{"id":5058,"date":"2012-04-17T18:29:23","date_gmt":"2012-04-18T01:29:23","guid":{"rendered":"http:\/\/www.functionalps.com\/blog\/?p=5058"},"modified":"2018-12-21T19:54:49","modified_gmt":"2018-12-22T03:54:49","slug":"calcium-to-phosphorus-ratio-pth-and-bone-health","status":"publish","type":"post","link":"https:\/\/www.functionalps.com\/blog\/2012\/04\/17\/calcium-to-phosphorus-ratio-pth-and-bone-health\/","title":{"rendered":"Calcium to Phosphorus Ratio, PTH, and Bone Health"},"content":{"rendered":"

Also see:
\nCalcium Paradox<\/a>
\nSource of Dietary Calcium: Chicken Egg Shell Powder<\/a>
\nLow CO2 in Hypothyroidism
\n<\/a>Blood Pressure Management with Calcium & Dairy<\/a>
\nHypertension and Calcium Deficiency<\/a>
\nExcess Dietary Phosphorus Lowers Vitamin D Levels<\/a>
\nFatty Acid Synthase (FAS), Vitamin D, and Cancer<\/a>
\nPhosphate, activation, and aging<\/a>
\nParmigiano Reggiano cheese and bone health<\/a>
\nDairy, Calcium, and Weight Management in Adults and Children<\/a><\/strong><\/p>\n

\"Picture<\/a><\/p>\n

Quotes by Ray Peat, PhD:<\/strong>
\n\u201cThe ratio of calcium to phosphate is very important; that\u2019s why milk and cheese are so valuable for weight loss, or for preventing weight gain. For people who aren\u2019t very active, low fat milk and cheese are better, because the extra fat calories aren\u2019t needed.\u201d<\/em><\/p>\n

“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.”<\/em><\/p>\n

“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.”
\n<\/em>
\n\u201cRecent publication are showing that excess phosphate can increase inflammation, tissue atrophy, calcification of blood vessels, cancer, dementia, and, in general, the processes of aging.\u201d <\/em><\/p>\n

Br J Nutr. 2006 Sep;96(3):545-52.
\nHigh phosphorus intakes acutely and negatively affect Ca and bone metabolism in a dose-dependent manner in healthy young females.<\/a>
\n<\/strong>Kemi VE, K\u00e4rkk\u00e4inen MU, Lamberg-Allardt CJ.
\nCa 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<\/a>. <\/strong>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.<\/strong><\/p>\n

Br J Nutr. 2008 Apr;99(4):832-9. Epub 2007 Oct 1.
\nIncreased calcium intake does not completely counteract the effects of increased phosphorus intake on bone: an acute dose-response study in healthy females.<\/a>
\nKemi VE, K\u00e4rkk\u00e4inen MU, Karp HJ, Laitinen KA, Lamberg-Allardt CJ.
\nA 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.<\/strong> 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.<\/strong><\/p>\n

Br J Nutr. 2010 Feb;103(4):561-8. Epub 2009 Sep 28.
\nLow calcium:phosphorus ratio in habitual diets affects serum parathyroid hormone concentration and calcium metabolism in healthy women with adequate calcium intake.<\/a>
\n<\/strong>Kemi VE, K\u00e4rkk\u00e4inen MU, Rita HJ, Laaksonen MM, Outila TA, Lamberg-Allardt CJ.
\nExcessive 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.<\/strong> 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.<\/strong><\/p>\n

Academic Dissertation by Virpi Kemi
\nEffects of dietary phosphorus and calcium-to phosphorus ratio on calcium and bone metabolism in healthy 20- to 43-year-old Finnish women<\/a><\/strong>
\n“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.<\/strong><\/p>\n

Specific findings of each study were as follows:<\/p>\n

Study I
\nIn a controlled study with healthy young women, the oral intake of P in doses
\ncomparable with normal dietary intakes (495, 745, 1245 and 1995 mg\/d) with a low
\nCa intake (250 mg\/d) increased serum parathyroid hormone (S-PTH) concentration in
\na dose-dependent manner. The highest P dose had the most negative effects, as with
\nthe highest dose there was also a decrease in serum ionized Ca (S-iCa) concentration
\nand bone formation and an increase in bone resorption. Furthermore, a high P intake
\n(1995 mg\/d) inhibited the increase in serum 1,25(OH)2D in response to a low dietary
\nCa intake, implying that the normal relationship between Ca intake and Ca absorption
\nis 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
\nis low. An acutely high P intake adversely affects bone metabolism by decreasing bone
\nformation and increasing bone resorption.<\/strong><\/p>\n

Study II
\nIn 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,
\nthe S-iCa concentration increased and bone resorption decreased dose-dependently.
\nThis study showed that a dietary Ca intake above the recommended level offers
\nseveral advantages in preventing the negative effects of a high P intake. However, not
\neven the highest Ca intake (1680 mg\/d) could counteract the effect of high dietary P on
\nbone formation, as indicated by unchanged bone formation activity.<\/strong><\/p>\n

Study III
\nIn a cross-sectional study with healthy 31- to 43-year-old women, a high habitual
\ndietary 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
\nstudy. Furthermore, in the habitual diets, phosphate additives, unlike other P sources,
\nwere associated with higher mean S-PTH concentrations. The association of S-PTH
\nwith natural P was the opposite of that with foods containing phosphate additives.
\nThus, these results suggest that P sources might differ in their effects on the central
\nregulator of Ca and bone metabolism, parathyroid hormone.<\/strong><\/p>\n

Study IV
\nIn a cross-sectional study of healthy 31- to 43-year-old women with an adequate Ca
\nintake, low habitual dietary Ca:P ratios (Ca:P molar ratio \u00020.50) were associated with
\nboth higher S-PTH and U-Ca levels. Interestingly, the lowest Ca:P quartile with a Ca:P
\nmolar ratio \u00020.50 differed from all other quartiles by having the most deleterious
\nassociations with Ca metabolism. These results imply that a cut-off Ca:P ratio may
\nexist that is lower than the suggested Ca:P molar ratio of 1, below which the effects on
\nmineral metabolism and bone health are more severe. None of the study subjects
\nachieved the suggested dietary Ca:P molar ratio of 1.<\/strong><\/p>\n

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.<\/strong> 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.<\/p>\n

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.”<\/strong> (pp. 85, 86)<\/p>\n","protected":false},"excerpt":{"rendered":"

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 […]<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[1],"tags":[367,748,1770,566,582,399,1116,1774,2035,1329,2033,569,1880,453,4],"class_list":["post-5058","post","type-post","status-publish","format-standard","hentry","category-general","tag-aging","tag-bone","tag-calcification","tag-calcium","tag-osteopenia","tag-paleo","tag-parathyroid","tag-phosphate","tag-phosphate-poisoning","tag-phosphorus","tag-phosphorus-poisoning","tag-pth","tag-ratio","tag-ray-peat","tag-stress"],"_links":{"self":[{"href":"https:\/\/www.functionalps.com\/blog\/wp-json\/wp\/v2\/posts\/5058","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.functionalps.com\/blog\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.functionalps.com\/blog\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.functionalps.com\/blog\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/www.functionalps.com\/blog\/wp-json\/wp\/v2\/comments?post=5058"}],"version-history":[{"count":5,"href":"https:\/\/www.functionalps.com\/blog\/wp-json\/wp\/v2\/posts\/5058\/revisions"}],"predecessor-version":[{"id":11927,"href":"https:\/\/www.functionalps.com\/blog\/wp-json\/wp\/v2\/posts\/5058\/revisions\/11927"}],"wp:attachment":[{"href":"https:\/\/www.functionalps.com\/blog\/wp-json\/wp\/v2\/media?parent=5058"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.functionalps.com\/blog\/wp-json\/wp\/v2\/categories?post=5058"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.functionalps.com\/blog\/wp-json\/wp\/v2\/tags?post=5058"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}