Milk Alkali Syndrome (explicit)

[j.]

what did Ray Peat say about your emergency?

It goes away on its own in most cases after stopping consumption of calcium carbonate and baking soda. Once it got better, I asked him about kidney disease in general and he advised thyroid and progesterone. I posted in the email depository.

 

[j.]

Bad Plastic Experience

So I haven't had any kidney symptoms for weeks, maybe months. I was able to drink all the milk and protein I wanted without a problem.

However, I've always had a problem with milk from plastic containers, for years. Lately, I've been able to drink a lot of the milk from the plastic container, but not the last few cups, I guess because the plastic accumulates at the bottom of the container. So last night I thought, I'll drink it anyway, even if I feel a strong aversion to it, because maybe that will make my body get used to it. I downed 2 (disgusting) cups.

Bad idea. Today I woke up and couldn't stand because I had lower back pain when I did. Since plastic is estrogenic and estrogens are bad for the kidney, I wondered if it was kidney related, but I don't know. So I had to spent a few hours in bed, took a few drops of progresterone, and the pain did gradually go away during the day. It feels a lot better now. I consumed a lot of farmer cheese today to avoid the milk from plastic containers, and overall I got better.

 

[dukez07]

Is that true about the plastic being at the bottom of the the container?

I've never noticed any plastic like taste. Not saying the plastic doesn't leach into the milk, it most probably does. But is it even that significant? Milk doesn't have a very long shelf life from the moment it comes from the cow. Not going to be like some fruit juices, where it might be steeped in these plastic containers for months or longer?
Maybe I'm wrong?

I find your thread worrying, too. I take calcium carbonate, drink litres of OJ, I eat lemons, I eat lots of salt and I've started taking sodium bicarbonate. Not good then?

 

[j.]

Is that true about the plastic being at the bottom of the the container?

All I can say is that I believe so because it tends to taste disgusting to me. But there are studies showing that water from plastic is estrogenic. So I don't think it's a big leap for me to believe that so is milk from plastic, maybe to a lesser extent.

I've never noticed any plastic like taste. Not saying the plastic doesn't leach into the milk, it most probably does. But is it even that significant?

I think if one is healthy, a bit of an estrogenic substance might be harmless. If you already have low progesterone and excess estrogen or something like that, then I believe it can provoke a reaction.

Not good then?

Good in the right quantities. Excess bicarbonate I think is bad.

 

[Blossom]

j. wrote: Good in the right quantities. Excess bicarbonate I think is bad.

I think j. summarizes a recurring theme often seen in a Peat inspired approach. Most of the protective measures can be taken to an extreme if we are not careful in monitoring ourselves for changes. I did it myself with thyroid a while back. I have to say that I think the amounts of the various supplements needed will vary with each individual according to their unique context and even vary within the same person as their situation changes. What is excess for one may be perfect or not even enough for someone else.

 

[Bejva]

I had this happen to me twice. First time because of egg shells and now because of to much Vit D. I found exercise to help alot. Also ive noticed that the recovery from exercise is just ridiculous, its insane how fast you recover and how hard you can exercise before lactate is produced. I had to do 20 pull-ups before even feeling lactate.

 

[Giraffe]

I found a review of pubmed articles dealing with milk-alkali-syndrome. Here is a recap:

Daily calcium intakes of up to 2,000 mg are generally safe, unless someone has a history of bulimia or anorexia. How much is "excessive" calcium intake is unclear, but it seems to be at least 4-5 g calcium carbonate daily.

Pre-exististing kidney disease is a risk factor as are medications that interfere with calcium excretion, dehydration and hypochloremia.

----------

From the article:

DIAGNOSIS AND CLINICAL COURSE

The first symptoms may occur within a few days. Nausea, vomiting, anorexia, distaste for milk, headache, dizziness, vertigo, apathy, and confusion are early signs of toxemia.32 Muscle aches, psychosis, tremor, polyuria, polydipsia, pruritus, and abnormal calcifications are typical of the chronic phase.7,11 Ocular calcification is a classic physical sign that consists of keratopathy and calcium deposits in the conjunctiva. Keratopathy can be mistaken for arcus senilis.9

Withdrawal of the offending agents generally leads to quick resolution of the symptoms, except for renal failure, which invariably improves but does not always resolve completely.7 Keratopathy and conjunctival calcium deposits can be reversible.9,75

PATHOGENESIS

Despite extensive clinical experience, scant data are available on the pathogenesis of MAS. Throughout the years, several contributing factors have been proposed, including loss of gastric juice, preexisting renal disease, insufficient chloride intake, hemorrhage, anemia, impaired liver function, and warm weather.16,26-31 Ingestion of excessive quantities of calcium and absorbable alkali is a prerequisite for establishing the diagnosis. What constitutes “excessive” is unclear but generally indicates at least 4 to 5 g of calcium carbonate daily.32,33 However, ingesting large amounts of alkali and calcium alone does not result in alkalosis and hypercalcemia, respectively. McGee et al34 administered 1.3 to 2.0 g of a mixture of calcium carbonate and magnesium oxide hourly from 7 am to 9 pm for 8 days to 17 individuals with healthy kidneys. No significant changes in serum bicarbonate levels were observed. The authors speculated that hypochloremia and dehydration were key factors in the development of alkalosis.35 In the first reports of toxicity due to the Sippy program, Hardt and Rivers5 noted a definite correlation between the incidence of alkalosis and the presence of kidney disease. Subsequent reports confirmed that preexisting renal disease seemed to be a predisposing factor.20,26,27,36 However, it is widely recognized that MAS can develop without renal impairment.37 Furthermore, even in patients with impaired renal function, large amounts of absorbable alkali do not lead to alkalosis in most individuals.14,38,39 Some authors found no preexisting kidney disease in most of their patients with MAS.1,15 Underlying renal disease does not seem to be a prerequisite but rather a contributing factor in the pathogenesis of MAS.

For hypercalcemia to develop, calcium intake must be excessive, but inability to excrete the excess calcium is also an essential part of the process. Because the skeletal system does not have unlimited calcium buffer capacity, tight regulation of calcium absorption from the small intestine and excretion by the kidneys are paramount to maintain serum calcium levels. Individual variations in the buffering capacity of bone may also have a role in the susceptibility to development of hypercalcemia.40

Although controversial (as previously discussed), preexistent renal insufficiency has been implicated in the pathogenesis of MAS. Medications that interfere with calcium excretion have also been considered risk factors. Thiazides decrease calcium excretion by inhibiting the thiazide-sensitive sodium chloride cotransporter and promote intravascular depletion and alkalemia.48-50 It is well recognized that alkalosis decreases calcium excretion by increasing its tubular reabsorption.51,52 The mechanism seems to be PTH independent.51 However, hypercalcemia impairs the kidneys' ability to excrete excess bicarbonate, possibly closing a vicious cycle that in susceptible individuals may lead to severe hypercalcemia and renal failure. The increased serum calcium level causes afferent arteriole constriction and reduction in the glomerular filtration rate (GFR).53,54 Also, hypercalcemia has a well-known natriuretic and diuretic effect, presumably by activating the calcium-sensing receptor, and leads to intravascular depletion.55,56 Aspiration of gastric content to control acidity in the original Sippy regimen can further exacerbate intravascular depletion, as does hypercalcemia-induced renal hyposthenuria.56,57 The resulting GFR reduction further limits excretion of bicarbonate and calcium. The increasing serum calcium level propagates the toxic effects of calcium on the kidneys. Long-term exposure to high calcium levels can result in nephrocalcinosis, tubular necrosis, and other structural changes.58 An alkalotic environment is known to facilitate calcium precipitation.9,59 Aging results in a decreased capacity to handle excess calcium, probably because of decreased renal function and down-regulation of the calcium-sensing receptor in chronic renal disease, and may predispose patients to developing hypercalcemia.40,60 Hypokalemia due to gastric suctioning and vomiting may have an additional renal deleterious effect. The combination of calcium and absorbable alkali seems to be necessary for the development of MAS. Absorbable alkali alone does not produce alkalosis. Even large administered amounts of sodium bicarbonate are readily excreted by the kidneys without persistent alkalemia. This has been well documented in humans and animals.61-63

The PTH level should be depressed by the high serum calcium level in patients with MAS. However, data are limited. Occasional reports showed inappropriately elevated PTH levels.33,64 In at least some of those cases, use of C-terminal assays to measure PTH levels in the setting of renal failure could explain the high levels. Decreasing serum calcium levels have been contemplated as the cause of high PTH levels even if the patient is still hypercalcemic.64 Data to support this theory are lacking, but a similar phenomenon has been observed in hypercalcemia seen in the polyuric phase of rhabdomyolysis.65 Intact PTH measurements generally reveal appropriately suppressed hormone levels,2 but available data are scant. The low serum PTH level further contributes to alkalemia by increasing urinary resorption of bicarbonate.66,67 Temporary hypocalcemia is not unusual after treatment of MAS and likely reflects a suppressed PTH level.2

 

[Such_Saturation]

post 103106
The first symptoms may occur within a few days. distaste for milk

I'm safe

 

[Dan W]

Very helpful (and reassuring), thanks Giraffe.

 

[Parsifal]

I've heard Peat saying in an interview that he used to drink 1 quart of milk/day for very long and that the Masai drink 5L/day so I guess this is not really an issue .

 

[DaveFoster]

@Giraffe
Great information.

I've been doing about 2 TSP baking soda, 1 TBSP regular salt, and 1 TSP calcium carbonate per day in addition to around a gallon of milk (and OJ, liver, oysters, chocolate, etc.)

I believe Buteyko breathing helps counter milk alkali syndrome, but please correct me if I'm wrong so I don't die.

I'll use some urine test strips tomorrow morning.

 

[raypeatclips]

I'll use some urine test strips tomorrow morning.

What would the urine strips show in milk alkali syndrome compared to normal? I can't find anything on Google about urine strips and MAS.

 

[Dan W]

What would the urine strips show in milk alkali syndrome compared to normal? I can't find anything on Google about urine strips and MAS.

Just a guess, but if the MAS involves metabolic alkalosis, the urine might be more basic than normal as the kidneys try to lower PH.

This person suggests your saliva might actually go acidic, which is interesting. If true, I wonder if saliva PH could be used to monitor CO2 in general.

 

[DaveFoster]

@raypeatclips Dan Wich is right; urine would be more basic according to tara.

@Dan Wich

"Which also means when saliva is moving more acid it could be telling you that contrary to thinking you have an "acid" issue, the issue may be quite the opposite. Respiration is automatic. You have no control over this. The body just does it to deal with its chemistry. You get too alkaline and your respiration rate will decrease. For point of reference, a normal breath rate per minute is around 14 breaths per minute, much lower than that and an alkalosis situation may be being revealed."

This conflicts with Buteyko, who thinks four breaths per minute equals ideal health. I don't feel good breathing every 4 seconds.

 

[Pet Peeve]

I assume magnesium bicarbonate would have the same effect as sodium bicarbonate in this context?

 

[Mage]

@Giraffe

One of the studies you've quoted say:

What constitutes “excessive” is unclear but generally indicates at least 4 to 5 g of calcium carbonate daily.32,33 However, ingesting large amounts of alkali and calcium alone does not result in alkalosis and hypercalcemia, respectively

Many of us here are ingesting around this daily dose of calcium (I'm currently at 2500-3000mg but I've seen several posts of 4000-5000mg). Do you think this should be a problem? I don't have any evidence to this, but I'm trying to find out if excess calcium consuption, even with proper Magnesium, K2 and D, is a problem. I know that low calcium is bad because PTH gets upregulated, but the other extreme doesn't seem good either..

 

[Amazoniac]

MilkCalcium-Alkali Syndrome in the Modern Era

"In the 1970s, the incidence of milk-alkali syndrome fell dramatically as the use of antacids decreased with the introduction of histamine blockers. The 1990s were marked by a resurgence of the milk-alkali syndrome, in large part due to the widespread use of calcium and vitamin D supplementation among post-menopausal women for the treatment and prevention of osteoporosis"

"The modern version of milk-alkali syndrome is now known as calcium-alkali syndrome. This evolution in terminology reflects the current pathogenesis of the disorder, which is related to excess calcium supplementation or calcium containing antacids [9]."

"The true incidence of calcium alkali syndrome is unknown. In a recent retrospective study at a single center, from 1998 to 2003, calcium-alkali syndrome was the third most common cause of hypercalcemia (8.8%) and second most common cause of severe hypercalcemia (>14 mg/dL). About 34% of the patients had malignancy and 30% had primary hyperparathyroidism [11]. Many of the patients reported consuming less than 2 g of elemental calcium per day in the form of calcium carbonate. With the caveat that self-reported calcium ingestion may not be accurate, the amount described is much lower than the usual minimum 4 g of calcium intake that was previously associated with the milk-alkali syndrome [11]. The lower threshold for calcium intake associated with calcium-alkali syndrome may be due to increased vitamin D intake resulting in enhanced intestinal calcium absorption."

"The integral features of calcium-alkali syndrome are excess ingestion of calcium and often absorbable alkali leading to the classic triad of hypercalcemia, metabolic alkalosis, and varying degrees of renal insufficiency [10,13,20]. Initially, the traditional milk-alkali syndrome was characterized by elevated serum phosphate concentration, probably secondary to the ingestion of phosphate-rich milk and cream in the Sippy diet [21]. In contrast, calcium-alkali syndrome is associated with hypophosphatemia or low-normal serum phosphorus level as a result of the phosphate-binding capacity of calcium carbonate and other calcium containing supplements resulting in decreased phosphate absorption. These effects are more pronounced in elderly patients and patients with eating disorders who have reduced dietary phosphate and protein intake [6]. The vast majority of cases are associated with calcium carbonate supplements [10]."

"Hypercalcemia occurs when the influx of calcium into extracellular fluid exceeds the excretion by the kidney [22]. Calcium-alkali syndrome can be divided into generation and maintenance phases. In the generation phase, the intestinal component is the most important since it is the site of calcium absorption. Factors affecting the amount of calcium absorption include dietary intake, vitamin D level, and acidity. An acidic environment increases the availability of free calcium for absorption in the gut, predominantly in the proximal small intestine through a combination of active vitamin D-dependent transport (saturable) and passive unregulated paracellular diffusion [6,16]. Therefore, meals that raise gastric acidity such as animal protein and carbohydrate-based meals are associated with increased calcium absorption [6]. The threshold amount of calcium generally considered to predispose to calcium-alkali is above 4 g; however, there are reports of calcium-alkali with as little as 1–1.5 g of calcium supplementation, a dose that is consistent with many dietary guidelines [11,13,23]."

"Natural protective mechanisms against the development of calcium-alkali syndrome also operate[], including decreased intestinal absorption of calcium, decreased sensitivity to vitamin D supplementation, and reduced gastric acidity [6]."

"In the event that hypercalcemia occurs, counter-regulatory mechanisms re-establish normocalcemia. First, the high calcium level suppresses parathyroid hormone (PTH) secretion, which reduces bone efflux of calcium. A decreased PTH concentration also functions to suppress calcitriol production, resulting in decreased intestinal absorption of calcium. Despite these modifying mechanisms, other features of the calcium-alkali syndrome may further perpetuate the syndrome."

"Calcium-alkali syndrome is often confused with hyperparathyroidism as both may have combined hypercalcemia and hypophosphatemia." "While serum concentrations of 1,25-hydoxyvitamin D are elevated in primary hyperparathyroidism, the levels of 1,25-hydroxyvitamin D are generally low in calcium-alkali syndrome because PTH is suppressed. However, reports exist of 1,25-hydroxyvitamin D levels that are not suppressed, perhaps identifying a subset of patients that are at high risk of developing calcium-alkali syndrome [10]."

"calcium carbonate and citrate can reduce phosphate absorption, which may be detrimental for bone mineralization"

"In general, ingestion of equivalent doses of calcium from dairy products has a smaller effect on serum calcium level than calcium supplements, which may explain the lack of detrimental vascular effect by dietary calcium intake as found in observational studies [35,37,38]. Calcium in food is less bioavailable because of the presence of calcium-binding agents, such as oxalic acid, phytates, fiber, and phosphate."

"the peak absorption of calcium occurs at around a 400 mg calcium load and then it levels off. Absorption of calcium may be as high as 60% at very low intake and as low as 20% at a high intake [40]."

"It is advisable to monitor calcium levels periodically in patients who are also receiving calcium and/or vitamin D supplementation."

 

[mimmo123]

this happened to me years ago I was drinking a gallon of milk for like 4 years then all of a sudden I noticed all my upper teeth turned white I was in a very stressful job when it happened and my calcium levels were a little high

Not good I realized I was extremely alkaline and my right kidney was hurting. You need to monitor your urine ph multiple times per day and adjust
what your eating/taking to bring the ph in balance. I started to drink massive amounts of Coke and breathing in co2 and taking K2 and t3 this brought my ph back down to normal. and the white teeth went back to normal.

Now a days I'm breathing in a lot of co2 from the tank and I noticed, it can drop my urine ph below 6 if I breath it in for hours at 7%. Co2 will acidify the blood
I just take baking soda and it goes back up to 7.0-7.5 I have it nailed down on how much baking soda to take to bring me back to perfect level. and if you take aspirin its the same thing you should be monitoring your urine ph and take baking soda based on the amount needed to bring the ph to normal, exercise will make you acidic as well and you can take baking soda to bring you back to normal levels.
taking baking soda and inhaling co2 like that you feel amazing by the way!

If I go to high in urine ph by taking too much baking soda I can just bring it down by inhaling co2 or you can do breathing exercises but co2 much easier and faster you can also try and drink soda take salt and k2,t3 etc

 

[Giraffe]

"The true incidence of calcium alkali syndrome is unknown. In a recent retrospective study at a single center, from 1998 to 2003, calcium-alkali syndrome was the third most common cause of hypercalcemia (8.8%) and second most common cause of severe hypercalcemia (>14 mg/dL). About 34% of the patients had malignancy and 30% had primary hyperparathyroidism [11]. Many of the patients reported consuming less than 2 g of elemental calcium per day in the form of calcium carbonate. With the caveat that self-reported calcium ingestion may not be accurate, the amount described is much lower than the usual minimum 4 g of calcium intake that was previously associated with the milk-alkali syndrome [11]. The lower threshold for calcium intake associated with calcium-alkali syndrome may be due to increased vitamin D intake resulting in enhanced intestinal calcium absorption."

I looked up the study cited here. The researchers did not come to the conclusion that increased vitamin D intake might be causative with the exception of ergocalciferol and calcitriol (see below).

Of this 11 patients with milk alkali syndrome:

• vitamin D levels were reported only for five of them: it was low (< 25 ng/ml)
• elemental calcium from calcium carbonate alone: 1-9 g
• all had underlying diseases and were taking pharmaceuticals drugs, some of those drugs are known to cause hypercalcemia.

The most common underlying diagnoses included hypertension (eight patients), osteoporosis (five patients), chronic kidney disease (five patients) and upper gastrointestinal diseases such as peptic ulcer, gastritis and gastroesophageal reflux disease (four patients) (Table 3).

The doses of calcium carbonate that caused the syndrome in our series ranged from 1 to 9 g of elemental calcium daily, but eight patients were ingesting 2000 mg or less, a dose that is not higher than the current recommended upper limit for elemental calcium intake (2000 mg/day) and much lower than the usually reported threshold of 4 g daily. Possibly, coadministered medications decreased this threshold: ergocalciferol and calcitriol promote absorption of calcium, thiazide-like diuretics decrease renal calcium excretion, and loop diuretics can cause volume depletion.

• Ergocalciferol is vitamin D2. It is formulated in capsules of larger dose (50,000 international units) to allow for less frequent administration.
• Calcitriol is the active form vitamin D. It is tightly regulated by the body, and you don't want to mess up with it.

 

[Giraffe]

"Hypercalcemia occurs when the influx of calcium into extracellular fluid exceeds the excretion by the kidney [22]."

The article they reference there is a must-read. Hypercalcemia is most often the result of an underlying disease, and the article explains some of the mechanisms.

What serum calcium can tell us and what it can't

"Factors affecting the amount of calcium absorption include dietary intake, vitamin D level, and acidity."

The vitamin D level has only a very small effect on calcium absorption.

The Effect of Vitamin D on Calcium Absorption in Older Women