the enzyme, pepsin, is also under nervous control. The stimulation of these nerves is caused by food entering the mouth or even by the thought of food, so that the stomach will be ready for processing the food when it reaches there. In nervous people, smokers, excessive drinkers, or individuals under stress, this nervous stimulation does not turn off at the proper sequence or turns on when there is no food in the stomach. When no food is present to take the full brunt of the corrosive chemical attack of the stomach juices, gastric distress is felt and, if long continued, actual attack of the lining may result.
Animal experiments have been conducted since the early 1930s on ascorbic acid and its relation to gastric and duodenal ulcers. In 1933, Smith and McConkey (1), working in a New York State tuberculosis hospital, performed autopsies on 1,000 guinea pigs that had been fed a normal diet and failed to find a single spontaneous stomach ulcer. Of seventy-five guinea pigs fed a diet deficient in ascorbic acid, twenty, or approximately twenty-six percent, developed ulcers. In eighty guinea pigs fed the same deficient diet but supplemented with added ascorbic acid, only one developed ulcers. In other experiments, they found that diets deficient in vitamins A, B, and D did not produce ulcers if the ascorbic acid supply was adequate. Mechanical injury to the duodenum lining of guinea pigs fed an adequate diet was followed by rapid and complete healing, while similar injury to guinea pigs on an ascorbic acid-deficient diet resulted in the formation of duodenal ulcers. They also gave a small group of their tuberculous patients with chronic duodenal ulcers tomato juice supplements (their only source of ascorbic acid in those early days) with favorable responses. They also advised adding tomato juice or orange juice to the scurvy-producing Sippy or Lenhartz diets used for ulcer treatment. Hanke (1), in Germany in 1937, confirmed this work.
There is an extensive medical literature on clinical tests going as far back as 1934 correlating deficiency of ascorbic acid with high incidence of gastric and duodenal ulcers, bleeding ulcers, and poor healing after surgery. Many of the papers point out that the ulcer patient should receive adequate amounts of ascorbic acid.
Over the years, the author has collected over fifty medical research papers on this subject with no claim that this represents all the papers which have been published. Complete reference to all these papers is obviously beyond the scope and space of this book. Instead, a limited illustrative selection of twelve papers is included in the bibliography covering the period from 1936 to 1968 (2). The earliest papers show that ulcer patients have higher requirements for ascorbic acid than normal subjects. The patients have low, inadequate intakes of ascorbic acid and are in a state of subclinical scurvy and there is poor healing of the ulcers and the wounds after surgery. The papers recommend that ulcer patients receive plenty of ascorbic acid. The following are quotes from a few of these early papers:
It is important for the clinician to make sure that patients with peptic ulcers are receiving an adequate amount of vitamin C... The severest degrees of vitamin C deficiency were found in the patients with haematemesis (vomiting of blood). It is suggested that large doses of vitamin C should be given to all subjects of peptic ulcerations and haematemesis in order to saturate them as rapidly as possible (2).
The results and suggestions contained in these early references have been repeated in the later papers and have continued up to the present time.
In 1968, Russell and coworkers (2) compared a series of sixty hospitalized patients with gastrointestinal hemorrhage -- 2 with peptic ulcer -- with a group having uncomplicated peptic ulcer and with healthy controls. They found significantly lower ascorbic acid levels in the bleeding group than in the uncomplicated peptic ulcer group, which was much lower than the healthy controls. The differences were more striking with advancing age over forty-five. They stated That only six of the bleeders had any clinical evidence of scurvy but that the ret suffered from a subclinical form of the disease. They believed this subclinical scorbutic state prevented healing of the bleeding ulcers and maintained hemorrhage in the gastric erosions precipitated by other factors such as aspirin or alcohol.
Certain drugs, such as aspirin, cortisone, and other anti-inflammatory agents, and cinchophen, are known to provoke ulcers and gastric hemorrhage. This is especially the case when a deficiency of ascorbic acid is present. In animal experiments, the administration of ascorbic acid along with the toxic drug reduced the incidence of peptic ulcer and gastric hemorrhage to such an extent that it prompted one author (Aron) to suggest, "Therefore it would seem judicious in human therapeutics to include ascorbic acid in every prescription for an anti-inflammatory drug" (3).
In any surgery, the importance of ascorbic acid has long been known (see Chapter 27). Patients undergoing surgery for ulcers are no exception. In a 1947 paper, Zerbini (4) discusses two surgical cases of patients with ascorbic acid deficiency. One patient exhibited severe surgical shock during the operation and the other patient showed no evidence of healing of the surgical wounds when the stitches were removed on the seventh postoperative day. This latter patient had been given a daily injection of 200 milligrams of ascorbic acid, but obviously this low, vitaminlike dosage was insufficient to supply the patient's high demands and as a result the wounds did not heal.
Williamson, in 1967, again confirmed the low ascorbic acid levels in patients subjected to gastric surgery and said that in these patients, "the administration of ascorbic acid would seem obligatory." Cohen, in the same year, stated that all patients with gastrointestinal disorders should be suspected of having subclinical scurvy. He also pointed out that this concept was proposed by Lazarus in 1937 but was "not yet generally acknowledged." This was over three decades ago -- the medical mills certainly grind slowly. Three other papers and a review added further confirmation to the pathogenetic role played by low levels of ascorbic acid in gastrointestinal disorders. In the paper by Cohen and Duncan they state:
[Patients should] be given routine ascorbic acid supplements before surgery and during the phase of early wound healing ... There are no known hazards of ascorbic acid therapy, and overdosage is therefore of no practical importance (4).
In a thirteen-page government bulletin (5) entitled "Peptic ulcer, " prepared by The National Institute of Arthritis and Metabolic Diseases of the National Institutes of Health, there is not a single mention of ascorbic acid in the entire booklet. Nothing is said of its possible role in ulcer formation or in the ulcer treatment, in spite of the worldwide background of nearly four decades of research, some of which has been cited above. This is a bulletin sold to the general public for its information on the causes and treatments of this disease. "The Medical Letter, " which is a semimonthly publication for doctors and is designed to convey authoritative recommendations for current medical treatments, devoted a large part of its December 26,1969 issue to a discussion of the "Medical Treatment of Peptic Ulcer" (5). Here again no mention is made of ascorbic acid in the two and a half pages of discussion. It seems rather fantastic that, in both these publications, all of the suggestive work reported in the medical literature on ascorbic acid in ulcer therapy, can be so blatantly ignored. It also indicates that the use of ascorbic acid in ulcer therapy is not widely practiced and that ulcer patients are generally denied the possible benefits indicated in the above review of medical literature.
The following clinical research proposal is made in the hope that it will be picked up and tested by the government health agencies, by the publicly endowed health foundations with clinical testing facilities, or by doctors in the gastrointestinal field. The proposed rationale for the use of sodium ascorbate instead of ascorbic acid in ulcer prevention and therapy at megascorbic levels combines the antacid and buffering capacity of sodium ascorbate with its wound healing and antihemorrhagic effects. The research protocol would include the use of 0.5 to 1 teaspoonful (1.5 to 4 grams) of sodium ascorbate, dissolved in a glass of milk, taken before meals and at bedtime. For gastric distress at other times, 0.5 teaspoon of sodium ascorbate, dissolved in about 2 ounces of water, will usually provide immediate relief. This simple regime was very successful in several ulcer volunteers who were thus able to avoid surgery. The use of sodium ascorbate should be subjected to large-scale clinical testing to determine its value as a new approach to peptic ulcer prevention and therapy.
Re: Vitamin C for Cataracts
26 days agoEYE CONDITIONS: ASCORBIC ACID (PURE VITAMIN C)
From the Book: Healing Factor Vitamin C Against Disease – by Irwin Stone, Linus Pauling, Albert Szent-Gyorgyi 1972.
Source on-line: https://vitamincfoundation.org/stone/
Source download book: https://welib.org/md5/35609ae8abf6e1dcb1cc701374943358
Of all the disorders afflicting man, blindness causes the most widespread disability. Aside from the cost in terms of economic loss and the personal expenses of family care and dependency, the annual bill for aid to the blind approaches a billion dollars. It is estimated that a million people in the United States have visual impairment so severe that they cannot read a newspaper. Yet, in spite of significant advances in eye research, the incidence of blindness is increasing. Megascorbic therapy might one day help to reverse this trend.
Structurally, the eye is a spherical camera aimed by exterior muscles. It has a transparent window in the front (cornea) composed of a special protein and a large optic nerve exiting at the rear. The interior is divided into two chambers separated by a flexible lens which focuses the image on a thin, biochemically active membrane (retina) which transforms light energy into nerve impulses. These nerve impulses are gathered into the optic nerve and transmitted to the brain where the color pictures are "seen" and recorded. As would be expected of an organ of such biochemical activity, the eye was early found normally to contain high levels of ascorbic acid and seemed to have the ability to extract it from the blood and to concentrate it for its many vital functions.
The 1962 paper by Heath (1), with forty references to the literature, reviewed the work on ascorbic acid and the eye. He cited twelve separate biochemical processes in which ascorbic acid is involved and speculated on the functions of ascorbic acid in the eye and its possible involvement in diabetic retinopathy, detachment of the retina, and maintenance of the proper consistency of the internal fluids of the eye. It has been known since the early 1930s that ascorbic acid is normally found in the eye at much higher levels than in the blood and in many other tissues. Heath confirmed this by showing that the ascorbic acid levels in different bovine eye tissues were (in milligram percent) the cornea, 30; corneal epithelium, 47 to 94; lens, 34; retina, 22; and were higher than in the skeletal muscle, 2; heart, 4; kidney, 13; and brain 17' but were not as high as in the adrenal gland, 97-160; or the pituitary gland, 126. He states:
Animals which are capable of synthesizing their own ascorbic acid usually have tissue levels approaching saturation. It would, therefore, seem desirable to ensure that the intake of ascorbic acid by man is sufficiently high for tissue saturation. Lower intakes, although not leading to scurvy, may affect some metabolic processing in which ascorbic acid is involved.
Glaucoma
Glaucoma usually appears in middle life and is the second leading cause of blindness in the United States. High pressure within the afflicted eyeball eventually destroys the nerve cells within the retina and progressive loss of vision results. Glaucoma as present in about 2 percent of the population over forty, and 8 to 10 percent over sixty-five. It brings creeping blindness to 3,500 Americans a year.
The prevention of glaucoma is achieved by merely maintaining low intraocular pressure during the lifetime of the individual. The treatment of the disease, once it occurs, is to endeavor to reduce the intraocular pressure to normal levels to prevent further nerve damage. About a million Americans over forty years of age have glaucoma without knowing it. Many cases go undetected for years in spite of the availability of a simple, rapid, and painless tonometer test procedure. Control and prevention of the disease in its early stages is preferable to waiting for the agony of acute glaucoma to strike.
There was a period of intense research activity from 1964 to 1969 on the use of megascorbic levels of ascorbic acid or sodium ascorbate for reducing the intraocular eye pressure. Linner (2), in 1964 in Sweden, showed that 0.5 grams of ascorbic acid administered twice daily produced a significant drop in the intraocular pressure of normal eyes. He published another paper, in 1969, in which he showed that 2 grams of ascorbic acid a day, orally, produced the same significant decrease in glaucomatous eyes.
The year 1965 saw the beginning of a four-year period when numerous papers reported on the prompt reduction of the intraocular pressure, with no side effects, by the intravenous injection of 20 percent sodium ascorbate solution at doses of about 70 grams per treatment. Virno and coworkers (3) in Rome published five papers in this period, the group from the University of Rome's Ocular Clinic (4) presented seven papers, one came from Switzerland (5), and one from Finland (5). Even though two papers were published in American journals in 1966 and 1967 by the Italian workers (3), no papers coming from American authors could be found on this exciting line of research.
Such a research silence on the part of American scientists can only be interpreted as an indication that no work has been carried out in the United States in the past six years in this field. Yet, during this same time, numerous government bulletins have appeared describing the urgent need for solving the problem of glaucoma and the daily mail is filled with repeated requests for donations to eye research charities. Where is the money going? What is being done with the available funds?
Research should be started immediately on population groups near forty years of age and older to determine the long-term effect on the inhibition of glaucoma by means of the continued daily intake of about 3 to 5 grams of ascorbic acid. The use of higher dosages, both orally and intravenously, for the therapy of incipient and advanced glaucoma should be included in the research protocols. This will help to determine if a simple and harmless ascorbic acid regimen can be worked out which will prevent blindness in our senior citizens.
Cataracts
A Public Health Service government bulletin (6) starts the discussion of cataracts with:
Cataracts are the leading cause of blindness in this country. They occur when the chemical composition of the crystalline lens changes, making it opaque rather than transparent. When cataracts form, the only way to restore sight is to remove the afflicted lens. In the majority of cases, cataracts appear to be part of the aging process. Uveitis (inflammation of the eye) and physical and chemical injury are other causes.
Let us discuss these authoritative statements individually:
1. That cataract is now the leading cause of blindness there is no argument -- but need it be? The proper long-term use of ascorbic acid may have a profound effect in reducing the incidence of this condition and preventing blindness.
2. Changes in the chemical composition of the lens makes it opaque -- correct, no argument. But what is the chemical composition of the lens? It is made from a specially oriented helical protein (7). Dische and Zil (8), in 1951, start their paper, "The most striking chemical change in the lens during the cataractous process is the decrease in sulfhydryl groups." Sulfhydryl groups, like ascorbic acid, are strong, normally occurring reducing agents, and are destroyed by oxidative processes. Possibly, the high levels of ascorbic acid found in the normal eye are there to protect against the loss of these sulfhydryl groups by oxidation. Studies in India (9), from 1963 to 1969, where senile cataract is rampant, occurs at an early age, and matures more quickly, show that cataractous eyes have a much lower content of ascorbic acid than normal eyes. One of these papers (Nema and Srivastava) suggests that the chronically low ascorbic acid content may be responsible for the high incidence of senile cataract.
3. When cataracts form, the only way to restore sight is to remove the afflicted lens -- right and wrong. This is the opinion of many present-day ophthalmologist. While some research shows that it is possible to slow down the cataractous process, no work could be found which would indicate that the proper use of ascorbic acid has been tried to reverse the cataractous process.
4. In the majority of cases, cataracts appear to be part of the aging process -- right. But let us do something about this by inhibiting aging (see Chapter 18).
5. Uveitid and physical and chemical injury are other causes -- right. All these stresses reduce the ascorbic acid levels in the eye. The 1941 paper f Lyle and McLan of the Royal Air Force on corneal inflammations should not be ignored. They stated:
Treatment by means of ascorbic acid intravenously is of therapeutic value. The improvement in most cases is almost dramatic. In most cases there is no reason to believe that a general vitamin C deficiency exists. It appears, therefore, that the beneficial results are obtained by flooding the bloodstream with excess of ascorbic acid.
This work was confirmed by Summers in 1946. The profound effects of ascorbic acid on the healing of deep corneal ulcers caused Boyd and Campbell, in 1950, to state and recommend, "We therefore suggest that ascorbic acid, in such massive doses as 1.5 grams daily, has a value in therapy apart from its normal role as a vitamin at accepted levels of intake." The additional work of Campbell and coworkers, in 1950, and Boyd, in 1955, on experimental eye burns, supplies additional confirmation for the need for adequate levels of ascorbic acid in the eye for recovery from heat injury 10).
The answers to this discussion of cataracts seem to be supplied by ascorbic acid. Are they not sufficiently suggestive to warrant further research and investigation?
The literature cited in this discussion of cataracts is but a small fraction of the total which has been published on ascorbic acid and the eye since the early 1930s. To thoroughly review this voluminous work is beyond the scope of a short monograph. We have to omit the work done on experimental diabetic cataracts, naphthalene cataracts, and dinitrophenol cataracts. But before closing this chapter, let us consider only four of the papers on senile cataract.
As long ago as 1939, Muhlmann and corworkers (11), in the Argentine, obtained 90 percent good results in sixty patients with 113 incipient senile cataracts by 2 series of daily injections, for ten days each, of 50 to 100 milligrams of ascorbic acid. He concluded that the treatment had no contraindications, should be tried in all incipient cases, and is more effective the earlier it is used.
In another 1939 paper, "Vitamin C and the Aging Eye, " Bouton (11) of Detroit found "ascorbic acid deficiency can be held partly responsible for impairment of vision associated with senescence of the human eye and that the administration of ascorbic acid by mouth can counteract this process." He gave 350 milligrams of ascorbic acid a day for four to eight weeks and obtained improvement in vision in 60 percent of the treated group; marked improvement usually set in within the first two weeks of treatment. He believed that cataracts already formed were not affected and the benefits obtained were due to clearing of the other optic media and to some degree to a beneficial effect on the retinal vessels and the head of the optic nerve. While 350 milligrams of ascorbic acid a day was considered a huge dose in 1939, the administration of multigram daily levels would have obtained even better results.
Atkinson, an ophthalmologist of more than thirty years' experience, published in 1952, a scholarly paper on the senile cataract (11). He stated, "...in a larger percentage of cases than most surgeons have realized, cataract is a preventable disease." In 1952 he had over 450 cases of incipient cataract under his treatment which included, among other dietary suggestions, the administration of about 1 gram of ascorbic acid a day. He noted that untreated incipient cataracts matured in four years or less, some taking only one year, Of his over 450 patients under prophylaxis, only a limited number matured and went to surgery, whereas formerly nearly all had to submit to surgery. He states that in a number of his patients the cataracts have remained incipient over a period of eleven years.
The promising leads relating to ascorbic acid cited above, have not been picked up or been the subject of intensive research in an effort to help prevent this annual plague of blindness. Why? A search of the government bulletin (6) entitled, "Research Profile -- Summary of Progress in Eye Disorders, " discussed before, fails to reveal a single mention of ascorbic acid in its 16 pages. This indicates that no research on the use of ascorbic acid for the prevention of blindness is being conducted at the National Institutes of Health or the National Institute of Neurological Diseases and Blindness. The same situation probably exists in the research facilities of the many publicly supported charitable foundations for the blind.
Most of the investigators using ascorbic acid in the treatment of eye pathology employed it orally or by injection. It is also possible to use it as a solution of sodium ascorbate applied topically. This is especially effective when the topical application is done iontophoretically. This method uses a harmless mild electric current to force the ascorbate into the eye tissues. As pointed out by Erlanger (12), in 1954, after many years of research, iontophoresis is another neglected principle of therapy which should find much wider use in the treatment of eye diseases. Topical megascoric therapy and iontophoresis should be a most valuable combination.
Retinal Detachment
Another area for eye research is in retinal detachments. A 1964 paper by Weber and Wilson (12) showed that the ascorbic acid levels in the subretinal fluid decreased with the length of time of the retinal detachments. Possibly, individuals on high levels of ascorbic acid would have less chance of suffering retinal detachment. The research on this condition could be combined with the above suggested tests on glaucoma and cataracts to determine whether the prophylactic daily dosage of 3 to 5 grams of ascorbic acid would also reduce the incidence of retinal detachments.
Re: Colchicine
26 days agoBorax Dosage For Children
26 days agoSomeone PLEASE help ASAP!
Does anyone know dosages for a kids? Ages 2,4,7,8 and 14? Thanks so much. More specifically for my 4 year old, she has candida overgrowth in the intestines since she was 5 months old and has blotchy skin JUST LIKE ME. I have had this since I was 8ish and am now 34! I need this detox! Also, can this be taken the same day as DE? TIA😊
Re: Food Grade Hydrogen Peroxide for Cancer
26 days agoRed Light Therapy For Torn Rotator Cuff
26 days agoAround the start of 2025, I was doing deep dips on some bars in the park. I ended up tearing both my rotator cuffs, especially my right one, which had previously been injured throwing the football too much at a Halloween party in 2008.
After this, I found out about Dr. Kirsch and his "dead hang" protocol from a pullup bar, which I started doing around April 2025. It's now September 2025 and my rotator cuffs are almost back to 100%, except the right one has limited mobility and some pain still. But the pain has reduced at least 90%, it was excruciating pain when I started doing the Dr. Kirsch dead hang protocol. Now I barely feel any pain at all.
I have a Red Light Therapy RLT panel and have been using it on my right shoulder (front and back) about 15 to 30 minutes every night, for only the past week (since the start of September) and already my mobility in the right arm is now extremely increased.
Before this week, I couldn't put my right arm behind my back and reach very high up the back (and it was somewhat painful to do so), it was only half the mobility of the left arm up the back. Now from just one week of the Red Light Therapy, it doesn't hurt and it can almost reach the same height up the back as the left arm now.
I FOUND THIS ABOUT RED LIGHT THERAPY AND SCAR TISSUE (SPECIFICALLY IN THE SHOULDER) BELOW
Red Light Therapy and Scar Tissue in Rotator Cuff Injuries
How Red Light Therapy Works
Red light therapy, also known as photobiomodulation, uses specific wavelengths of light to penetrate tissues. This process stimulates cellular activity, promoting healing and reducing inflammation. It is particularly effective for conditions like rotator cuff injuries, where scar tissue can limit mobility.
Benefits for Scar Tissue and Mobility
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Pain Reduction: Red light therapy can alleviate pain associated with scar tissue in the shoulder, making movement easier.
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Improved Circulation: The therapy enhances blood flow, which is crucial for healing damaged tissues and reducing stiffness.
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Tissue Regeneration: It supports the body's natural healing processes, helping to regenerate nerves and tissues affected by scar formation.
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Increased Range of Motion: Regular sessions can lead to improved flexibility and mobility in the shoulder joint, counteracting the restrictions caused by scar tissue.
Cod Liver Oil for Dry Eyes
26 days agoRe: Utis Caused By Super Bugs
26 days agoHi Wendy,
I use pure D-Mannose powder for UTIs with no fillers the way capsules have and the 1.5 teaspoon per bottle is a lot stronger dose. I've never weighed the 1.5 teaspoon dose on my digital milligram scale, but it is a lot larger dose than the capsules.
I thought you might find the following of interest :
https://pmc.ncbi.nlm.nih.gov/articles/PMC8944421/
Here is a relevant quote from the link :
' Here, we present data from a post hoc analysis of this study to compare the cure rate of d-mannose monotherapy with that of antibiotics. The results show that d-mannose is a promising alternative to antibiotics in the treatment of acute uncomplicated UTIs in women. '
Please keep us updated on how you do!
Art
Re: Utis Caused By Super Bugs
26 days agoThanks Art. I found out recently from an UrgentCare doc (@60yo female, and pleasantly conversant, soon-to-retire) that D-Mannose works only for e-coli, not the superbugs (I don't understand how this could be, actually). In any case, I've been taking three 150mg capsules every morning for years, but I'll try your recommendations & recipe. Thanks again!
Re: Utis Caused By Super Bugs
27 days agoHi Wendy,
Since D-Mannose also binds to Citrobacter freundii, of course I would have started there and added others, only if needed. Since you are still having symptoms, I would then add the D-Mannose drink three times per day until after all symptoms have stopped. Since the UTI is currently active I would add a little sea salt, I use pink, to the D-Mannose drink.
Here is how to make the D-Mannose drink :
https://www.earthclinic.com/cures/bladder_infection11.html#dmannose
Art
Terrasil for Impetigo
27 days agoHi! I had impetigo as a child, then again as an adult when I started working at a school. It was horrible! Its very painful and embarrassing. And I was searching online one day and came across Terrasil, I figured it couldn't hurt so I ordered it. It is made of volcanic ash, beeswax and other natural ingredients. It is 22 times stronger than antibiotics. Now this impetigo covered the whole bottom half of my face! It was taking over! I got the Max strength. I did what the directions say, I applied it liberally and covered it with gauze and taped it on. I had to cut a mouth slit for my straw to drink. It had me healed in 2 days! I was still red and kept applying it every night with the gauze, there's something about the gauze holding it against the skin and keeping it moist that healed my skin. I don't represent this product, but we use it on every skin thing now! It took me almost a year to never have a cold sore try to turn into impetigo again. I apply it in my nose too, because I think blowing your nose blows the germs onto your cold store and would tingle like it wanted to turn into impetigo. I've Never had it come back and rarely ever get a sun blister again! And I shared this with teachers and students and their parents and they all got their skin conditions healed.
Re: Utis Caused By Super Bugs
27 days agoQuestion for Art, and anyone else who's experienced UTIs caused by superbugs:
Background:
I recently was diagnosed, via urine culture, with Citrobacter freundii. I believe it's a superbug. This is the FOURTH (4th) different superbug I've contracted since 2018 which is when I discovered Oil of Oregano. Oregano oil was the only thing, IMHO, that got rid of my FIRST superbug, Klebsiella pneumoniae. Since then, I've also contracted Klebsiella oxytoca, Morganella morganii, and now the Citrobacter freundii (currently on a 10-day script for Cefdinir, 300mg). According to my Urologist, this antibiotic CAN kill the Citrobacter freundii.
The problem is, I'm still experiencing UTI symptoms while on the antibiotic! I've messaged my Urologist, but anything he's advised I've heard before, and follow.
NOTE: I've also been on the GLP injection, Zepbound, since October 2024. Successful weight loss, BUT, I've read recently that these GLPs actually cause UTI symptoms in people who've had UTIs in the past, and in those who've never had one! Despite wanting to lose more weight, I'm considering stopping the GLP in the hopes that these recurring UTIs will stop.
I'm generally a very health-conscious 70-year-old, kidney transplant recipient from a live doner in 2016 (CKD Stage 2; perfect bloodwork since 2016), eat healthfully and exercise moderately (although whenever I have a UTI, I feel like crap and the exercise is limited to forcing myself to walk, just to do something! ). I also check with ALL my doctors whenever I want to try a new med or supplement.
Questions: While I have this particular UTI, I've decided to take the Oregano Oil capsules 2x/day, 2-3 hours after I take my antibiotic. Would you recommend anything else? Also, what's your opinion about GLPs possibly (likely?) causing UTI symptoms. Actually, a couple of doctors have recently agreed with me that this side effect is indeed possible, but it's just that the GLPs are so new, and the side effects are still being documented (as far as I know).
Re: Mung Bean Soaked Fermented Water for Diabetes Type II
27 days agoI have taken 10 bags of moong beans. I soaked in water over night . I drank in the morning first thing for several months maybe 5 or 6, however, I can't really see a change in the way I feel. I found another article and it said the moong beans have to be heated and then left over night wish I had of known before all of the beans...loling Please help me to know for sure the correct way to take ...Fran
Re: Xylitol or Erythritol for the Prevention of Cavities
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27 days agoApple Cider Vinegar Recipe
27 days agoMung Bean Soaked Fermented Water for Diabetes Type II
27 days agoRe: Nebulizing Iodine
27 days agoRe: Testing for Excitotoxicity
27 days agoHow do you test for excitotoxicity? What I have found is regularly taking your blood pressure multiple times a day can reveal a lot and give you some idea how and what your food is doing to your blood pressure. For instance you need to find out what your normal blood pressure. Resting 15 min and compare before you eat in the morning and about 3hours after you eat and see if there is dramatic changes in blood pressure .This will clue you in as to how what you ate effected your blood pressure. My wife who suffers from AFIB and dramatic swings in blood pressure depending on what she eats this is how you can test for excitotoxicity. You need to have a daily food journal and write down everything you take orally such as medication as well as food so you can compare episodes of toxicity and what foods caused it and what foods contributed to it There are multiple causes depending on each person . IT could be glutamate, Histamine, tyramine, msg or any number of its derivatives, or just free glutamate in food or foods that are high in aspartic acid. As well as medications that contribute to your problems. For instance a case of AFIB in my wife is usually preceded by first a dramatic up swing in blood pressure, it could be 70 points higher systolic in 3hours of eating a few slices of peaches, and than it tops and starts dropping. If you take a blood pressure pill when it is high it can cause your blood pressure to swing far to low and that swing low is usually when she goes into A Fib. I hope this answers the above question and gives you an Idea how to get on top of your problems as if you want to figure it out this will help.
