Does fluoride cause kidney stones? How Supplemental Iodine Supports Healthy Urinary Tract Function...

Iodine Deficiency and Bromine/Fluorine Toxicity in the Kidneys and Beyond...

Iodine deficiency significantly increases the risk of cystitis and urinary tract infections, especially in people who also are bromine/fluorine toxic. Indeed, a surprisingly high number of iodine receptors are present in the kidneys, which demonstrates the importance of iodine in maintaining kidney health. 

The presence of iodine receptors in the kidney also suggests that toxic halides like bromide and fluoride that masquerade as iodine in the body, would be particularly toxic to the kidneys. These toxic halides would be able to bind to iodine receptors in the kidney and essentially hijack these receptor sites, causing an array of possible kidney and urinary tract problems.

If you aren’t yet familiar with the interplay of iodine deficiency with bromide and fluoride toxicity, be sure to click here to read this introductory article about how iodine deficiency makes the body more vulnerable to bromide and fluoride toxicity and how to treat this problem with iodine therapy.

A Brief Introduction to the Urinary Tract 

The urinary tract system includes the kidneys, the ureters (the tubes that connect the kidneys to the bladder), the urinary bladder, and the urethra. The urinary system is ultimately responsible for waste filtration and removal (as blood passes through the kidneys to be filtered), blood pressure regulation, maintenance of electrolyte levels in the blood, pH homeostasis regulation, red blood cell production (in the kidneys), and the synthesis of calcitriol. Calcitrol is the active form of vitamin D; the kidneys work with the skin and liver to produce and activate vitamin D naturally in the body. 

Notably, many of the functions of the kidneys and the rest of the urinary system are regulated by hormones, such as aldosterone, antidiuretic hormone, and parathyroid hormone. Since iodine plays a significant role in general endocrine health, some people may experience the effects of iodine deficiency via endocrine imbalances that ultimately affect the urinary system (as well as other related areas of the body). In other words, iodine impacts the kidneys both directly and indirectly via iodine receptor sites in the kidneys as well as via the endocrine hormones that circulate in the blood supply. 

Many people experience extreme bladder irritation / cystitis, chronic urinary tract infections, kidney infection, or kidney disease as a result of iodine deficiency, or rather, bromide toxicity. If the iodine deficient patient is also being exposed to bromide and fluoride (which is likely), that patient will then become “bromide toxic” or “fluoride toxic”. To the human body, bromide and fluoride both look almost identical to iodine. When the body becomes deficient in iodine, the body becomes desperate for this mineral and welcomes bromide and fluoride into receptor sites throughout the body. But as the patient then begins to take iodine daily in high doses (over 3 mg per day up to 100 mg per day), bromide and fluoride are then purged from the body. These toxic halides, as they are removed from the tissues, must travel through the bloodstream to then be removed permanently from the body by the kidneys and urinary tract. As the bromide and fluoride travel through the urinary tract, they cause severe bladder irritation that can feel and seem like a urinary tract infection. 

Often, people who suffer from chronic cystitis experience bladder irritation when they eat a food item that’s higher in iodine. When the body takes in iodine, it kicks out bromide and fluoride. These toxic halides then travel through the blood supply to be removed from the kidney causing irritation to urinary tract tissues along the way. Some people may begin to believe that the food itself is causing cystitis symptoms. For example, if a person always experiences cystitis after eating seaweed (a high-iodine food), they might believe the seaweed is causing cystitis when in fact, the seaweed is healing the root cause of the cystitis by causing bromide and fluoride to be removed from the body. So, the problem of iodine deficiency and bromide or fluoride toxicity can be confusing especially as it pertains to the effects of iodine on the urinary tract.

The Relationship Between the Thyroid and the Urinary Tract System: How Thyroid Health Affects Urinary Tract Health

The relationship between the urinary tract and the thyroid gland has been observed largely through the known correlation between hypothyroidism and chronic kidney disease (CKD). Patients with CKD are significantly more likely than the average person to develop hypothyroidism, which has been acknowledged to be the most common endocrine disorder that affects CKD patients. As another indication of the connection between the thyroid and the urinary tract, children with congenital hypothyroidism often also will have renal (kidney) and urinary abnormalities. Note that hyperthyroidism is generally not as common in kidney disease patients as hypothyroidism.    The connection between thyroid disease and kidney disease has also been well documented in cats and dogs. Older cats are at high risk of developing both hyperthyroidism and chronic kidney disease, and research shows that these two conditions are extremely likely to exist simultaneously in geriatric feline populations. In dogs, hypothyroidism has been associated with decreased glomerular filtration rates.    To understand this kidney-thyroid connection, let’s start at the beginning with thyroid hormones. There are 2 kinds of thyroid hormones: thyroxine (T4) and triiodothyronine (T3). T4 is the “inactive” form of thyroid hormone, and it is produced exclusively by the thyroid gland. In contrast, T3, the “active” form of thyroid hormone, is produced by deiodination of T4 in areas of the body like the kidneys, liver, brain, and skeletal muscle. The basic recipe for T3 is one Tyrosine amino acid plus 3 iodine atoms. The basic recipe for T4 is one Tyrosine amino acid and 4 iodine atoms. So the “T” in T3 stands for “Tyrosine” and the number that follows tells you how many iodine atoms are found in that particular form of thyroid hormone. In any case, if the inactive thyroid hormone (T4) is circulating in the body and the kidneys, liver, brain, or skeletal muscles are not able to remove the extra iodine to create the active T3 form, a person will have symptoms of hypothyroidism. In other words, in a situation like this, the thyroid gland may be functioning just fine, but the kidneys are not able to remove the extra iodine atom to activate thyroid hormone.   In hypothyroidism, a person will have lower-than-normal levels of T3 and/or T4. Patients with CKD have also been shown to have abnormalities with thyroid hormone levels, with many patients exhibiting low levels of circulating T3 levels. Some research speculates that hypothyroidism may develop in cases of nephrotic syndrome as a result of heavy protein losses, since most thyroid hormones in the body are protein-bound and thus, if the body doesn’t have enough protein available, thyroid hormones wouldn’t be able to do their job in the same way and hypothyroid symptoms would develop. Also, Tyrosine (also known as “L-Tyrosine”) is an amino acid that’s derived from protein. Without Tyrosine, thyroid hormone cannot be produced properly. So patients with kidney disease or thyroid hormone need to make sure that they are getting all of their essential amino acids along with plenty of iodine.   

Click here to subscribe to the Living Database!

Hypothyroidism: Effect on the Kidneys

Hypothyroidism, or below average thyroid hormone levels, can affect the kidneys by: 

• Decreasing kidney-to-body-weight ratio
• Changing glomerular basement membrane (GBM) architecture (GBM thickening, increased glomerular capillary permeability, decreased GBM volume, mesangial matrix expansion, etc.)
• Causing glomerular hyperfiltration (resulting in thyroid-related obesity)
  • Glomerular hyperfiltration occurs when the glomeruli in the kidneys (these are the main “filters”) produce excess amounts of pro-urine. Other than chronic kidney disease, diabetes mellitus, polycystic kidney disease, sickle cell anemia, obesity, high altitude renal syndrome, and secondary focal segmental glomerulosclerosis caused by a reduction in renal mass (note that decreased kidney weight is another symptoms of hypothyroidism) have all been associated with glomerular hyperfiltration.
• Decreasing cardiac output
  • Decreased cardiac output leads to decreased renal perfusion, which ultimately causes a decrease in urine output. Decreased urine output can lead to all kinds of problems, but one of the most relevant potential issues related to this discussion includes the increased potential for accumulation of bromine and fluorine in the kidneys and the rest of the urinary system (as well as the rest of the body).
• Increasing tubuloglomerular feedback
  • Tubuloglomerular feedback is the process through which the renal tubules communicate with the glomerulus in order to regulate glomerular filtration rate.
• Altering the RAAS (renin-angiotensin-aldosterone system)
  • This can impair autoregulation in the kidneys of blood flow/perfusion 
  • Altered function of the RAAS can also reduce the synthesis of renal vasodilators (nitric oxide, adrenomedullin, etc.), which is a contributing factor in the inhibition of blood flow in the kidneys
  • Specifically, hypothyroidism can cause reduced production of renin, angiotensin, and aldosterone, all hormones ultimately involved in sodium-potassium balance and the release of antidiuretic hormone. 
  • Click here for a more detailed description of the RAAS
• Reducing renal plasma flow (RPF) and single nephron glomerular filtration rate (GFR)
  • These are measures of how efficiently (or inefficiently) the kidneys are filtering the plasma and blood. Generally speaking, reduced RPF and GFR is a negative thing, especially in cases where there are toxins present in the body. 
• Causing development of truncated tubular mass
• Increasing renal vasoconstriction and peripheral vascular resistance

Hyperthyroidism: Effect on the Kidneys

Hyperthyroidism is generally less closely associated with kidney disease / renal dysfunction, but nevertheless can still negatively affect the kidneys. Patients with hyperthyroidism may experience kidney damage as a result of proteinuria, oxidative stress, or glomerulosclerosis (scarring of the glomeruli in the kidneys). 

Some of the ways that hyperthyroidism can affect the kidneys include: 

• Decreased systemic vascular resistance by up to 50%
  • This decreased vascular resistance ultimately causes the RAAS system to upregulate, thus increasing sodium absorption in the kidneys in the loop of Henle and the proximal tubule.
• Increased cardiac output by up to 60%
• Increased renal blood flow (RBF) 
• Increased glomerular filtration rate (GFR)
• Increased glomerular capillary hydrostatic pressure
• Hypertrophic and hyperplastic tubuli
• Increased RAAS activity
• Elevated blood urea nitrogen levels
• Elevated creatinine levels

Selenium Deficiency in Kidney Disease and Thyroid Dysfunction

Selenium deficiency is another problem seen in both patients with thyroid dysfunction as well as those with chronic kidney disease. Given the importance of selenium in converting thyroid hormones from the inactive T4 form to the active T3 form, this connection between selenium deficiency in thyroid dysfunction and selenium deficiency in kidney dysfunction seems especially important. Indeed, selenium is one of the most important supportive nutrients that must be taken alongside Lugol’s iodine to ensure that iodine is properly metabolized by the body. Click here to read about each of the supportive nutrients that the body needs to be able to properly process iodine and use Lugol’s iodine to cure kidney disease and urinary tract dysfunction naturally.

Click here to read more about selenium deficiency symptoms.

Inflammation in Kidney Disease and Thyroid Dysfunction

Inflammation in the body that causes the release of inflammatory cytokines like TNF-alpha and IL-1 has also been known to potentially inhibit the conversion of T4 to T3, thus leading to symptoms of hypothyroidism. This indicates that inflammation in the kidneys may, through the presence of inflammatory cytokines, have a negative effect on thyroid hormone conversion from the inactive to the active form leading to symptoms resembling hypothyroidism.

Thyroid Hormone Replacement Treatment for Kidney Disease

Also of special interest is that, in conventional medicine, thyroid hormone replacement therapy is sometimes used to preserve renal function in patients with CKD or subclinical hypothyroidism. Illness in cats and dogs also provides some additional insight into the connection between the kidneys and thyroid gland. In cats, lower-than-normal serum thyroid hormone levels are associated with the potential for more severe non-thyroidal illness (such as chronic kidney disease), while in dogs, the same situation is associated with increased mortality. 

The thyroid-kidney connection is important in understanding the argument that iodine therapy is vital for general urinary tract health. Above, we talked about the fact that the kidney tissues have iodine receptor sites. Iodine directly impacts the kidneys through these receptor sites and toxic halides like bromide and fluoride can also impact the kidneys by hijacking these iodine receptor sites. But iodine deficiency also causes endocrine system dysfunction which causes endocrine hormones to become imbalanced in the bloodstream. These endocrine hormones impact the kidneys. And above, we listed several other connections between the thyroid gland function and kidney function to further support the argument that both the thyroid gland and the kidneys benefit from iodine in part through the mutual support that the thyroid and kidneys give to each other.

The Iodine Loading Test…

A person’s iodine levels can be measured by administering what’s called an Iodine Loading Test. With this test, a person first starts by taking 50 mg of iodine. Then, they collect their urine over the course of 24 hours. This urine is then analyzed for iodine content. Normally, when a person is iodine sufficient (meaning that their body has adequate iodine levels), approximately 90% or more of the 50 mg of iodine will be excreted in the urine. However, if a person is iodine deficient, more of the iodine will be retained, and thus, less iodine will be in the urine. So, an iodine sufficient person will excrete 45 mg of iodine in their urine over a 24-hour period. In contrast, if a person is iodine deficient, they’ll excrete less iodine than this (for example, a 20% excretion rate would mean that the person excreted only 10 mg of iodine, and retained 40 mg). 

There are some home iodine loading tests available, but because 50 mg is a fairly high initial dose for patients with certain conditions (like thyroid disease, for instance), it may be wise to seek the supervision of a medical practitioner while doing this test, since higher doses of iodine from the start can cause a halide detoxification reaction. In any case, it’s by no means essential to test your iodine levels before taking iodine. This description of the Iodine Loading Test is mostly intended to illustrate the importance of the urinary tract system in filtering and/or retaining halides, including iodine, in the body. 

Fluoride Toxicity and the Urinary Tract

There exist plenty of reports of fluoride toxicity on the kidneys and urinary tract in both humans and animals. In fact, the kidneys are among the most sensitive organs in the body when it comes to fluoride toxicity.

One case study observed end-stage kidney failure and osteosclerosis in one individual who had drunk copious amounts of Vichy water, a mineralized water containing 8.5 mg/liter of fluoride. The same study cited other research whereby methoxyflurane, an inhaled pain medication, induced renal damage. Other human studies have indicated that fluoride toxicity in the urinary tract specifically has been linked to development of pyaemic abscesses in the kidneys, the appearance of pyelonephritis, and ureter dilation. In workers exposed to high levels of fluoride, some research has also observed impaired renal function. 

There are comparatively more animal studies in regard to the effects of fluoride on the kidneys and the rest of the urinary tract. For example, in one study, rats given water containing varying levels of fluoride were observed to develop renal injury in all cases (even in cases where lower levels of fluoride were present in the water). For reference, the 4 groups of rats in the study were given 190 ppm, 210 ppm, 452 ppm, 904 ppm, and 1356 ppm of fluoride in their drinking water. Other damages to the rats’ urinary systems included inflammation in the urinary tract, urinary tract fibrosis, dilation of convoluted tubules, tubular degeneration, cloudy swellings, and parenchymatous nephritis. Renal degeneration has also been seen in cattle receiving drinking water with high fluoride levels. 

Another study completed on rabbits, 10 mg/kg of body weight of sodium fluoride per day (a high dose) resulted in cloudy swellings in the convoluted tubules, hypertrophic changes to the glomeruli, and interstitial nephritis. Rabbits given 20 mg/kg of body weight per day also showed extensive vacuole formation, some cell necrosis, slight thickening of the glomerular basement membrane, and interstitial edema. Finally, the rabbits in this study who were given 50 mg/kg of body weight daily showed extensive cell necrosis, degeneration of convoluted tubules, widening of the tubular lumen, disintegration of nuclei, atrophy of the glomeruli, further thickening of the glomerular basement membrane, and vacuolization of the cytoplasm and glomerular cells. Interstitial edema, nephritis, and interstitial cell necrosis were the most pronounced in rabbits given this dose of fluoride. 

In pigs, sodium fluoride was also shown to produce kidney damage. Some of the various forms of renal damage observed in the pigs consuming sodium chloride included: 

• Necrosis of glomeruli and tubules
• Atrophy of the glomeruli and glomerular capsules
• Dilation of tubules
• Severe tubular leakage
• Damages to the architecture of the proximal tubular epithelia (such as cell swelling and lysis)
• Vacuoles of the mitochondria
• Nuclear membrane breakdown
• Nuclear condensation
• Cellular apoptosis
• Necrosis
• Nuclear condensation
• Elevated serum levels of urea nitrogen and creatinine
• Decreased serum levels of sodium and chloride (this indicates that the kidneys were less able to effectively eliminate toxic metabolite substances)

While most of these animal studies involved administration of (very) high doses of fluoride, far higher than the dose that most people would take during any 24-hour period, they effectively illustrate the acute toxicity of fluoride on the kidneys and the entire urinary system. And, although it’s unlikely that the average person would reach a daily dose of even 10 mg/kg of bodyweight of fluoride, it’s still important to note that fluoride builds up in the body. So therefore, chronic exposure to higher fluoride levels can and does ultimately lead to the development of kidney and urinary tract problems over time. 

In the United States, Australia, Canada, the UK, and some other industrialized countries, fluoride is added to the water supply (note that some areas of the world have water that’s naturally higher in fluoride; this still can cause health problems, but is somewhat of a different discussion than the active adding of fluoride to drinking water in the public water supply, and so I’m not going to discuss that here). Water fluoridation is a major issue in the United States specifically, where (according to data from 2010) somewhere between 66-74% of the population receives fluoridated water. Another shocking statistic is that from 1999 to 2004, about 40.7% of kids aged 12-15 years old in the US had dental fluorosis. In Australia, about 70% of the population receives fluoridated drinking water; in Ireland, 71% of the population (or more) received fluoridated water, in Chile, the number is 70.5%, and in Brazil, about 41% of people drink artificially fluoridated water. 

Chronic exposure to fluoride at levels as low as 1.5 ppm in drinking water have been associated with fluoride toxicity (including symptoms like infertility, renal impairment, diminished IQ, dental and skeletal fluorosis, and more). 

Besides the problem of fluoride being added to the drinking water (NOTE: a reverse osmosis water filter that specifically processes out halides can help remove fluoride from your drinking water, even if you live in an area with fluoridated water), many people are also exposed to fluoride in the form of toothpastes and other dental care products, pharmaceutical medications, pesticides and other airborne chemicals, and even foods that have been grown with fluoridated water or in soil with a high fluoride content. 

Click here to learn how to remove fluoride from the body naturally.

Click here to buy vitamin K2 / MK-7.

Fluoride and Urolithiasis / Kidney Stones

A strong connection exists between high fluoride exposure and the development of kidney stones. While there are potentially a variety of causes for the development of kidney stones, the research indicates that high fluoride intake may cause an increased risk for the development of urolithiasis (especially in relation to other factors, such as vitamin K2 deficiency, for example). 

One study done in India observed that, firstly, the overall occurrence of urolithiasis was 4.6 times higher in tribal populations where fluoride levels were “endemic” than in populations where fluoride was not endemic. In the endemic areas, fluoride levels in the drinking water ranged from 3.5 ppm to 4.9 ppm, and study subjects were also found to excrete higher levels of fluoride and oxalates in their urine than the subjects in the non-endemic areas. The actual urinary stones in the subjects from the endemic areas also had notably higher levels of fluoride, oxalate, and calcium than the individuals from the non-endemic areas. Ultimately, this particular study concluded that, indeed, fluoride may function as a causative agent in the development of urolithiasis / kidney stones through increased oxalate excretion and oxidative stress.

Other research supports the finding that kidney stones tend to contain higher levels of fluoride. One other study compared fluoride content between kidney stones and gallstones and observed that kidney stones had overall higher fluoride levels than the gallstones (which suggests that fluoride toxicity probably plays a greater role in kidney stone formation than in gallstone formation). This study observed that people in areas with drinking water containing 2.6 ppm of fluoride had kidney stones with 0.37% fluoride content, whereas people with kidney stones in areas with lower fluoride in the drinking water had renal calculi containing only about 0.25% fluoride content. 

Leukocytosis, False Lab Results, and Fluorine Toxicity

Fluoride has been observed to affect leukocyte function and leukocyte levels in some cases. Leukocytes are white blood cells (such as neutrophils, eosinophils, monocytes, etc.) that show up on a urinalysis strip in response to infection or inflammation. They are an essential part of the body’s immune system. Fluoride can affect all types of leukocytes, but it’s important to note here that fluoride has been known to activate mast cells and stimulate histamine release from this particular type of leukocyte. This is important information for anyone who is looking for a natural cure for Mast Cell Activation Syndrome (MCAS). The link between iodine deficiency and fluoride exposure in activating mast cells is worth contemplating. Indeed, many patients who have contacted us about finding a cure for MCAS believe that iodine supplementation is causing their symptoms to worsen because they don’t understand that iodine is removing fluoride from the body. We refer readers with Mast Cell Activation Syndrome to our natural fluoride detoxification page at this link.

Leukocytosis is a condition where leukocytes are found in plasma in above average quantities. When there’s an infection, this is a normal immune response. However, the presence of other conditions, including leukemia, some types of bone cancer, certain parasitic infections, epilepsy and other convulsive disorders, and pregnancy/labor, or the use of medications like lithium carbonate or epinephrine, can also cause an increase in leukocytes. Strenuous exercise and emotional stress have also occasionally been known to cause leukocytosis. High leukocyte levels in the urine can thus be attributed either to a urinary tract infection, OR to inflammation caused by other factors. Fluoride toxicity is another rarely noted potential cause of leukocytosis when an infection isn’t present. 

Why exactly is this important? 

There are 2 reasons… First of all, the fact that fluoride increases leukocyte levels indicates that it stimulates an abnormal immune response in the body (which can be misdiagnosed as something serious like an autoimmune disease). Second, fluoride causes inflammation (which can cause symptoms like cystitis or other types of swelling in the urinary tract and beyond). Third, an increase in leukocyte levels that’s caused by an increase in fluoride levels may cause false UTI test results, leading to misdiagnosis of “infections” and the potential for unnecessary medical interventions. 

Most home UTI test strips will only tell you whether or not you have leukocytes and/or nitrites in your urine. Some may also include other parameters, such as blood levels, glucose levels, protein levels, or pH of the urine, but most popular test strips only include information about leukocyte and nitrite levels. What we’ve been taught (or told by the instruction pamphlet in the UTI test strip package) is that the presence of either one of these in the urine is a clear, definitive indicator of a urinary tract infection. 

But, if something like fluoride or even a medicine like lithium can also cause leukocytosis, then there’s a huge potential for UTIs to be misdiagnosed regularly. Which means that all kinds of people will end up on antibiotics or other drugs that will then seem to “not work” to treat the infection (at least, according to the UTI test strip). In reality, bladder irritation / cystitis or the sensation that one has a UTI may actually be caused by fluoride or bromide being removed from the body. The “cure” for the bladder irritation in this case would be Iodine therapy along with salt loading or salt flushing.

Click here to read more about the Iodine therapy protocol.

Click here to read how to do salt flushing and salt loading.

Click here to read more about the use of Chlorine Dioxide Solution to cure cystitis or urinary tract infection naturally. Note that Chlorine / Chloride is another NON-toxic halide that, like iodine, is essential for human health. 

Bromine / Bromide Toxicity and the Urinary Tract

Some sources suggest that bromine / bromide accumulation in the kidneys and other tissues in the body is the result of a kind of “limit” on its excretion from the kidneys. Research indicates that bromine / bromide is only excreted from the kidneys up to a certain level, and that beyond that level, the bromine / bromide will be reabsorbed into the bloodstream rather than being excreted via the urine. Thus, when bromine / bromide is present in abnormally high levels in the body, it can accumulate relatively easily, especially when the body is chronically exposed to higher-than-normal levels of bromine / bromide. Some studies show that urinary excretion of bromine / bromide generally varies from 1 mg - 2.5 mg in a 24-hour period, and that its degree of excretion correlates with 1) the amount of bromine consumed, and 2) the amount of chlorine excreted in the urine. Higher bromine / bromide excretion levels are also always associated with higher blood bromine / bromide levels. 

 

One study done on rats observed that liquid bromine administered at 20 mg/kg/day increased the rats’ blood cell count, hemoglobin levels, and hematocrit/packed cell volume (these effects on the blood were reversible within 14 days after stopping bromine administration). This quantity of bromine also increased serum glucose levels and urinary volume with protein. Other research also has noted that potassium bromate (KBrO3), a common food additive in wheat flours and breads, is specifically carcinogenic to the kidneys and is directly linked to the development and promotion of renal cell tumors (it has also been noted to cause mesothelioma of the peritoneum and follicular cell tumors of the thyroid). As such, anyone who is looking for a cure for mesothelioma should work with Iodine therapy as a front-line treatment. Click here to read how to do Iodine therapy properly.

 

Renal failure has also been observed in patients given potassium bromide, a substance once commonly prescribed as an anticonvulsant and sedative until around 1975 in the US. Specifically, this bromide-containing drug was correlated with obstruction of the urinary tract due to fibrosis and fat necrosis (the death of fat cells), as well as with papillary necrosis. Sodium bromide given to rabbits has also been shown to cause similar types of damage to the kidneys and urinary tract. In one animal study on rats, sodium bromide was also shown to displace chloride by up to 50% in not only the kidneys, but also in the brain, liver, and plasma, in addition to increasing the overall weight of the kidneys in the group that received the highest “dose” of sodium bromide. Chloride, as we mentioned above, is an essential electrolyte that the body requires in fairly high quantities in order for our cells to work properly. Chloride and iodide are the NON-TOXIC halides while both bromide and fluoride are toxic halides that are toxic, in large part, because they are able to fit into many of the same receptor sites as chloride and iodide. 

 

Click here to learn more about over-the-counter and prescription drugs that contain bromide / bromine.

 

Methyl bromide, a pesticide otherwise known as bromomethane, has been known to cause severe damage to various organ systems, including the urinary system. Case reports exist of early renal failure and anuria in cases of methyl bromide poisoning or acute exposure to this chemical. While methyl bromide use isn’t all that common in the US anymore as a general pesticide, this chemical is still in use in other countries in the world, and still permitted for use in cases of quarantine of imported products (such as for fumigation of logs), pre shipment fumigations, and in cases where a “critical use exemption” applies (what exactly this means is pretty vague). 

Click here to read more about bromide / bromine toxicity.

Bromine Toxicity and Alport Syndrome

One study carried out on rats observed that rats with Alport syndrome had decreased bromine excretion rates than healthy rats. Supplementation with bromine in the rats with Alport syndrome resulted in a more rapid disease progression, suggesting that bromine accumulation in the kidneys may be at least partially responsible for the decline in kidney function associated with this syndrome. The study acknowledged that bromine accumulation may specifically be responsible in some cases for kidney fibrosis and general kidney dysfunction in patients with Alport syndrome.

The AlivenHealthy Iodine Bible - Everything you need to know to get started taking iodine and more!

The Bladder: Pissed Off and Ready for a Change - BUY HERE!

Resources: