Thanks, Bonnie

Correction on classic 4:1 ketogenic diet. It is 80% fat and 20% combined protein and carbs. It is often supplemented with MCT (i.e. coconut oil).

Here is another piece of information on ketogenic diets. The very best way to prevent the following side-effect is by drinking lots of water.

Pediatr Nephrol 2000 Nov;15(1-2):125-8

Risk factors for urolithiasis in children on the ketogenic diet.

Furth SL, Casey JC, Pyzik PL, Neu AM, Docimo SG, Vining EP, Freeman JM, Fivush BA.

Kidney stones have been associated with use of the ketogenic diet in children with refractory seizure disorders. We performed a case-control study examining risk factors for the development of stones on the ketogenic diet, and prospectively followed children initiating the ketogenic diet to evaluate the incidence of urolithiasis. Clinical characteristics of 18 children presenting with stones (8 uric acid stones, 6 mixed calcium/uric acid stones, 1 calcium oxalate/phosphate stone, 3 stones not evaluated) were compared with characteristics of non-stone-forming children initiating the ketogenic diet at Johns Hopkins since July 1996. Since July 1996, 112 children initiating the ketogenic diet have been followed for development of stones. Follow-up times on the diet range from 2 months to 2.5 years. Of 112 children, 6 have developed stones (3 uric acid, 3 mixed calcium/uric acid stones) (0.8 children developing stones/ 100 patient-months at risk). Comparisons of children presenting with stones on the ketogenic diet with characteristics of the entire cohort initiating the ketogenic diet suggest younger age at diet initiation and hypercalciuria are risk factors for the development of stones. Prospective evaluation of children initiating the ketogenic diet revealed that almost 40% of patients had elevated fasting urine calcium: creatinine ratios at baseline; this increased to 75% after 6 months on the diet. Median urine pH was 5.5 at diet initiation, and remained at 6.0 thereafter. In a subset of patients tested, urinary citrate excretion fell from a mean of 252 mg/24 h pre diet initiation to 52 mg/24 h while on the diet. Uric acid excretion remained normal. Patients maintained on the ketogenic diet often have evidence of hypercalciuria, acid urine, and low urinary citrate excretion. In conjunction with low fluid intake, these patients are at high risk for both uric acid and calcium stone formation.

What Is a Kidney Stone?

Kidney stones are non-life-threatening, however, they can be painful.

A kidney stone develops from crystals that separate from urine and build up on the inner surfaces of the kidney. Normally, urine contains chemicals that prevent or inhibit the crystals from forming. These inhibitors do not seem to work for everyone, however, and some people form stones. If the crystals remain tiny enough, they will travel through the urinary tract and pass out of the body in the urine without even being noticed.

Kidney stones may contain various combinations of chemicals. The most common type of stone contains calcium in combination with either oxalate or phosphate. These chemicals are part of a person's normal diet and make up important parts of the body, such as bones and muscles.

A less common type of stone is caused by infection in the urinary tract. This type of stone is called a struvite or infection stone. Much less common are the uric acid stone and the rare cystine stone.

Urolithiasis is the medical term used to describe stones occurring in the urinary tract. Other frequently used terms are urinary tract stone disease and nephrolithiasis. Doctors also use terms that describe the location of the stone in the urinary tract. For example, a ureteral stone (or ureterolithiasis) is a kidney stone found in the ureter. To keep things simple, the term "kidney stones" is used throughout this e-text document.

Gallstones and kidney stones are not related. They form in different areas of the body. If a person has a gallstone, he or she is not likely to develop kidney stones.

Absorptive hypercalciuria occurs when the body absorbs too much calcium and empties the extra calcium into the urine. This high level of calcium in the urine causes crystals of calcium oxalate or calcium phosphate to form in the kidneys or urinary tract.

Other causes of kidney stones are hyperuricosuria (a disorder of uric acid metabolism), gout, excess intake of vitamin D, and blockage of the urinary tact. Certain diuretics (water pills) or calcium-based antacids may increase the risk of forming kidney stones by increasing the amount of calcium in the urine.

Calcium oxalate stones may also form in people who have a chronic inflammation of the bowel or who have had an intestinal bypass operation, or ostomy surgery. As mentioned above, struvite stones can form in people who have had a urinary tract infection.

A patient may be asked to collect his or her urine for 24 hours after a stone has passed or been removed. The sample is used to measure urine volume and levels of acidity, calcium, sodium, uric acid, oxalate, citrate, and creatinine (a byproduct of protein metabolism). The doctor will use this information to determine the cause of the stone.

Calcium and Kidney Stone

Although patients with calcium stones have been encouraged to restrict calcium intake in the past, studies are now strongly indicating that dietary calcium is actually protective against many cases of calcium oxalate stones. Large studies of both men and women found that those with the highest intake of dietary calcium had a much lower risk for stones than those who had little calcium in their diets. Some experts believe that dietary calcium may help by binding the oxalate in foods, preventing it from being absorbed into the blood and excreted into the urine. In one study of women, however, those who took calcium supplements, had a 20% higher risk. Some experts speculate that this higher risk may occur because supplements are usually taken in the morning either without food or with breakfast, which is typically low in oxalates. Taking supplements with later meals may not incur the same risk. It should also be noted that many people with calcium stones have reduced bone density from resorption (the breakdown of bone that releases calcium into the blood stream). Limiting calcium intake in such people could actually promote further bone loss. Some calcium stone patients who have supersaturation of calcium in the urine and who are not at risk for bone loss may need to restrict calcium, but more studies are needed to define this group precisely.

UROLITHIASIS (Kidney Stones)

Canadians appear to have a very high incident of kidney stones and the occurence is particularly high in Newfoundland (11, 12). In U.S., South Carolina has the highest urolithiasis rate. South Carolina also has the highest U.S. rate for cardivascular deaths (10). Both Newfoundland and South Carolina regions have "very soft" drinking waters with little magnesium (11).

In Canada, calcium urolithiasis accounts for 70 to 80% of the total kidney-stone problems (12). In the U.S., about 67% of all kidney stones are composed of calcium oxalate or calcium hydroxyapatite (11).

Several researchers have used the magnesium/calcium ratio as an index of susceptibility of urine to form kidney-stones in patients (10,13,14). In general, patients with a urinary magnesium/calcium ratio of 0.7 is normal, whereas a value lower than 0.7 may be considered as stone-forming. The ratio is especially low in the Canadian "Kidney Stone Patients", indicating inadequate magnesium intake.

The oral magnesium supplementation has proven very effective in the prevention of kidney-stone formation (14).

The traditional ratio is 2 mg of calcium for every 1 mg of magnesium.