Calcium to Phosphorus Ratio, PTH, and Bone Health

Also see:
Calcium Paradox
Source of Dietary Calcium: Chicken Egg Shell Powder
Low CO2 in Hypothyroidism
Blood Pressure Management with Calcium & Dairy
Hypertension and Calcium Deficiency
Excess Dietary Phosphorus Lowers Vitamin D Levels
Fatty Acid Synthase (FAS), Vitamin D, and Cancer
Phosphate, activation, and aging
Parmigiano Reggiano cheese and bone health
Dairy, Calcium, and Weight Management in Adults and Children

Quotes by Ray Peat, PhD:
“The ratio of calcium to phosphate is very important; that’s why milk and cheese are so valuable for weight loss, or for preventing weight gain. For people who aren’t very active, low fat milk and cheese are better, because the extra fat calories aren’t needed.”

“The foods highest in phosphate, relative to calcium, are cereals, legumes, meats, and fish. Many prepared foods contain added phosphate. Foods with a higher, safe ratio of calcium to phosphate are leaves, such as kale, turnip greens, and beet greens, and many fruits, milk, and cheese.”

“Free unsaturated fatty acids turn on the stress hormones, and cortisol blocks oxidation of sugar and turns it into fatty acids and triglycerides. Keeping cortisol and stress low is the main thing. Keeping a high ratio of calcium to phosphate helps to oppose the stress metabolism.”

“Recent publication are showing that excess phosphate can increase inflammation, tissue atrophy, calcification of blood vessels, cancer, dementia, and, in general, the processes of aging.”

Br J Nutr. 2006 Sep;96(3):545-52.
High phosphorus intakes acutely and negatively affect Ca and bone metabolism in a dose-dependent manner in healthy young females.
Kemi VE, Kärkkäinen MU, Lamberg-Allardt CJ.
Ca and P are both essential nutrients for bone and are known to affect one of the most important regulators of bone metabolism, parathyroid hormone (PTH). Too ample a P intake, typical of Western diets, could be deleterious to bone through the increased PTH secretion. Few controlled dose-response studies are available on the effects of high P intake in man. We studied the short-term effects of four P doses on Ca and bone metabolism in fourteen healthy women, 20-28 years of age, who were randomized to four controlled study days; thus each study subject served as her own control. P supplement doses of 0 (placebo), 250, 750 or 1500 mg were taken, divided into three doses during the study day. The meals served were exactly the same during each study day and provided 495 mg P and 250 mg Ca. The P doses affected the serum PTH (S-PTH) in a dose-dependent manner (P=0.0005). There was a decrease in serum ionized Ca concentration only in the highest P dose (P=0.004). The marker of bone formation, bone-specific alkaline phosphatase, decreased (P=0.05) and the bone resorption marker, N-terminal telopeptide of collagen type I, increased in response to the P doses (P=0.05). This controlled dose-response study showed that P has a dose-dependent effect on S-PTH and increases PTH secretion significantly when Ca intake is low. Acutely high P intake adversely affects bone metabolism by decreasing bone formation and increasing bone resorption, as indicated by the bone metabolism markers.

Br J Nutr. 2008 Apr;99(4):832-9. Epub 2007 Oct 1.
Increased calcium intake does not completely counteract the effects of increased phosphorus intake on bone: an acute dose-response study in healthy females.
Kemi VE, Kärkkäinen MU, Karp HJ, Laitinen KA, Lamberg-Allardt CJ.
A high dietary P intake is suggested to have negative effects on bone through increased parathyroid hormone secretion, as high serum parathyroid hormone (S-PTH) concentration increases bone resorption. In many countries the P intake is 2- to 3-fold above dietary guidelines, whereas Ca intake is too low. This combination may not be optimal for bone health. In a previous controlled study, we found that dietary P dose-dependently increased S-PTH and bone resorption and decreased bone formation. The aim of the present study was to investigate the dose-response effects of Ca intake on Ca and bone metabolism with a dietary P intake higher than recommended. Each of the twelve healthy female subjects aged 21-40 years attended three 24-h study sessions, which were randomized with regard to a Ca dose of 0 (control day), 600 or 1200 mg, and each subject served as her own control. The meals on each study day provided 1850 mg P and 480 mg Ca. S-PTH concentration decreased (P < 0.001) and serum ionized Ca concentration increased (P < 0.001) with increasing Ca doses. The bone formation marker, serum bone-specific alkaline phosphatase, did not differ significantly (P = 0.4). By contrast, the bone resorption marker, urinary N-terminal telopeptide of collagen type I, decreased significantly with both Ca doses (P = 0.008). When P intake was above current recommendations, increased Ca intake was beneficial for bone, as indicated by decreased S-PTH concentration and bone resorption. However, not even a high Ca intake could affect bone formation when P intake was excessive.

Br J Nutr. 2010 Feb;103(4):561-8. Epub 2009 Sep 28.
Low calcium:phosphorus ratio in habitual diets affects serum parathyroid hormone concentration and calcium metabolism in healthy women with adequate calcium intake.
Kemi VE, Kärkkäinen MU, Rita HJ, Laaksonen MM, Outila TA, Lamberg-Allardt CJ.
Excessive dietary P intake alone can be deleterious to bone through increased parathyroid hormone (PTH) secretion, but adverse effects on bone increase when dietary Ca intake is low. In many countries, P intake is abundant, whereas Ca intake fails to meet recommendations; an optimal dietary Ca:P ratio is therefore difficult to achieve. Our objective was to investigate how habitual dietary Ca:P ratio affects serum PTH (S-PTH) concentration and other Ca metabolism markers in a population with generally adequate Ca intake. In this cross-sectional analysis of 147 healthy women aged 31-43 years, fasting blood samples and three separate 24-h urinary samples were collected. Participants kept a 4-d food record and were divided into quartiles according to their dietary Ca:P ratios. The 1st quartile with Ca:P molar ratio < or = 0.50 differed significantly from the 2nd (Ca:P molar ratio 0.51-0.57), 3rd (Ca:P molar ratio 0.58-0.64) and 4th (Ca:P molar ratio > or = 0.65) quartiles by interfering with Ca metabolism. In the 1st quartile, mean S-PTH concentration (P = 0.021) and mean urinary Ca (U-Ca) excretion were higher (P = 0.051) than in all other quartiles. These findings suggest that in habitual diets low Ca:P ratios may interfere with homoeostasis of Ca metabolism and increase bone resorption, as indicated by higher S-PTH and U-Ca levels. Because low habitual dietary Ca:P ratios are common in Western diets, more attention should be focused on decreasing excessively high dietary P intake and increasing Ca intake to the recommended level.

Academic Dissertation by Virpi Kemi
Effects of dietary phosphorus and calcium-to phosphorus ratio on calcium and bone metabolism in healthy 20- to 43-year-old Finnish women
“This thesis contributes novel information related to the effects of dietary phosphorus (P) and the combined effects of P and calcium (Ca) on Ca and bone metabolism in healthy individuals. It is already well established that high P intake is detrimental for patients with impaired renal functioning, but the effects of high P intake in healthy humans have been investigated seldom. In this thesis, an excessively high P intake, which is common in Western countries, was observed to negatively affect Ca and bone metabolism. Moreover, P doses affected Ca and bone metabolism in a dose-dependent manner, and P sources also differed in their effects on the essential regulator of Ca and bone metabolism. Finally, we demonstrated that by increasing dietary Ca intake the negative effects of a high P intake could be reduced. However, based on the findings of the controlled study, even a high dietary Ca intake could not completely overcome all of the negative effects caused by a high dietary P intake.

Specific findings of each study were as follows:

Study I
In a controlled study with healthy young women, the oral intake of P in doses
comparable with normal dietary intakes (495, 745, 1245 and 1995 mg/d) with a low
Ca intake (250 mg/d) increased serum parathyroid hormone (S-PTH) concentration in
a dose-dependent manner. The highest P dose had the most negative effects, as with
the highest dose there was also a decrease in serum ionized Ca (S-iCa) concentration
and bone formation and an increase in bone resorption. Furthermore, a high P intake
(1995 mg/d) inhibited the increase in serum 1,25(OH)2D in response to a low dietary
Ca intake, implying that the normal relationship between Ca intake and Ca absorption
is disturbed in diets high in P and low in Ca. This study showed that P has a dose dependent effect on S-PTH and increases PTH secretion significantly when Ca intake
is low. An acutely high P intake adversely affects bone metabolism by decreasing bone
formation and increasing bone resorption.

Study II
In a controlled study of healthy 20-to 40-year-old women with a dietary P intake that was 3-fold above the dietary guidelines (1850 mg/d), by increasing the Ca intake from 480 mg/d to 1080 mg/d and then to 1680 mg/d, the S-PTH concentration decreased,
the S-iCa concentration increased and bone resorption decreased dose-dependently.
This study showed that a dietary Ca intake above the recommended level offers
several advantages in preventing the negative effects of a high P intake. However, not
even the highest Ca intake (1680 mg/d) could counteract the effect of high dietary P on
bone formation, as indicated by unchanged bone formation activity.

Study III
In a cross-sectional study with healthy 31- to 43-year-old women, a high habitual
dietary P intake was associated with increased S-PTH and decreased S-iCa concentrations. These results are in line with observations in our controlled short-term
study. Furthermore, in the habitual diets, phosphate additives, unlike other P sources,
were associated with higher mean S-PTH concentrations. The association of S-PTH
with natural P was the opposite of that with foods containing phosphate additives.
Thus, these results suggest that P sources might differ in their effects on the central
regulator of Ca and bone metabolism, parathyroid hormone.

Study IV
In a cross-sectional study of healthy 31- to 43-year-old women with an adequate Ca
intake, low habitual dietary Ca:P ratios (Ca:P molar ratio 0.50) were associated with
both higher S-PTH and U-Ca levels. Interestingly, the lowest Ca:P quartile with a Ca:P
molar ratio 0.50 differed from all other quartiles by having the most deleterious
associations with Ca metabolism. These results imply that a cut-off Ca:P ratio may
exist that is lower than the suggested Ca:P molar ratio of 1, below which the effects on
mineral metabolism and bone health are more severe. None of the study subjects
achieved the suggested dietary Ca:P molar ratio of 1.

A question arising from the findings of this thesis is how to reduce the current excessively high dietary P intake. The answer to this is not straightforward, as the current P intakes are not well known since the use of phosphate additives has not been taken into consideration when establishing food composition databases. In the future, food composition databases should be updated and the actual P contents of foodstuffs determined by laboratory analyses. In addition, it is impossible for an individual to know how much P foods contain because P is not included in the compulsory food ingredient list. While waiting for these issues to be addressed, one can reduce dietary P intake by restricting the consumption of highly processed foods and increasing the consumption of raw or unprocessed foods.

As there are still many open questions concerning the effects of high P intake on bone health, we will continue to investigate whether dietary P intakes and different P sources affect bone mass and structure in adult Finns. However, nowadays, when considering public health, it is not only osteoporosis but also other public health diseases in which a high P intake may play an important role in a negative sense. An alarming rise has been seen among Western populations in the incidence of type 2 diabetes, a major cause of end stage renal disease, in which dietary P restriction is a part of the treatment. Among patients with end-stage renal disease and diabetes, vascular calcification correlates highly with cardiovascular disease mortality. Recent results suggest that an excessive P intake may be involved in this vascular calcification process, even in healthy humans. Therefore, in the near future, our studies will expand to investigate the relationship between dietary P and vascular calcification in Finnish adults.” (pp. 85, 86)