Evidence map›Paper›PMID 24425727›Full record

ReviewAdvances in nutrition (Bethesda, Md.)2014

Increasing dietary phosphorus intake from food additives: potential for negative impact on bone health.

Eiji Takeda, Hironori Yamamoto, Hisami Yamanaka-Okumura, Yutaka Taketani

Open access · bronzeAbstract readReview
In one paragraph

Review in Advances in nutrition (Bethesda, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
6.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Supplements for bone health.Archives of endocrinology and metabolism · 2025
    Review
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  7. Review
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  10. Mineral Supplements in Ageing.Sub-cellular biochemistry · 2024
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Eiji TakedaDepartment of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima City, Tokushima, Japan.
Hironori Yamamoto
Hisami Yamanaka-Okumura
Yutaka Taketani
Tokushima University · JPJin-ai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is important to consider whether habitual high phosphorus intake adversely affects bone health, because phosphorus intake has been increasing, whereas calcium intake has been decreasing in dietary patterns. A higher total habitual dietary phosphorus intake has been associated with higher serum parathyroid hormone (PTH) and lower serum calcium concentrations in healthy individuals. Higher serum PTH concentrations have been shown in those who consume foods with phosphorus additives. These findings suggest that long-term dietary phosphorus loads and long-term hyperphosphatemia may have important negative effects on bone health. In contrast, PTH concentrations did not increase as a result of high dietary phosphorus intake when phosphorus was provided with adequate amounts of calcium. Intake of foods with a ratio of calcium to phosphorus close to that found in dairy products led to positive effects on bone health. Several randomized controlled trials have shown positive relations between dairy intake and bone mineral density. In our loading test with a low-calcium, high-phosphorus lunch provided to healthy young men, serum PTH concentrations showed peaks at 1 and 6 h, and serum fibroblast growth factor 23 (FGF23) concentrations increased significantly at 8 h after the meal. In contrast, the high-calcium, high-phosphorus meal suppressed the second PTH and FGF23 elevations until 8 h after the meal. This implies that adequate dietary calcium intake is needed to overcome the interfering effects of high phosphorus intake on PTH and FGF23 secretion. FGF23 acts on the parathyroid gland to decrease PTH mRNA and PTH secretion in rats with normal kidney function. However, increased serum FGF23 is an early alteration of mineral metabolism in chronic kidney disease, causing secondary hyperthyroidism, and implying resistance of the parathyroid gland to the action of FGF23 in chronic kidney disease. These findings suggest that long-term high-phosphorus diets may impair bone health mediated by FGF23 resistance both in chronic kidney disease patients and in the healthy population.

Indexed as

AnimalsBone and BonesBone ResorptionCongresses as TopicFast FoodsFeeding BehaviorFibroblast Growth Factor-23Fibroblast Growth FactorsFood AdditivesHumansParathyroid GlandsParathyroid HormonePhosphorus, DietaryFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsFood AdditivesParathyroid HormonePhosphorus, DietaryPTH protein, human

Identifiers

PMID24425727
PMCPMC3884105
OpenAlexW2100820099

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.