FAQs

Please click on a frequently asked question to view our response:

• What is UTI?
• Who gets UTI?
• What are the symptoms of UTI?
• Conventional Antibitoic Treatment
• What happens when we take D-mannose to treat a UTI?
• How taking D-mannose can treat or prevent UTI?
• Is D-mannose safe for people with Diabetes?

A UTI is a bacterial infection (caused by the bacteria E. coli over 90% of the time) that effects the inside lining tissue of the urinary system (or tract). This system includes two kidneys , which form urine from liquid waste in the blood: two narrow ureters , tubes that carry urine from the kidneys to the muscular bladder , which stores it; and a single urethra , the final common path from the bladder to the outside world.

The urinary tract reacts to a bacterial infection in much the same way that the upper respiratory system reacts to a cold virus. The tissues become inflamed, irritated and swollen. Just as it's hard to breathe through swollen and inflamed nasal passages, swollen and inflamed urinary ducts can partially obstruct normal flow, making it painful and difficult to pass urine.

Ordinarily, the urinary system is hostile territory for bacteria, viruses or any other microorganisms. Bugs that do make their way into a healthy urinary tract are likely to find an inhospitable acidic environment (pH <5.5). They are also subject to attack by the body's immune defenses. (Adult men have the added protection of a specific bacterial growth inhibitor squirted directly into the urinary system by their prostate gland.) Even if micro organisms manage to overcome these considerable obstacles, they would typically be flushed out with the normal flow of urine. So effective are these natural antibacterial defenses that in a study in which bacteria were instilled into the bladders of guinea pigs, simple urination expelled 99.9% of the bugs. 5

Despite all these built-in safeguards, each year millions of people, overwhelmingly women, still develop UTIs. Most UTIs begin when bacteria originating in the bowels travel to and grow in the urethra. Infections limited to the urethra are known as "urethritis." When bacteria travel upstream to the bladder, the infection is called " cystitis ." Infections that reach the kidneys are known as "nephritis" or "pyelonephritis."

The E. coli that cause most UTIs are among the most common "friendly" bacteria in the GI tract, where they aid digestion, produce a few vitamins, and in general, behave themselves without bothering us. If, however, when E. coli and other bugs exit the lower GI tract, they manage to gain entry to the urinary tract via the urethra, then they attach to the internal lining of the bladder, multiply and spread.

Although up to 90% of UTIs are caused by E. coli , the remaining 10% are caused by bacteria known as Chlamydia , Mycoplasma , Neisseria gonorrhoeae , and others. Unlike E. coli , these bugs tend to be transmitted via sexual contact and rarely cause the more serious bladder and kidney infections. Chlamydia, Mycoplasma and N. gonorrhoeae infections do not respond to D-mannose treatment and will probably require antibiotic treatment. In addition, a few UTIs are caused by other bacteria, such as Proteus or Staphylococcus (" Staph "). Still, all of these non- E. coli infections combined amount to no more than 10% of all UTIs.

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Anatomy is UTI destiny. Women are far more likely to develop UTI than men. The reason lies in a difference in anatomy between the two sexes. Normal female anatomy, in which the urethral opening, vagina, and anus are all in close proximity, in tailor-made for UTI, because it makes it relatively easy for bacteria from the bowel to gain a "foothold" in the vagina or the urethra or both. Even small differences in the location of these openings can make a big difference. In one study of women who tended to get UTIs over and over again, the urethral opening was just 0.2 cm closer to the anus than women who never got UTI. 6 In males, of course, the urethra exits the body via the penis, making it too far a distance for most E. coli to travel.

The female urethra is also far shorter than the male's. This means that the distance bacteria have to travel to reach the female bladder is much shorter, increasing the chances that a urethral infection will quickly become a bladder infection, or cystitis.

Poor hygiene . Failure to remove bacteria from the region surrounding the urethra is an important cause of UTI. Because the urethra is in front of the anus, mothers teach their small daughters to "always wipe from front to back" to avoid introducing bacteria from the anus into the urethra. In uncircumcised males, the foreskin, if not cleansed properly, can serve as an excellent breeding ground for bacteria, which could then easily gain access to the urethra.

Blocking the flow of urine. Normally, the flow of urine from kidneys to bladder to the urethra washes out most bacteria. However, anything that inhibits the flow of urine can increase the risk of UTI. Thus, people with certain anatomic anomalies, as well as blood clots, stones, tumours or strictures (narrowings) are more likely to have recurrent UTIs. In men, enlargement of the prostate gland can impede the flow of urine. Bladder weakness due to diabetes, stroke, or other neurologic disorder can sometimes lead to the "pooling" of urine in the bladder after urination. In time, this stagnant, residual urine can serve as a growth medium for bacteria. UTI is also quite common in people who are severely debilitated and require a urinary catheter (a tube inserted into the urethra to drain the bladder), which can easily become contaminated. Although blockages can promote infection in both sexes, they are the primary cause of UTI in males.

Taking the joy out of sex. For many women, the best way to get UTI is to have sexual intercourse. " Honeymoon cystitis " results when bacteria move from the vagina and the perianal area to the urethra during intercourse. (In a similar manner, it is possible to "inoculate" the urethra during masturbation and same-sex sexual activity).

Some contraceptive methods also increase the chances of UTI. Research has shown that women who use a diaphragm with a spermicidal jelly or foam, or just the spermicide itself, are much more likely to develop a UTI the next day. The same thing is true for condoms with spermicide. 7

Not only do spermicides promote the growth of E. coli , they also allow yeasts and other bacteria to thrive in the vagina. 8 It seems that nonoxynol-9, the most commonly used spermicide, kills a lot more than just sperm. It also kills the friendly bacteria, known as Lactobacilli that inhibit the vagina. One of Lactobacilli's main functions is to produce lactic acid, which lowers the pH of the vagina. The relatively acidic normal environment helps keep the population of yeasts and unfriendly bacteria, like E. coli , under control. With Lactobacilli out of the way, the pH rises (less acid), allowing pathogenic organisms to grow unchecked. Nonoxynol-9 may also promote infection by making it easier for E. coli to stick to the epithelial cells that line the vagina, urethra, and bladder. 9

Antibiotics! Yes, it's true that antibiotics are widely used to treat UTI, but it's also true that antibiotics given for UTI or any other infection can actually increase the risk of UTI. How can that be? Like spermicide, many antibiotics kill vaginal Lactobacilli . Once the antibiotic treatment ceases, the absence of Lactobacilli leaves the vagina vulnerable to E. coli (and yeast) infection. 10 Once in the vagina, E. coli can more easily reach the urethra and bladder and begin the infection cycle all over again.

Getting older. The incidence of UTI increases after women reach menopause. The lack of youthful levels of oestrogen leads to a loss of Lactobacilli with a subsequent rise in vaginal pH leading to E. coli (and yeast) colonisation. 11 In very old (and very young) people, urinary and faecal incontinence can also pave the way to UTI.

In the genes. Some people have a genetic predisposition to UTI. In other words, if your mother had recurrent UTI, you have a good chance of having it too. The reasons are not entirely clear, but one possibility is that some UTI-prone women have a protein that makes it easier for E. coli to "stick" to their urinary tract tissue. Other women seem to lack certain antigens that normally inhibit bacterial adhesion ("stickiness"). Still other women have elements in their urine, such as low pH, that actively discourage bacterial growth, making them more resistant to infections. In some fortunate instances, urine may be naturally fatal to many bacteria. 12

Immune impairment. Any condition that impairs normal immune function can make the urinary tract a more hospitable place for bacteria. Thus, people with diseases, such as diabetes or AIDS or people taking immunosuppressive drugs (e.g., corticosteroids), should be extra careful.

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Some people with UTI have no symptoms and are completely unaware of their infection. However, it is far more common to have at least some symptoms. The most common symptoms of UTI include:

• A frequent urge to urinate
• Trickling of urine, despite a strong urge to urinate
• A painful, burning feeling in the area of the bladder or urethra during urination or even when not urinating
• An uncomfortable pressure above the pubic bone (in women) or a fullness in the rectum (in men)
• Cloudy, milky or reddish urine

When these symptoms are combined with a fever, one or both kidneys may be infected. Other symptoms of kidney infections are nausea, vomiting and back or side pain below the ribs.

In children, the symptoms of UTI are not always obvious. This is especially true in very young children, who may not be able to describe how they feel. Parents should be on the lookout for UTI if their kids are irritable, have no appetite, have no low-grade fever with nausea and vomiting, and/or if their urine smells "funny". If children are sick for more than a day with a high temperature but have no "cold" symptoms, they may have UTI.

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Conventional medical treatment of UTI involves the use of antibiotic drugs, which typically cure most infections within one or two days. Even though the infection may appear to be gone in a couple of days, doctors often recommend taking antibiotics for 10 to 14 days just to make sure no relatively resistant bacteria survive. Longer treatment is especially indicated in cases where symptoms have lasted more than a week, when the infection is recurrent, or when the individual has diabetes (or other diseases in which the immune system may be impaired). When women are subject to recurrent UTI, many doctors prescribe daily low dose antibiotics for as long as two or three years ! One problem with such long-term treatment is that it is guaranteed to seriously disrupt the body's normal ecological balance by eradicating friendly bacteria, including E. coli in the GI tract and Lactobacilli in the vagina. The antibiotic drugs most often prescribed for UTI include:

• Trimethoprim (Trimpex)
• Trimethoprim/sulfamethoxazole (Bactrim, Septra, Cotrim)
• Amoxicillin (Amoxil, Trimox, Wymox)
• Nitrofurantoin (Macrodantin, Furadantin; technically termed "urinary tract antispetics")
• Fluoroquinolones (Floxin, Noroxin, Cipro, Trovan)
• Ampicillin (Many brands)
• Treating UTI Naturally with D-Mannose

When faced with a potentially pathogenic germ like E. coli , conventional, pharmaceutically based medicine typically confronts the problem by throwing the most potent poisons it can find at the bugs. While there's nothing essentially wrong with killing disease-causing bacteria, this approach does have some very serious drawbacks, as we have noted earlier. Happily, "bacteria-cide" is not the only possibly avenue of attack. Another, more natural way to eliminate E. coli infections from the urinary tract is to beat them at their own game. If they're going to cause trouble, bacteria usually have to find a way to adhere (stick) to the body tissue they're infecting. In UTI, E. coli attach to cells lining the bladder and urinary tract using filmy hair-like projections called fimbria on their cell walls. 13 At the tip of each fimbrium is a glycoprotein (a combination carbohydrate and protein) called a lectin that is programmed to bind to the first molecule of the sugar mannose that it encounters. 14

It turns out that molecules of mannose (produced inside urinary tract lining cells) naturally dot the surfaces of these cells. Here they act as "receptors", inviting the fimbria of E. coli to attach, and allowing them to bind to the tissue in a right, Velcro-like grip. 14 If not for this attachment to the cells's mannose, any E. coli that had successfully ventured up the urethral river would be unable to stick to the slippery surface and would be washed right back out on the next tide of urination.

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Now imagine what would happen to E. coli in the urinary tract if those sweet little mannose molecules they crave were present not just on the surface of the epithelial cells but surrounding them in the urine as well. The E. coli couldn't turn around without bumping into D-mannose "just floating around" in the urine. Unable to resist the tasty bait they suddenly find themselves swimming in, they would latch on to the nearest mannose molecules, and happily sail off into the porcelain sunset. Those few E. coli left clinging to mannose molecules on cells then become easy prey for white blood cells and other agents of the immune system. 15-17

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In addition to its natural occurrence in the cells lining the epithelial tract, the sugar D-mannose is also found in relatively large quantities in fruit such as peaches, apples, oranges and certain berries, like cranberries and blueberries. Extracted in the form of D-mannose ,* a white crystal sugar similar to glucose, it can be easily dissolved in a liquid and swallowed. (Mannose can also be synthesized from other simple sugars.)

When someone with UTI consumes a dose of D-mannose , the sugar is absorbed in the upper GI tract, but at a much slower rate than most other sugars. (For example, glucose is absorbed more than eight times faster.) Moreover, unlike other sugars, D-mannose is not readily converted to glycogen (and stored) in the liver, but instead passes directly into the bloodstream largely unchanged. 18,19

As the D-mannose-laden blood passes through the kidneys, a considerable proportion of the sugar is extracted and added to the urine. The D-mannose-sweetened urine flows from the kidneys through the ureters to the bladder and on to the urethra, literally sugar-coating any free-floating E. coli it might encounter, so they can's stick to cells any more. It also unsticks most of the E. coli already "Velcro-ed" to the inner surface of the bladder and urinary tract, ultimately flushing them all down the drain.

(* Not all varieties of E. coli find the mannose molecule such a treat. Those that do are said to be "mannose-specific," and they are the ones that can potentially cause UTI. 14 + Many molecules have D- (dextro-) and an L- (levo-) (literally, right and left) forms. It is not uncommon for the D- and L- forms of a molecule to have very different activity profiles. In the case of mannose, only the D- form is useful for dislodging E. coli .)

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People with diabetes usually need to limit their intake of sugar. How does this affect their use of D-mannose? Fortunately, very little. There are anecdotal reports that some people with diabetes experience a transient increase in blood sugar levels, but the effect is not great and never permanent, lasting only for the length of time mannose is used.

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