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MyDeficiencies

Teriparatide

parathyroid hormone analog, PTH(1-34), bone anabolic

Also sold as Forteo, Bonsity.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Teriparatide is the opposite case from a typical depletion drug: it does not chelate, does not induce liver enzymes, and is not absorbed through the gut at all, since it is a 34-amino-acid peptide given by subcutaneous injection and cleared by ordinary proteolysis. Its nutrient-relevant signal instead comes directly from its own pharmacology: it is PTH(1-34), so once-daily receptor activation reproduces the core actions of parathyroid hormone on the calcium, phosphate, and vitamin D axis, deliberately and predictably. The regulatory label documents this in detail and at scale: 11.1% of women and 6% of men on teriparatide had at least one serum calcium above the upper limit of normal versus 1.5% and 0%, respectively, on placebo, with a distinct 4-6 hour post-dose transient peak. That is graded red. In the same pivotal-trial population, the label also reports a mild, transient reduction in serum phosphorus (phosphaturia, with no clinical hypophosphatemia observed), a rise in active 1,25-dihydroxyvitamin D (calcitriol, +19% in women, +14% in men at 12 months) paired with a fall in storage 25-hydroxyvitamin D (-19% in women, -10% in men) against a background where every trial participant received supplemental vitamin D, and a small increase in serum uric acid (3% vs 1% above normal, without a corresponding rise in gout). Each of these is graded orange: real, drug-specific, and bounded.

parathyroid hormone analog, PTH(1-34), bone anabolic · ATC H05AA02 · also sold as Forteo and Bonsity · reviewed 2026-09-28. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Teriparatide in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe
Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate
At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit.
Yellow — Low
Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction.
Not graded — disclosed evidence gap
Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: Not gradeable under the rules above because nothing has been measured. Published as a documented gap, never as reassurance that there is no effect.

What the research found

Calcium, frequent, dose-related, monitored hypercalcemia

Red — Severe

See study details

Teriparatide reliably raises serum calcium in a meaningful minority of treated patients through a well-characterized PTH-receptor mechanism, with defined monitoring built into labeling.

Full detail and limits

What the grade means here: Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence. Red

Limits on what this shows

  • Key negative/null findings: The label states hypercalcemia remained below 11 mg/dL in the large majority of patients and that calcium supplement and/or drug-dose adjustment resolved elevated values in clinical trials, arguing against an unmanageable or progressive process at approved dosing.
  • At-risk subgroups: Patients with any underlying hypercalcemic disorder (avoid use; not studied), patients on digoxin (label-flagged risk of digitalis toxicity potentiated by transient hypercalcemia), and patients with pre-existing hypercalciuria or urolithiasis for the related urinary-calcium risk.
  • Counter-evidence on record: None found contradicting direction or frequency; independent access to the original Fracture Prevention Trial (Neer et al, NEJM 2001) was blocked by a paywall during this review, so this entry rests on the label's own reporting of that and the companion male-osteoporosis trial rather than the primary journal article directly.

Regulatory status

Labeling requires periodic serum calcium monitoring, describes a characteristic 4-6 hour post-dose transient peak returning near baseline by 16-24 hours, and instructs avoiding use in patients with pre-existing hypercalcemic disorders such as primary hyperparathyroidism (drug not studied in that population).

Population evidence

DailyMed label, pooled pivotal-trial data, two independent development-program trials. Women: 11.1% of teriparatide-treated patients had at least one calcium value above the upper limit of normal (10.6 mg/dL) versus 1.5% on placebo; 3% versus 0.2% had elevated calcium on consecutive measurements; median peak calcium 9.68 mg/dL at 12 months, remaining below 11 mg/dL in >99% of women. Men: 6% above ULN versus 0% on placebo; 1.3% (2 men) versus 0% on consecutive measurements; median peak 9.44 mg/dL at 12 months, below 11 mg/dL in 98%. Transient post-dose hypercalcemia (4-6 hours): 11% (women) and 6% (men) on drug versus 2% and 0% on placebo.

Mechanism

Named: PTH1-receptor activation increases osteoclast-mediated bone resorption release of calcium, renal tubular calcium reabsorption, and (via calcitriol) intestinal calcium absorption, all core, intended PTH physiology rather than an incidental drug effect.

Counter-evidence held on record

This is an excess-direction, not a depletion-direction, finding: it should never be used to suggest increasing calcium intake beyond the co-prescribed calcium/vitamin D supplementation already built into standard teriparatide care, and any calcium-related monitoring question belongs with the prescriber, not with a supplementation prompt.

Phosphate, transient renal wasting, bounded, no clinical hypophosphatemia

Orange — Moderate

See study details

Teriparatide produces a real, drug-specific transient phosphaturia and mild reduction in serum phosphorus, but the label reports no clinical hypophosphatemia in trials, bounding the finding.

Full detail and limits

What the grade means here: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit. Orange

Limits on what this shows

  • Key negative/null findings: The label's own statement that hypophosphatemia was not observed clinically is the bounding null finding reported here rather than omitted.
  • At-risk subgroups: Not separately quantified in the label; patients with baseline low-normal phosphate or concurrent phosphate-lowering therapy are the plausible, though unquantified, higher-risk group by mechanism.
  • Counter-evidence on record: None found beyond the bounding null finding itself.

Regulatory status

Phosphate is described directly in the label's pharmacodynamics section alongside calcium; no phosphate-specific warning or monitoring requirement beyond routine bone-panel labs.

Population evidence

DailyMed label, same pivotal-trial population as the Calcium entry: "transient phosphaturia and mild transient reductions in serum phosphorus concentration," with hypophosphatemia (<2.4 mg/dL) not observed clinically in either the women's or men's development-program trials.

Mechanism

Named: PTH1-receptor activation in the renal proximal tubule reduces sodium-phosphate cotransporter activity, producing phosphaturia, standard endogenous PTH physiology reproduced by the drug.

Counter-evidence held on record

Do not present as a phosphate-deficiency risk requiring supplementation; the label explicitly reports no clinical hypophosphatemia, and phosphate is already part of routine bone-metabolism monitoring for this drug.

Vitamin D, storage form falls as active calcitriol rises, against a supplemented background

Orange — Moderate

See study details

Teriparatide measurably shifts the vitamin D axis: active 1,25-dihydroxyvitamin D rises while storage 25-hydroxyvitamin D falls, a real and drug-specific but mechanistically expected and background-supplemented finding.

Full detail and limits

What the grade means here: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit. Orange

Limits on what this shows

  • Key negative/null findings: The rise in the active hormone, occurring in parallel with the storage-form decline, is itself evidence against a true depletion narrative; this is an axis shift, not a net vitamin D deficit, and is explicitly reported that way here rather than isolating only the falling number.
  • At-risk subgroups: Not separately quantified; patients whose vitamin D supplementation is inconsistent or below the trial-level dosing are the plausible group where the storage-form decline could become clinically relevant, though this was not directly tested.
  • Counter-evidence on record: The background universal-supplementation design of the pivotal trials limits generalization to unsupplemented patients; no unsupplemented teriparatide cohort with vitamin D data was found.

Regulatory status

Reported directly in the label's pharmacodynamics section; all patients in the primary studies received at least 400 IU/day supplemental vitamin D (800 IU/day in the glucocorticoid-induced osteoporosis trial), so the finding is against a supplemented, not deficient, background by design.

Population evidence

DailyMed label, same pivotal-trial population. Active 1,25-dihydroxyvitamin D: +19% (women) and +14% (men) at 12 months versus baseline (placebo -2% women, +5% men). Storage 25-hydroxyvitamin D: -19% (women) and -10% (men) at 12 months versus baseline (placebo unchanged in women, +1% in men).

Mechanism

Named: PTH1-receptor activation stimulates renal 1-alpha-hydroxylase, accelerating conversion of storage 25-hydroxyvitamin D into active 1,25-dihydroxyvitamin D; the storage-form decline is a direct, mechanistically expected consequence of accelerated conversion rather than reduced dietary intake or absorption.

Counter-evidence held on record

Do not present as evidence that teriparatide "depletes" vitamin D outright; the active hormone rises while the storage form falls, and every source patient was already vitamin-D-supplemented. This should surface only as a reason to keep standard co-supplementation consistent, never as a prompt to increase vitamin D dosing beyond a prescriber's plan.

Magnesium, real decline in a single retrospective cohort, bounded by design

Orange — Moderate

See study details

A single-center retrospective cohort found more than a third of teriparatide-treated patients developed hypomagnesemia, with a statistically significant decline at every timepoint measured, though the finding has not been independently replicated.

Full detail, limits and 1 references

What the grade means here: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit. Orange

Limits on what this shows

  • Key negative/null findings: Stable calcium, creatinine, and endogenous PTH across the same cohort argue the magnesium decline is not simply a marker of general renal deterioration or of calcium/PTH-axis disruption.
  • At-risk subgroups: Older age (71.1 vs 65.1 years in hypomagnesemic vs normomagnesemic patients, p=0.05) and lower baseline magnesium (0.81 vs 0.85 mmol/L, p=0.03) independently predicted hypomagnesemia in this cohort.
  • Counter-evidence on record: This is a single-center, single-cohort, retrospective, non-placebo-controlled design; no second independent human cohort was found or could be opened during this review, so the finding is not replicated and is graded accordingly rather than higher.

Regulatory status

Not addressed in labeling.

Population evidence

Begin et al, Journal of Bone and Mineral Research, 2018. Retrospective cohort, 53 patients treated for severe osteoporosis with teriparatide for 6 to 24 months (May 2008 to January 2016), single center. Hypomagnesemia defined as serum magnesium <0.7 mmol/L: incidence 35.9% (19 of 53). Magnesium decline versus baseline: -0.075 mmol/L at 3 months, -0.069 mmol/L at 6 months, -0.085 mmol/L at 12 months, -0.086 mmol/L at end of treatment (all p<0.0001). Serum calcium, creatinine, and (endogenous, suppressed) PTH remained normal throughout, arguing against confounding by renal impairment.

Mechanism

Present but not fully elaborated in the primary cohort study (mechanism class C, renal tubular handling): a separate case-series abstract (SAT-801, could not be opened during this review, see Sources) proposes renal magnesium wasting via hypermagnesuria as the driver, consistent with known PTH effects on distal tubular magnesium handling.

Counter-evidence held on record

This is a genuine depletion-direction finding, unlike the calcium entry above; periodic serum magnesium monitoring is a reasonable prompt, particularly in older patients or those with lower baseline magnesium, but any magnesium supplementation decision belongs with a prescriber given teriparatide's own renal and calcium-axis effects.

Uric acid, small, low-frequency elevation, no downstream clinical effect observed

Orange — Moderate

See study details

Teriparatide produces a small, drug-specific rise in serum uric acid in a minority of patients, with the label explicitly noting no corresponding increase in gout, arthralgia, or urolithiasis.

Full detail and limits

What the grade means here: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit. Orange

Limits on what this shows

  • Key negative/null findings: The label states directly that "the hyperuricemia did not result in an increase in gout, arthralgia, or urolithiasis," the key bounding null finding for this entry.
  • At-risk subgroups: Not separately quantified; patients with pre-existing gout or hyperuricemia are the plausible, though unquantified, higher-risk group.
  • Counter-evidence on record: The absence of a clinical gout signal in the same trial population is itself the counter-evidence limiting this entry's severity.

Regulatory status

Reported in the label's adverse reactions/laboratory findings section.

Population evidence

DailyMed label, pivotal-trial population: 3% of teriparatide-treated patients had serum uric acid above the upper limit of normal versus 1% of placebo-treated patients.

Mechanism

Not elaborated in the label; a plausible but unconfirmed link runs through PTH's known effects on renal tubular urate handling, paralleling its effects on renal calcium and phosphate transport, though this specific pathway was not directly tested for teriparatide in sources reviewed.

Counter-evidence held on record

This is an excess-direction, not a depletion-direction, finding and carries no established clinical consequence at approved dosing; it should surface only as a minor lab-monitoring note for patients with pre-existing gout, never as a supplementation or dietary-restriction prompt.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden, tissue-specific metabolic reprogramming in osteoblasts, not a systemic deficit

Yellow — Low

See study details

In mouse osteoblasts, PTH(1-34) signaling shifts energy metabolism toward aerobic glycolysis and away from mitochondrial oxidative metabolism as part of its own bone-anabolic mechanism, a tissue-specific finding that must not be read as a systemic mitochondrial burden.

Full detail, limits and 1 references

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Key negative/null findings: None found directly contradicting the direction; the main limitation is that this entry is one step removed from the primary source (characterized via a review) and confined to mouse osteoblasts, not a whole-organism or human mitochondrial measurement.
  • At-risk subgroups: Not applicable; this describes a localized, cell-type-specific metabolic program in bone-forming cells, not a patient subgroup risk.
  • Counter-evidence on record: None found; the entry's main caveat is scope (osteoblast-specific, mouse, review-mediated citation) rather than a contradicting result.

Regulatory status

Not addressed in labeling.

Population evidence

Accessed via a narrative review (Journal of Bone and Mineral Research, 2024, "multifaceted roles of mitochondria in osteoblasts") that directly characterizes a mouse osteoblast study: PTH(1-34) "was shown to enhance bone formation by activating aerobic glycolysis and preventing glucose entry into the TCA cycle via IGF signaling in mouse osteoblasts," and pharmacologically forcing glucose back into the TCA cycle (dichloroacetate) abrogated the PTH-induced bone-mass increase. The primary study behind this citation was not independently opened during this review; this entry rests on the review's characterization, disclosed here rather than presented as if the primary paper were read directly.

Mechanism

Named: IGF-signaling-mediated diversion of glucose from mitochondrial oxidative phosphorylation toward aerobic glycolysis (a Warburg-like shift) in differentiating osteoblasts, functionally required for PTH's anabolic bone effect per the dichloroacetate-reversal experiment described.

Counter-evidence held on record

This is a mechanism clarification, not a nutrient-style deficiency claim, per hard rule 2: it describes how teriparatide builds bone in osteoblasts specifically, and must never be presented as evidence of systemic mitochondrial harm or as a reason to recommend mitochondrial-support supplementation. Shares its underlying source with the ATP production entry below; see Overlap map.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress, reduced in two independent animal/cell models, no human data, protective direction

Yellow — Low

See study details

Two independent drug-specific animal and cell studies found teriparatide reduces oxidative stress markers and activates antioxidant pathways, a consistent protective signal with no human confirmation yet.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Key negative/null findings: No human oxidative-stress-marker study in teriparatide-treated patients was found; both supporting sources are animal/cell models in disease contexts (glucocorticoid-induced osteoporosis, spinal cord injury) outside teriparatide's primary osteoporosis indication population.
  • At-risk subgroups: Not applicable; this is a described benefit signal in disease models, not a described risk, and has not been tested in the general osteoporosis population using teriparatide for its approved indication.
  • Counter-evidence on record: No study found showing teriparatide worsening oxidative stress markers; the main limitation is the total absence of human data and the use of non-approved-indication disease models.

Regulatory status

Not addressed in labeling.

Population evidence

Study 1 (in vitro/in vivo): MLO-Y4 osteocyte cell line (teriparatide 10 nmol/L) and Sprague-Dawley rats (n=20, 10/group, dexamethasone-induced osteoporosis model, intramuscular teriparatide). ROS (DCFH-DA assay) reduced with teriparatide co-treatment; SOD2 mRNA (control 1.0 ± 0.13, dexamethasone 0.42 ± 0.11, dexamethasone+teriparatide 0.72 ± 0.04, p<0.05) and catalase mRNA (control 1.0 ± 0.14, dexamethasone 0.37 ± 0.17, dexamethasone+teriparatide 0.64 ± 0.21, p<0.05) both partially restored. Study 2 (in vivo): 138 male Sprague-Dawley rats, spinal cord injury model, teriparatide 20 mcg/kg/day subcutaneously for 14 days. Malondialdehyde fell (day 14: 0.42 ± 0.03 vs saline 1.22 ± 0.13, p<0.001); glutathione peroxidase activity rose (0.5 ± 0.03 vs 0.16 ± 0.03, p<0.001); Nrf2 rose (2.87 ± 0.13 vs 0.82 ± 0.06, p<0.001) with elevated downstream HO-1 and SOD2, partially reversed by the Nrf2 inhibitor ML385, confirming pathway specificity.

Mechanism

Named in both: study 1 proposes an AKT-pathway route suppressing caspase-3-driven apoptosis; study 2 identifies the Nrf2/HO-1 antioxidant-response pathway directly, with pharmacological blockade partially reversing the effect, the stronger mechanistic case of the two.

Counter-evidence held on record

This is a reverse-direction (protective) finding in animal/cell models only: it should never be presented as evidence that antioxidant supplementation is unnecessary during teriparatide treatment, nor generalized to humans or to the approved osteoporosis indication without direct confirmation.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Copper

Not graded — disclosed evidence gap

See study details

No tier B or C evidence, and no circulating consumer claim, connecting teriparatide to copper status was found.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: The dual condition for ungraded is met: a Crossref API query for teriparatide plus copper returned only generic teriparatide regulatory/pharmacopoeia entries with no copper content, and web searches across several phrasings (serum copper, trace elements, copper and osteoporosis) returned only general copper-and-bone-density literature with no teriparatide-specific study and no consumer nutrient-depletion claim naming copper for this drug. Teriparatide's pharmacokinetic profile (Step 1) gives no plausible mechanism either: it is a subcutaneously injected peptide with no gastrointestinal absorption step to chelate or compete at, no CYP450 involvement, and no known copper-cofactor dependency in its proteolytic clearance pathway. Access note: PubMed's article pages, PMC full-text pages, and the Europe PMC and Semantic Scholar search interfaces returned bot-verification challenges or were disallowed by robots.txt for direct querying during this review, and this session's web-search allowance was exhausted before every possible phrasing could be tried; this is disclosed as a tooling limitation, not treated as further confirming the gap.

Iron

Not graded — disclosed evidence gap

See study details

No tier B or C evidence, and no circulating consumer claim, connecting teriparatide to iron status (ferritin, transferrin saturation, serum iron) was found; adjacent hematopoietic stem cell and anemia data (see Oxygen delivery/utilization) do not measure iron status itself and were deliberately not used to support a grade here.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. Ungraded

Limits on what this shows

  • Why no grade: The dual condition for ungraded is met: a Crossref API query for teriparatide plus iron/ferritin returned entirely unrelated iron-metabolism literature with no teriparatide-specific match, and web searches (serum iron, ferritin, transferrin, "teriparatide iron metabolism erythropoiesis hemoglobin") returned only general erythropoiesis-iron physiology reviews with no teriparatide-specific connection. The hematopoietic stem cell mobilization finding and the reversible-anemia case report under Oxygen delivery/utilization concern red-cell production and marrow progenitor activity, not ferritin, transferrin saturation, or other direct iron-status markers; using them here would double count one signal as two findings, so they were intentionally excluded from this entry. Access note: PubMed's article pages, PMC full-text pages, and the Europe PMC and Semantic Scholar search interfaces returned bot-verification challenges or robots.txt disallowals during this review, and this session's web-search allowance was exhausted before every possible phrasing could be tried; this is a disclosed tooling limitation, not a confirmed absence beyond what the channels actually used could show.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk, compositional shift toward SCFA-producing genera, protective direction

Orange — Moderate

See study details

A drug-specific human study found teriparatide measurably enriches two short-chain-fatty-acid-producing gut bacterial genera that correlate with bone density gains, a real but single-study compositional finding running in a protective, not disruptive, direction.

Full detail and limits

What the grade means here: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit. Orange

Limits on what this shows

  • Key negative/null findings: No diversity-loss or dysbiosis marker was reported for the teriparatide arm in the material reviewed; the direction found was enrichment of beneficial SCFA-producing taxa, not depletion.
  • At-risk subgroups: Not established; this is a described compositional shift, not a described risk, in a postmenopausal-fracture population.
  • Counter-evidence on record: Non-randomized, open-label design with no untreated control arm limits attribution; a denosumab comparator arm exists but does not test either drug against no treatment, so natural post-fracture or perimenopausal microbiome shifts cannot be fully excluded.

Regulatory status

Not addressed in labeling.

Population evidence

Archives of Osteoporosis, 2026. Non-randomized, open-label, head-to-head comparative study, 108 completers (mean age 64.8 ± 8.4 years): 68 on teriparatide 20 mcg/day subcutaneously, 40 on denosumab 60 mg every 6 months, both arms with concomitant calcium and vitamin D, 6-month duration. Fecal 16S rDNA sequencing found teriparatide significantly enriched Dubosiella and Butyrivibrio; Dubosiella abundance correlated positively with L4 and hip bone mineral density, Butyrivibrio with L2 bone mineral density. Osteocalcin, a bone-formation marker, rose significantly more with teriparatide than denosumab (p<0.001), consistent with teriparatide's anabolic mechanism.

Mechanism

Not fully elaborated in the source; the authors' framing links the microbiota shift to the drug's bone-anabolic, high-bone-turnover mechanism rather than to a gut-toxicity or absorption-interference pathway (mechanism class G, adjacent to microbiome disruption, but not disruption in this case).

Counter-evidence held on record

This is a protective-direction finding: it should never be presented as evidence of microbiome harm, and should never be used to suggest probiotic supplementation is necessary or that it substitutes for the drug's monitoring requirements; it is reported here to prevent a reader mistaking the required category as automatically a risk category.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

Oxygen delivery/utilization, stem-cell mobilization confirmed, red-cell effect null

Yellow — Low

See study details

A 24-month human cohort found teriparatide significantly increases circulating hematopoietic stem cells without changing red blood cell counts, while a separate case report describes mild, reversible anemia, leaving a genuinely mixed record short of a clear oxygen-delivery signal.

Full detail, limits and 2 references

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Key negative/null findings: The Yu et al cohort's explicit finding of no significant red blood cell change is the most informative result available and is reported here as a genuine null for the oxygen-delivery question specifically, distinct from the positive stem-cell-mobilization finding.
  • At-risk subgroups: Not established; the case report involved sequential use of two different PTH formulations, complicating attribution to teriparatide specifically.
  • Counter-evidence on record: A second relevant title (Grabmaier et al, Internal Medicine Journal 2015, on hematopoietic stem cell mobilization in teriparatide-treated patients) could not be opened during this review (403/429 responses); it is listed in Sources but not used as supporting evidence.

Regulatory status

Not addressed in labeling.

Population evidence

Yu et al, Journal of Bone and Mineral Research, 2014. Prospective longitudinal trial, 23 postmenopausal women at high fracture risk (18 with baseline hematopoietic stem cell measurements), teriparatide 20 mcg subcutaneously daily for 24 months, flow cytometry (ISHAGE-guideline CD34+/CD45-moderate) at baseline, 3, 6, 12, 18, and 24 months. Hematopoietic stem cells increased 40% ± 14% by month 3 (p=0.004), remained elevated at 6 months (p=0.013) and 18 months (p=0.044), and returned to baseline by 24 months. Complete blood count with differential showed no significant change in red blood cells, total B cells, T cells, or transitional B cells. Separately, a case report (Journal of Bone and Mineral Metabolism, 2009) of a postmenopausal woman treated sequentially with full-length PTH(1-84) and then teriparatide (PTH 1-34) described mild, asymptomatic, normochromic normocytic anemia that was more pronounced with PTH(1-84) than with teriparatide and reversed with discontinuation of each.

Mechanism

Proposed but not fully established: PTH signaling is known to act on the bone marrow hematopoietic stem cell niche (early osteoblast/osteoblastic niche cells), plausibly via Wnt signaling, which could mobilize stem cells without necessarily changing mature red-cell output; the case report's authors propose a general PTH-mediated suppression of erythropoiesis based on prior literature, a different and not fully reconciled mechanism from the stem-cell-mobilization finding.

Counter-evidence held on record

Do not present as an established anemia or oxygen-delivery risk; the best-powered human data found showed no red blood cell change, and the case report used a different PTH formulation as well as teriparatide. Anemia in an osteoporosis population has many causes; do not attribute a hemoglobin change to teriparatide without excluding these.

ATP production, glycolytic

Yellow — Low

See study details

The same mouse osteoblast mechanism that reprograms mitochondrial substrate use also means ATP generation shifts toward glycolysis during PTH(1-34)-driven bone formation, a tissue-specific finding about how the drug works, not a measurement of whole-body ATP output.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

  • Key negative/null findings: No direct ATP-output or whole-body energy-expenditure measurement in teriparatide-treated humans or animals was found; per the tightened evidentiary standard for functional claims, a pathway-level substrate shift in one cell type is not the same as a systemic ATP-production claim, and this entry is written and framed accordingly.
  • At-risk subgroups: Not applicable; cell-type-specific finding, not a patient subgroup risk.
  • Counter-evidence on record: None found; the gap is the absence of any direct systemic energetic measurement, not a contradicting result.

Regulatory status

Not addressed in labeling.

Population evidence

Same review-mediated source as the Mitochondrial burden entry: aerobic glycolysis activation with blocked TCA-cycle glucose entry in mouse osteoblasts under PTH(1-34) signaling, with the anabolic bone effect abolished when glucose was pharmacologically forced back into oxidative (TCA/mitochondrial) metabolism.

Mechanism

Named: aerobic glycolysis (substrate-level ATP generation) substitutes for mitochondrial oxidative phosphorylation as the dominant ATP source in differentiating osteoblasts during PTH-driven anabolism; this is upstream cell biology, not a direct whole-body ATP measurement.

Counter-evidence held on record

Do not present as evidence that teriparatide increases or decreases whole-body cellular energy or causes fatigue; the source describes a substrate-preference shift within bone-forming cells specifically, functionally tied to the drug's own therapeutic mechanism, not a systemic ATP deficit. Shares its underlying source with the Mitochondrial burden entry above; see Overlap map.

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

  • Coenzyme Q10

    Where it comes from: Automated "frequently checked together" interaction-checker listings (e.g. Drugs.com) that pair teriparatide with CoQ10 without describing any actual documented interaction or mechanism, echoing generic "drug mugging" style depletion lists built for the mevalonate-pathway drugs (chiefly statins).

    Why it fails: Teriparatide is a 34-amino-acid peptide administered subcutaneously and cleared by non-specific proteolysis; it does not act on the mevalonate/HMG-CoA reductase pathway or any other CoQ10 biosynthetic step, and has no gastrointestinal absorption step to interfere with co-administered CoQ10. No drug-specific or PTH-class study measuring CoQ10 status with teriparatide was found.

  • Vitamin B12

    Where it comes from: Automated "frequently checked together" interaction-checker listings that pair teriparatide with vitamin B12, echoing depletion lists more legitimately built for acid-suppressing drugs (PPIs, H2 blockers) and metformin.

    Why it fails: Teriparatide has no acid-suppression mechanism, no intrinsic-factor interference, and no metformin-like ileal-absorption mechanism; as a subcutaneous injection it bypasses the entire gastric-acid/intrinsic-factor/terminal-ileum B12 absorption pathway entirely. No drug-specific or PTH-class study measuring B12 status was found.

  • Zinc

    Where it comes from: Generic mineral-depletion lists that append zinc to long-term prescription-medication lists broadly, without drug-level stratification.

    Why it fails: No chelation, gastric-pH, or urinary zinc-wasting mechanism is documented for teriparatide, and no drug-specific or PTH-class study measuring zinc status with teriparatide was found despite a targeted Crossref and web search.

All references used above
  1. FORTEO (teriparatide) injection, solution, prescribing information. — DailyMed, U.S. National Library of Medicine, Eli Lilly and Company. Regulatory label, setid aae667c5-381f-4f92-93df-2ed6158d07b0.
  2. Begin MJ, et al. Hypomagnesemia During Teriparatide Treatment in Osteoporosis: Incidence and Determinants. — Journal of Bone and Mineral Research, 2018;33(8):1444. Retrospective cohort, n=53, single center. Abstract accessed via Oxford Academic.
  3. SAT-801: Hypomagnesemia associated with Teriparatide (Forteo) administration due to Hypermagnesuria. — Endocrine society abstract/case series, mechanism proposal for the Begin et al finding.Could not be opened: PMC returned a bot-verification (reCAPTCHA) challenge page on every fetch attempt during this review. Listed only, not used as supporting evidence beyond its title.
  4. A clinical study on the effects of teriparatide and denosumab on bone metabolism and gut microbiota in osteoporotic fracture patients. — Archives of Osteoporosis, 2026. Non-randomized, open-label, comparative study, n=108 (68 teriparatide, 40 denosumab), 6 months, 16S rDNA fecal sequencing.
  5. Yu EW, et al. Teriparatide (PTH 1-34) Treatment Increases Peripheral Hematopoietic Stem Cells in Postmenopausal Women. — Journal of Bone and Mineral Research, 2014;29(6):1380. Prospective longitudinal trial, n=23 (18 with longitudinal HSC data), teriparatide 20 mcg/day SC, 24 months. PMC4564394.
  6. Mobilisation of haemopoietic stem cells in teriparatide-treated patients. — Grabmaier, Internal Medicine Journal, 2015. Relevant to Oxygen delivery/utilization.Could not be opened: Wiley returned a 403 error, and a PubMed follow-up returned a 429/bot-verification response. Listed only, not used as supporting evidence.
  7. Normochromic normocytic anemia in a postmenopausal woman with severe osteoporosis treated with intermittent parathyroid hormone. — Journal of Bone and Mineral Metabolism, 2009. Case report, sequential PTH(1-84) then teriparatide (PTH 1-34) treatment.
  8. Role of Teriparatide in Glucocorticoid-induced Osteoporosis through Regulating Cellular Reactive Oxygen Species. — In vitro (MLO-Y4 osteocytes, teriparatide 10 nmol/L) and in vivo (Sprague-Dawley rats, n=20, dexamethasone-induced osteoporosis model) study. PMC6594530.
  9. Teriparatide mitigates oxidative stress following spinal cord injury and enhances neurological recovery via the Nrf2/HO-1 signaling pathway. — Frontiers in Pharmacology, 2025. In vivo rat study, n=138, teriparatide 20 mcg/kg/day SC, 14 days.
  10. Multifaceted roles of mitochondria in osteoblasts: from energy production to mitochondrial-derived vesicle secretion. — Journal of Bone and Mineral Research, 2024. Narrative review; characterizes a mouse osteoblast PTH(1-34) aerobic-glycolysis study (cited within as its reference 44, not independently opened during this review). Used for the Mitochondrial burden and ATP production entries.The primary mouse study this review characterizes was not independently opened; this entry relies on the review's characterization only, as disclosed in the relevant entries.
  11. Mechanisms limiting the long-term anabolic effects of teriparatide (PTH 1-34) on bone. — JBMR Plus. Reviewed for mitochondrial/ATP content; contains none relevant to those categories. Cited to document a checked-but-negative source.
  12. Increased fatty acid availability improves the osteo-anabolic effects of intermittent parathyroid hormone (iPTH) in murine models. — Animal study (mice), intermittent human PTH(1-34) 100 mcg/kg SC, 4 weeks, plus dietary/oleic-acid fatty-acid manipulation. Bone-outcome study without direct mitochondrial or ATP measurement; checked and not used to support the Mitochondrial burden/ATP entries beyond background context.
  13. Crossref API queries for teriparatide + copper and teriparatide + iron/ferritin. — Bibliographic search only (api.crossref.org), used to confirm the absence of drug-specific literature for the Copper and Iron ungraded entries. Not a citable study; recorded here for audit transparency.
  14. Teriparatide interactions checker. — Drugs.com. Consumer interaction-checker listing; used to identify CoQ10, vitamin B12, vitamin C, and vitamin K2 as commonly co-searched items with no described mechanism, supporting the Fails verification entries.
  15. Neer RM, et al. Effect of parathyroid hormone (1-34) on fractures and bone mineral density in postmenopausal women with osteoporosis. — New England Journal of Medicine, 2001 (the original Fracture Prevention Trial underlying the label's pooled pivotal-trial data).Could not be opened: NEJM returned a 403 (subscription/paywall) response during this review. The Calcium and Phosphate entries above rely on the DailyMed label's own reporting of this trial's pooled results, not on this primary article directly; listed here for completeness and future re-check.