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<article xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" article-type="case-report" xml:lang="en">
<front>
<journal-meta>
<journal-id journal-id-type="publisher-id">JMH</journal-id>
<journal-title-group>
<journal-title>Journal of Metabolic Health</journal-title>
</journal-title-group>
<issn pub-type="ppub">3105-4323</issn>
<issn pub-type="epub">2960-0391</issn>
<publisher>
<publisher-name>AOSIS</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="publisher-id">JMH-9-128</article-id>
<article-id pub-id-type="doi">10.4102/jmh.v9i1.128</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Case Report</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Synergistic management of metabolic syndrome with postmenopausal osteoporosis: A retrospective case report</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" corresp="yes">
<contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-6333-8514</contrib-id>
<name>
<surname>Tidman</surname>
<given-names>Melanie M.</given-names>
</name>
<xref ref-type="aff" rid="AF0001">1</xref>
<xref ref-type="aff" rid="AF0002">2</xref>
<xref ref-type="aff" rid="AF0003">3</xref>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-1721-4905</contrib-id>
<name>
<surname>Fazzina</surname>
<given-names>Mona</given-names>
</name>
<xref ref-type="aff" rid="AF0001">1</xref>
<xref ref-type="aff" rid="AF0004">4</xref>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-8910-9894</contrib-id>
<name>
<surname>White</surname>
<given-names>Dawn R.</given-names>
</name>
<xref ref-type="aff" rid="AF0005">5</xref>
<xref ref-type="aff" rid="AF0006">6</xref>
<xref ref-type="aff" rid="AF0007">7</xref>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-8550-3317</contrib-id>
<name>
<surname>White</surname>
<given-names>Tim A.</given-names>
</name>
<xref ref-type="aff" rid="AF0007">7</xref>
<xref ref-type="aff" rid="AF0008">8</xref>
<xref ref-type="aff" rid="AF0009">9</xref>
</contrib>
<aff id="AF0001"><label>1</label>School of Health Sciences, Liberty University, Lynchburg, Virginia, United States of America</aff>
<aff id="AF0002"><label>2</label>College of Graduate Health Studies, A.T. Still University, Mesa, Arizona, United States of America</aff>
<aff id="AF0003"><label>3</label>Department of Occupational Therapy, Nova Southeastern University, Ft Lauderdale, Florida, United States of America</aff>
<aff id="AF0004"><label>4</label>School of Education, Liberty University, Lynchburg, Virginia, United States of America</aff>
<aff id="AF0005"><label>5</label>School of Health Professions, National University, San Diego, California, United States of America</aff>
<aff id="AF0006"><label>6</label>Glaser Center for Grounded Theory, Institute for Research and Theory Methodologies, Poway, California, United States of America</aff>
<aff id="AF0007"><label>7</label>Benerd College, University of the Pacific, Stockton, California, United States of America</aff>
<aff id="AF0008"><label>8</label>School of Health Sciences, American Public University Systems, Charles Town, West Virginia, United States of America</aff>
<aff id="AF0009"><label>9</label>School of Health Sciences, University of Maryland Global Campus, Adelphi, Maryland, United States of America</aff>
</contrib-group>
<author-notes>
<corresp id="cor1"><bold>Corresponding author:</bold> Melanie Tidman, <email xlink:href="mtidman@liberty.edu">mtidman@liberty.edu</email></corresp>
</author-notes>
<pub-date pub-type="epub"><day>14</day><month>02</month><year>2026</year></pub-date>
<pub-date pub-type="collection"><year>2026</year></pub-date>
<volume>9</volume>
<issue>1</issue>
<elocation-id>128</elocation-id>
<history>
<date date-type="received"><day>03</day><month>09</month><year>2025</year></date>
<date date-type="accepted"><day>26</day><month>11</month><year>2025</year></date>
</history>
<permissions>
<copyright-statement>&#x00A9; 2026. The Authors</copyright-statement>
<copyright-year>2026</copyright-year>
<license license-type="open-access" xlink:href="https://creativecommons.org/licenses/by/4.0/">
<license-p>Licensee: AOSIS. This work is licensed under the Creative Commons Attribution 4.0 International (CC BY 4.0) license.</license-p>
</license>
</permissions>
<abstract>
<p>Metabolic syndrome (MetS) and postmenopausal osteoporosis (POP) commonly coexist, amplifying cardiovascular and fracture risk through shared mechanisms of insulin resistance, inflammation, and impaired energy metabolism. Conventional management often emphasises pharmacotherapy and calcium supplementation, while overlooking the optimisation of metabolic health. Emerging evidence supports nutritional and exercise-based strategies that target both metabolic and skeletal integrity. This study aimed to evaluate the synergistic effects of a low-carbohydrate and ketogenic diet (LCK), resistance training (RT), and bioavailable calcium supplementation on bone mineral density (BMD) and metabolic health in a patient with concurrent POP and MetS. A 65-year-old postmenopausal woman with baseline osteoporosis and MetS provided documentation for a 36-month, three-phase retrospective data analysis. Phase 1 intervention included an LCK (12 months); Phase 2 combined LCK with RT three times per week (12 months); and Phase 3 added daily bioavailable calcium supplementation (12 months). Bone mineral density was assessed via dual-energy X-ray absorptiometry at baseline, 12, 24, and 36 months. Secondary outcomes included metabolic markers, body composition, and inflammatory indices. Progressive increases in BMD <italic>T</italic>-scores were observed across major skeletal sites. Metabolic outcomes included improved biomarker levels and favourable changes in weight and waist circumference. No adverse effects occurred. Sometimes KD nutrition may not be enough to preserve BMD. The integration of ketogenic nutrition, RT, and calcium supplementation may synergistically enhance BMD while improving metabolic health in individuals with POP and MetS. This multimodal approach represents a promising adjunct to standard management of MetS and osteoporosis and warrants validation through controlled clinical studies.</p>
</abstract>
<kwd-group>
<kwd>postmenopausal osteoporosis</kwd>
<kwd>metabolic syndrome</kwd>
<kwd>bone mineral density</kwd>
<kwd>ketogenic diet</kwd>
<kwd>resistance training</kwd>
<kwd>bioavailable calcium supplementation</kwd>
<kwd>metabolic health</kwd>
<kwd>lifestyle interventions</kwd>
</kwd-group>
<funding-group>
<funding-statement><bold>Funding information</bold> This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.</funding-statement>
</funding-group>
</article-meta>
</front>
<body>
<sec id="s0001">
<title>Introduction</title>
<p>Metabolic syndrome (MetS) is prevalent in postmenopausal women and is characterised by central obesity, hypertension, dyslipidaemia, and impaired glucose regulation (Neeland, 2024). Insulin resistance (IR), a defining feature of MetS, contributes to systemic inflammation and the production of reactive oxygen species (ROS), which are implicated in chronic diseases such as obesity, type 2 diabetes, and cardiovascular disease.<sup><xref ref-type="bibr" rid="CIT0001">1</xref></sup> These inflammatory processes negatively affect bone turnover and remodelling, helping to explain the interactions between MetS and IR and the increased risk of osteoporosis.<sup><xref ref-type="bibr" rid="CIT0001">1</xref></sup> Often, changes in nutritional approaches to address MetS and IR are not sufficient to prevent the onset of postmenopausal osteoporosis (POP).</p>
<p>Fractures resulting from POP are among the most serious complications affecting older women, often leading to loss of independence, chronic pain, and increased mortality.<sup><xref ref-type="bibr" rid="CIT0002">2</xref></sup> Postmenopausal osteoporosis develops following menopause, which is clinically defined as the absence of menstruation (amenorrhoea) for 12 consecutive months, when oestrogen deficiency accelerates bone demineralisation and bone microarchitecture.<sup><xref ref-type="bibr" rid="CIT0003">3</xref></sup> Diagnosis is confirmed by dual-energy X-ray absorptiometry (DEXA) scans, which show a bone mineral density (BMD) <italic>T</italic>-score of &#x2013;2.5 or lower compared to young, healthy women, underscoring its role as a widespread skeletal disease affecting millions worldwide.<sup><xref ref-type="bibr" rid="CIT0002">2</xref></sup> Common recommendations for POP include calcium and mineral supplementation and progressive resistance training (PRT) with heavy weights.<sup><xref ref-type="bibr" rid="CIT0004">4</xref>,<xref ref-type="bibr" rid="CIT0005">5</xref></sup></p>
<p>Bone functions as a major endocrine organ, balancing osteoblastic and osteoclastic activity through insulin receptors, insulin-like growth factor-1 (IGF-1), and osteocalcin.<sup><xref ref-type="bibr" rid="CIT0006">6</xref></sup> Disruption of these pathways through IR alters bone metabolism, leading to further declines in BMD and structural integrity. Recent studies in postmenopausal women confirm that moderate forms of IR impair IGF-1 signalling and reduce bone matrix stability, demonstrating the multifactorial nature of POP and highlighting the need for further evidence in this area.<sup><xref ref-type="bibr" rid="CIT0007">7</xref></sup></p>
<p>Amid these complexities, one promising avenue for intervention lies in targeted physical activity such as resistance exercise. Evidence from systematic reviews of randomised controlled trials demonstrates that PRT improves femoral neck and lumbar spine BMD, enhances physical function, and reduces fracture risk, with adverse events being uncommon.<sup><xref ref-type="bibr" rid="CIT0004">4</xref></sup> These findings support PRT as a safe and effective approach for postmenopausal women at risk of osteoporosis, making it a central component of non-pharmacological management strategies.</p>
<p>Another potential strategy includes using calcium and mineral supplementation to address POP, although results remain mixed. Some studies report an increase in cardiovascular complications with calcium supplementation, while others find no adverse outcomes, emphasising the need for longer-term trials to clarify its safety and effectiveness in fracture prevention.<sup><xref ref-type="bibr" rid="CIT0005">5</xref>,<xref ref-type="bibr" rid="CIT0008">8</xref></sup> Despite uncertainty, supplementation remains part of management guidelines because of its potential role in bone density maintenance in older women.</p>
<p>Dietary modification has been explored as an adjunct therapy for MetS, particularly through low-carbohydrate and ketogenic diets (LCK).<sup><xref ref-type="bibr" rid="CIT0009">9</xref></sup> These approaches have demonstrated benefits in improving insulin sensitivity and addressing features of MetS, but their specific effects on POP are less well studied.<sup><xref ref-type="bibr" rid="CIT0010">10</xref></sup> Frequently, LCK limits dairy intake because of evidence of increased inflammation caused by dairy proteins, such as whey.<sup><xref ref-type="bibr" rid="CIT0011">11</xref></sup> As a result of this limitation in dairy intake, people following an LCK diet may need to supplement to preserve BMD, especially in older age. Because adverse effects limit the long-term viability of pharmacological therapies, many women turn to alternative strategies, such as PRT, dietary adjustments, and selective supplementation, to manage the combined symptoms of MetS, IR, and POP.</p>
<p>The purpose of this retrospective data analysis in the form of a single case report is to describe the potential impact of combining an LCK diet, bioavailable calcium and mineral supplementation with AlgaeCal Plus and Strontium Boost (AP-SB) and a structured PRT programme in a postmenopausal woman who initially presented with MetS and developed POP during the year she was on the LCK approach. The case report aims to explore how a multifaceted approach may help to preserve and potentially enhance BMD in a female with MetS on an LCK diet. By presenting a retrospective analysis of data collected from medical reports and DEXA scan documentation provided by the participant, the case offers insight into the potential role of integrative, non-pharmacological, synergistic strategies in managing POP and metabolic health.</p>
</sec>
<sec id="s0002">
<title>Methods</title>
<sec id="s20003">
<title>Participant</title>
<p>A 65-year-old woman from the southwestern United States (US) was recruited through osteoporosis and bone health Facebook groups. After providing informed consent, she participated in a retrospective three-phase study analysing medical records over time. Her history included pre-diabetes, MetS, hypertension, fibromyalgia, and obesity. Baseline assessments included DEXA, Haemoglobin A1c (HbA1c), lipid panel, fasting insulin, hs-CRP, weight, and waist circumference. Results showed metabolic values consistent with MetS (<xref ref-type="table" rid="T0003">Table 3</xref>) but normal bone density at baseline (<italic>T</italic>-score: AP spine = 1.0) (<xref ref-type="table" rid="T0002">Table 2</xref>).</p>
</sec>
<sec id="s20004">
<title>Interventions</title>
<p>The participant, initially diagnosed with MetS, began an LCK diet for 12 months. Medical records were reviewed as she completed three sequential 12-month interventions (<xref ref-type="fig" rid="F0001">Figure 1</xref>). Intervention A included a very low-carbohydrate, reduced-dairy, moderate-protein, high-fat ketogenic diet. After 12 months, she was diagnosed with POP. Intervention B continued the same diet, with the addition of structured PRT using compound barbell exercises three times a week. Intervention C maintained the diet and training while adding daily supplementation with algae-based calcium and minerals.</p>
<fig id="F0001">
<label>FIGURE 1</label>
<caption><p>Timeline of interventions and associated outcome measures.</p></caption>
<graphic xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="JMH-9-128-g001.tif"/>
</fig>
</sec>
<sec id="s20005">
<title>Dietary regimen: Low-carbohydrate and ketogenic diets</title>
<p>During Intervention A, the participant followed a strict reduced-dairy, moderate-protein LCK diet to address MetS. The well-formulated plan included only occasional cheese and cream cheese, with macronutrient targets of fats (65&#x0025; &#x2013; 70&#x0025;), protein (20&#x0025; &#x2013; 25&#x0025;), and carbohydrates (5&#x0025; &#x2013; 10&#x0025;). Nutritional ketosis was monitored daily with a KetoMojo metre; readings above 0.5 mmol/L indicated ketosis. The participant tracked their food intake through the MyFitnessPal app and submitted weekly summaries to the researcher for verification of adherence.</p>
</sec>
<sec id="s20006">
<title>Resistance training regimen</title>
<p>At the end of the first year on a LCK diet, the participant was diagnosed with POP and began Intervention B, which incorporated compound barbell exercises as prescribed by Dr Jonathon Sullivan and Andy Baker.<sup><xref ref-type="bibr" rid="CIT0012">12</xref></sup> Sullivan and Baker targeted four compound movements that incorporate all major muscle groups and mimic movements performed in daily life. The movement regimen included a combination of squats (related to reaching items on the floor), deadlifts (related to picking up heavy items from the floor), bench presses (related to pushing heavy items), and overhead presses (related to lifting heavy items overhead).<sup><xref ref-type="bibr" rid="CIT0012">12</xref></sup></p>
<p>The participant provided written exercise logs to researchers, documenting evidence of progressively adding weight to each exercise, with weights increasing by 0.9 kg per week as tolerated. The PRT protocol consisted of five sets of five repetitions for each exercise, completed in three 1-h sessions per week. The intervention adheres to Sullivan and Baker&#x2019;s resistance protocol, which provides for progression of resistance according to the participant&#x2019;s tolerance.<sup><xref ref-type="bibr" rid="CIT0012">12</xref></sup> High-intensity RT refers to any exercise above 90&#x0025; of the subject&#x2019;s 1-repetition maximum (1RM). Moderate-intensity RT is performed at 50&#x0025; &#x2013; 60&#x0025; of the subject&#x2019;s 1RM, while low-intensity RT, also known as a power-based training protocol, is conducted at 20&#x0025; &#x2013; 50&#x0025; of 1RM.<sup><xref ref-type="bibr" rid="CIT0010">10</xref></sup> During the study, the participant used a moderate-resistance protocol, lifting 50&#x0025; &#x2013; 60&#x0025; of her 1RM. She started at 50&#x0025; of her 1RM and gradually increased to 60&#x0025; as her training load progressed from Intervention B to Intervention C. The participant adhered to the prescribed programme and documented consistent progression within the training protocol.</p>
</sec>
<sec id="s20007">
<title>Supplementation</title>
<p>Intervention C added AP-SB supplementation to the LCK diet and PRT protocols. The selected supplement was AP, together with SB.<sup><xref ref-type="bibr" rid="CIT0013">13</xref></sup> These are proprietary algae-based calcium, mineral, and strontium citrate supplements. The prescribed doses were 2 AP capsules twice daily and 2 SB once daily with meals. The recommended dosage is 2 AP doses, more than 2 h apart, and 2 SB capsules 2 h after the last AP dose, administered daily (algaecal.com) (<xref ref-type="table" rid="T0001">Table 1</xref>).</p>
<table-wrap id="T0001">
<label>TABLE 1</label>
<caption><p>Supplement facts of the AlgaeCal bone health supplement.</p></caption>
<table frame="hsides" rules="groups">
<thead>
<tr>
<th valign="top" align="left">Ingredient</th>
<th valign="top" align="center">Amount</th>
</tr>
</thead>
<tbody>
<tr>
<td align="left">Elemental strontium (from citrate) (mg)</td>
<td align="center">680</td>
</tr>
<tr>
<td align="left">Trace minerals (mg)</td>
<td align="center">1608</td>
</tr>
<tr>
<td align="left">Calcium (mg)</td>
<td align="center">720</td>
</tr>
<tr>
<td align="left">Magnesium (mg)</td>
<td align="center">72</td>
</tr>
<tr>
<td align="left">Vitamin D3 (IU)</td>
<td align="center">1600</td>
</tr>
<tr>
<td align="left">Vitamin K as MK-7 (mcg)</td>
<td align="center">100</td>
</tr>
<tr>
<td align="left">Boron (mg)</td>
<td align="center">3</td>
</tr>
<tr>
<td align="left">Vitamin C (mg)</td>
<td align="center">50</td>
</tr>
</tbody>
</table>
</table-wrap>
</sec>
<sec id="s20008">
<title>Biomarker testing and imaging</title>
<p>Blood samples were collected at baseline and at 12-, 24-, and 36-month intervals, including measurements of triglycerides, high-density lipoprotein (HCL), fasting insulin, HbA1c, C-reactive protein, C-telopeptide (CTX), and procollagen type 1 N-terminal propeptide (P1NP), as well as weight and waist circumference. The P1NP/CTX ratio was calculated to assess bone turnover. Bone mineral density was measured by DEXA (GE Lunar iDXA) of the spine, femoral neck, and total hip at the same intervals. The World Health Organization (WHO) criteria guided the classifications of MetS and osteoporosis <italic>T</italic>-scores.<sup><xref ref-type="bibr" rid="CIT0002">2</xref></sup> All assays were chemiluminescence immunoassays (CLIA)-certified, and KetoMojo tracking confirmed sustained nutritional ketosis (&#x03B2;-hydroxybutyrate &#x003E; 0.5 mmol/L) throughout the 36-month study.</p>
<p>Results are presented for imaging and bone turnover markers (<xref ref-type="table" rid="T0002">Table 2</xref>) and for biomarkers (laboratory values, weight, and waist measurements) (<xref ref-type="table" rid="T0003">Table 3</xref>).</p>
<table-wrap id="T0002">
<label>TABLE 2</label>
<caption><p>Bone mineral density <italic>T</italic>-scores and biochemical bone marker results.</p></caption>
<table frame="hsides" rules="groups">
<thead>
<tr>
<th valign="top" align="left">BMD</th>
<th valign="top" align="center">Baseline</th>
<th valign="top" align="center">Intervention A (12 months)</th>
<th valign="top" align="center">Change (&#x0394;T units)</th>
<th valign="top" align="center">Intervention B (24 months)</th>
<th valign="top" align="center">Change (&#x0394;T)</th>
<th valign="top" align="center">Intervention C (36 months)</th>
<th valign="top" align="center">Change (&#x0394;T)</th>
</tr>
</thead>
<tbody>
<tr>
<td align="left">AP Spine (<italic>T</italic>-Score)</td>
<td align="center">1.0</td>
<td align="center">&#x2212;2.5</td>
<td align="center">&#x2212;1.5</td>
<td align="center">&#x2212;1.9</td>
<td align="center">+0.6</td>
<td align="center">&#x2212;1.2</td>
<td align="center">+0.7</td>
</tr>
<tr>
<td align="left">Rt Femoral Neck (<italic>T</italic>-Score)</td>
<td align="center">0.9</td>
<td align="center">&#x2212;1.9</td>
<td align="center">&#x2212;1.8</td>
<td align="center">&#x2212;1.4</td>
<td align="center">+0.5</td>
<td align="center">&#x2212;1.4</td>
<td align="center">0.0</td>
</tr>
<tr>
<td align="left">Rt Total Hip (<italic>T</italic>-Score)</td>
<td align="center">1.5</td>
<td align="center">&#x2212;1.4</td>
<td align="center">&#x2212;2.9</td>
<td align="center">&#x2212;1.5</td>
<td align="center">&#x2212;0.1</td>
<td align="center">&#x2212;1.4</td>
<td align="center">+0.1</td>
</tr>
<tr>
<td align="left">P1NP (ng/mL)</td>
<td align="center">1.5</td>
<td align="center">47.2</td>
<td align="center">&#x2212;13.8</td>
<td align="center">59</td>
<td align="center">+11.8</td>
<td align="center">61</td>
<td align="center">+2</td>
</tr>
<tr>
<td align="left">CTX (pg/mL)</td>
<td align="center">527</td>
<td align="center">324</td>
<td align="center">&#x2212;203</td>
<td align="center">564</td>
<td align="center">+240</td>
<td align="center">432</td>
<td align="center">&#x2212;132</td>
</tr>
<tr>
<td align="left">CTX/P1NP Ratio Desired Range (&#x003E; 10:1 &#x2013; &#x003E; 10:2)</td>
<td align="center">10:0.10</td>
<td align="center">10:1.14</td>
<td align="center">-</td>
<td align="center">10:1.36</td>
<td align="center">-</td>
<td align="center">10:1.08</td>
<td align="center">-</td>
</tr>
</tbody>
</table>
<table-wrap-foot>
<fn><p>BMD, bone mineral density; AP, AlgaeCal Plus; CTX, C-telopeptide; P1NP, procollagen type 1 N-terminal propeptide.</p></fn>
</table-wrap-foot>
</table-wrap>
<table-wrap id="T0003">
<label>TABLE 3</label>
<caption><p>Biomarkers.</p></caption>
<table frame="hsides" rules="groups">
<thead>
<tr>
<th valign="top" align="left">Biomarker</th>
<th valign="top" align="center">Baseline</th>
<th valign="top" align="center">Intervention A (12 Months)</th>
<th valign="top" align="center">Intervention B (24 Months)</th>
<th valign="top" align="center">Intervention C (36 Months)</th>
</tr>
</thead>
<tbody>
<tr>
<td align="left">Triglycerides (mmol/L)</td>
<td align="center">1.98</td>
<td align="center">1.670</td>
<td align="center">0.65</td>
<td align="center">0.395</td>
</tr>
<tr>
<td align="left">HDL (mmol/L)</td>
<td align="center">0.34</td>
<td align="center">0.730</td>
<td align="center">1.01</td>
<td align="center">1.060</td>
</tr>
<tr>
<td align="left">HbA1C (mmol/mol)</td>
<td align="center">44.00</td>
<td align="center">37.000</td>
<td align="center">38.00</td>
<td align="center">37.000</td>
</tr>
<tr>
<td align="left">Insulin (pmol/L)</td>
<td align="center">39.44</td>
<td align="center">38.194</td>
<td align="center">27.08</td>
<td align="center">30.000</td>
</tr>
<tr>
<td align="left">hs-CRP (umol/L)</td>
<td align="center">1.42</td>
<td align="center">0.790</td>
<td align="center">0.56</td>
<td align="center">0.330</td>
</tr>
<tr>
<td align="left">Weight (kg)</td>
<td align="center">77.11</td>
<td align="center">70.300</td>
<td align="center">67.58</td>
<td align="center">65.770</td>
</tr>
<tr>
<td align="left">Waist circumference (cm)</td>
<td align="center">88.90</td>
<td align="center">86.360</td>
<td align="center">83.82</td>
<td align="center">81.280</td>
</tr>
</tbody>
</table>
</table-wrap>
</sec>
<sec id="s20009">
<title>Ethical considerations</title>
<p>Participant recruitment, study design, methods, data collection strategies, and data analysis were subject to ethics review and oversight by the Institutional Review Board at Liberty University (Protocol # IRB-FY24-25-602), Lynchburg, Virginia, US.</p>
</sec>
</sec>
<sec id="s0010">
<title>Results</title>
<p>Results are presented for imaging and bone turnover markers (<xref ref-type="table" rid="T0002">Table 2</xref>), and for biomarkers (laboratory values, weight, and waist measurements) (<xref ref-type="table" rid="T0003">Table 3</xref>).</p>
</sec>
<sec id="s0011">
<title>Discussion</title>
<sec id="s20012">
<title>Intervention A</title>
<sec id="s30013">
<title>Dietary intervention</title>
<p>Problems related to IR, MetS, and BMD tend to increase with age, particularly among postmenopausal women.<sup><xref ref-type="bibr" rid="CIT0014">14</xref></sup> An increasing number of women in this group are choosing non-pharmacological approaches to manage metabolic dysfunction and bone loss, favouring nutrition, lifestyle modification, exercise, and supplementation. The present case describes a 65-year-old woman with MetS, who adopted this multifaceted strategy; however, adherence to the LCK diet alone did not prevent the development of POP after 12 months.</p>
<p>The relationship between POP and IR has been well documented, as has the effectiveness of an LCK diet in reducing IR and improving markers such as glucose, waist circumference, triglycerides, HDL, and blood pressure.<sup><xref ref-type="bibr" rid="CIT0015">15</xref></sup> In this study, baseline biomarkers showed progressive improvement. Fasting insulin declined from 39.44 pmol/L at baseline to 27.08 pmol/L at 24 months (Interventions A and B) before a slight rise to 30.0 pmol/L at 36 months. Waist circumference decreased from 88.90 cm to 81.28 cm, while weight dropped from 77.1 kg at baseline to 65.77 kg by 36 months (Intervention C) (<xref ref-type="table" rid="T0002">Table 2</xref>). Our participant met four of the five MetS criteria, qualifying her for the diagnosis, which can be managed through an LCK diet that lowers blood glucose, insulin, and IR.<sup><xref ref-type="bibr" rid="CIT0016">16</xref></sup> Greere et al. found that the functions of insulin and IGF-1 have a greater influence on BMD than previously recognised. As IGF-1 levels decline in postmenopausal women, the risk of fractures rises independently of BMD.<sup><xref ref-type="bibr" rid="CIT0014">14</xref></sup> The role of insulin and related growth factors in age-related BMD loss warrants further study. Despite improvements in MetS biomarkers during Intervention A, the participants&#x2019; BMD declined, likely because of reduced-dairy intake and a lack of calcium or mineral supplementation.</p>
<p>In a systematic review examining the relationship between low carbohydrate healthy fat (LCHF) or low carbohydrate and ketogenic diet (LCK) and bone health, seven trials were identified in which no significant effects on BMD were observed, despite participants experiencing greater weight loss and increases in serum vitamin D levels compared with controls.<sup><xref ref-type="bibr" rid="CIT0004">4</xref></sup> In contrast, a systematic review by Nieman et al.<sup><xref ref-type="bibr" rid="CIT0010">10</xref></sup> discussed the relationship between dairy product intake and inflammation, with potential effects on inflammatory markers. These results may prompt people on an LCK diet to limit their intake of dairy products to address symptoms of MetS and IR, which was the case in our participant between baseline and 12 months. Based on a review of our participants&#x2019; medical records, the onset of POP occurred after 12 months on an LCK diet. Taken together, these findings provide a rationale for using an LCK diet as the foundational dietary strategy to address symptoms of MetS and IR, as in Intervention A, and for the potential need for dairy products or supplementation to support BMD. Our case supports this supposition, as the participant experienced a decline in BMD during Intervention A while consuming an LCK diet, with no calcium or mineral supplementation and limited dairy intake; her lumbar spine <italic>T</italic>-score declined from 1.0 at baseline to &#x2013;2.5 at 12 months (&#x0394; = &#x2013;1.5 units).</p>
</sec>
</sec>
<sec id="s20014">
<title>Intervention B</title>
<sec id="s30015">
<title>Resistance training</title>
<p>Historically, heavy RT was not recommended for women with BMD problems because of the possible risk of fractures.<sup><xref ref-type="bibr" rid="CIT0017">17</xref></sup> Current research has shown that even low-repetition, light-load power training can facilitate BMD.<sup><xref ref-type="bibr" rid="CIT0017">17</xref></sup> Therefore, high-intensity RT may not be appropriate for some women, given their history of fractures and falls.<sup><xref ref-type="bibr" rid="CIT0018">18</xref></sup> This restriction may apply to sedentary women at risk for osteoporosis and those who are resistant to engaging in heavy loads. Our participants&#x2019; results were comparable to those of a previous study, in which BMD increased with the addition of PRT to an LCK diet during the Intervention B protocol period.<sup><xref ref-type="bibr" rid="CIT0018">18</xref></sup> A systematic analysis of RCTs reported that the average frequency of training across studies was three times per week (median, <italic>n</italic> = 2) and that the duration ranged from 1 month to 30 months (median, <italic>n</italic> = 6).<sup><xref ref-type="bibr" rid="CIT0004">4</xref></sup> These results are commensurate with our study, although our participants engaged in PRT three times a week.</p>
<p>The Lifting Intervention for Training Muscle and Osteoporosis Rehabilitation (LIFTMOR) trial was a randomized clinical trial (RCT) by Watson et al. investigating the use of multi-joint compound exercises &#x2013; squat and deadlift &#x2013; which involved extensive muscle recruitment to address BMD at the spine and hip. The study included postmenopausal women over 8 months, with a control group (<italic>n</italic> = 52) and an intervention group (<italic>N</italic> = 49).<sup><xref ref-type="bibr" rid="CIT0017">17</xref></sup> Intervention B for our patient involved thrice-weekly sessions of compound barbell exercise. Similarly, Watson et al.<sup><xref ref-type="bibr" rid="CIT0017">17</xref></sup> found that moderate exercise improved bone mineral content and modestly increased BMD compared with a control group. Consistent with these findings, the BMD <italic>T</italic>-scores of our participant improved from baseline to the 36-week assessment (<xref ref-type="table" rid="T0001">Table 1</xref>).</p>
<p>In addition, the study demonstrated that a combination of lower-frequency, moderate-intensity (50&#x0025; &#x2013; 60&#x0025; of 1RM) RT and weight-bearing exercise prevents bone loss in an older adult female, consistent with findings from a recent systematic review.<sup><xref ref-type="bibr" rid="CIT0019">19</xref></sup> The participant completed PRT three times a week and continued her other daily routines, including walking. In another study investigating RT, the exercise consisted of 8&#x2013;10 target repetitions, performed in 2&#x2013;3 sets, twice a week, under supervised PRT at moderate intensity (approximately 10 repetitions maximum), and progressed to high-intensity PRT (&#x2264; 6 repetitions maximum).<sup><xref ref-type="bibr" rid="CIT0010">10</xref></sup> Similarly, our participant performed five sets of five repetitions for each of four exercises (squats, deadlifts, bench press, and overhead press), increasing the load by 0.09 kg each week, aligning with previous interventions using compound movements and progressive loading.<sup><xref ref-type="bibr" rid="CIT0004">4</xref></sup> Resistance training increases insulin sensitivity by activating muscle through increased muscle mass and enhanced glucose uptake, thereby helping to regulate circulating blood glucose.<sup><xref ref-type="bibr" rid="CIT0014">14</xref></sup> Our participant had a baseline HbA1c of 44 mmol/mol. After starting the LCK diet, her HbA1c dropped from 44 mmol/mol to 37 mmol/mol (12 months). With the addition of PRT, her HbA1c level remained steady at 38 mmol/mol at 24 months and 37 mmol/mol at 36 months. In addition, we cannot ignore the improvements in BMD, specifically in the A-P Spine, from 12 months (<italic>T</italic> Score = &#x2013;2.5) to 24 months (<italic>T</italic> Score = &#x2013;1.9) with the addition of PRT to the LCK diet. This improvement in BMD may also be attributed to the combination of PRT and the reduction of IR in our subject, along with the associated reduction in her symptoms of MetS.<sup><xref ref-type="bibr" rid="CIT0007">7</xref>,<xref ref-type="bibr" rid="CIT0018">18</xref></sup></p>
</sec>
</sec>
<sec id="s20016">
<title>Intervention C</title>
<sec id="s30017">
<title>Bone mineral density and supplementation</title>
<p>Evidence from Kaats et al. suggests that, over several years, the use of calcium- and plant-based mineral-containing supplements increased BMD without adverse changes in blood chemistry or lipid profiles in a study population with demographics similar to those of our participant.<sup><xref ref-type="bibr" rid="CIT0008">8</xref></sup> Similarly, our participant experienced an increase in <italic>t</italic>-scores for BMD with the addition of the AP-SB supplement, which moved her from an osteoporosis diagnosis to the osteopenia range for her lumbar spine (&#x0394;<italic>T</italic> = &#x2013;1.5 units) (<italic>T</italic>-Score: &#x2013;1.9, increasing to &#x2013;1.2 at 36 months).</p>
<p>In our case report, the addition of a daily AP-SB calcium or mineral supplement to the LCK diet and PRT (Intervention B) was associated with improved lumbar spine BMD <italic>T</italic>-scores, with smaller gains at the femoral neck and total hip (<xref ref-type="table" rid="T0001">Table 1</xref>). These findings align with the improvements the women reported in Kaats et al. longitudinal trial and are noteworthy, given the age of our participant (65 years) at the onset of this case report. In the Bristow et al.<sup><xref ref-type="bibr" rid="CIT0020">20</xref></sup> study, outcomes for this age group were considered inconsistent. It is worth noting that our participant did not experience any adverse cardiovascular effects during the study, which is consistent with prior safety findings.<sup><xref ref-type="bibr" rid="CIT0020">20</xref></sup></p>
<p>For bone markers, Serum P1NP decreased from 61 ng/mL at baseline to 47.2 ng/mL after 12 months (&#x0394; = &#x2013;13.8 ng/mL), possibly indicating a decrease in bone-building markers during the LCK-only phase. Serum P1NP increased from 47.2 ng/mL at 12 months to 59 ng/mL at 24 months (&#x0394; = +11.8 ng/mL), possibly reflecting increased bone formation in response to the combined dietary and PRT interventions, consistent with studies using this combination.<sup><xref ref-type="bibr" rid="CIT0021">21</xref></sup> Serum CTX decreased from 527 ng/L at baseline to 432 ng/L at 36 months (&#x0394; = &#x2013;95 ng/L). The 18&#x0025; reduction in CTX indicates reduced bone resorption, which is consistent with stabilisation or improvement in BMD during the Intervention C period, which combined the LCK diet, PRT, and the AP or SB supplement (<xref ref-type="table" rid="T0002">Table 2</xref>).</p>
</sec>
</sec>
<sec id="s20018">
<title>General findings</title>
<p>It is notable that initially, the participant&#x2019;s baseline <italic>T</italic>-Scores were neither in the osteoporosis (OP) nor the osteopenia range, as she initially was seen for her MetS. In the first year of her MetS treatment with a LCK diet that omitted dairy products, her T Score decreased considerably. This decline in BMD was indeed dramatic. The point of the case report is to demonstrate that while LCK diets are excellent for resolving symptoms of MetS, LCK dairy-free diets in postmenopausal women without supplementation may result in decreased bone density in some cases. Once this was recognised, a stepwise intervention strategy was added, and the improvement in <italic>T</italic>-scores is notable. All dual-energy x-ray absorptiometry (DXA) scans were performed on the same device by the same technician for consistency.</p>
</sec>
<sec id="s20019">
<title>Study&#x2019;s limitations</title>
<p>As with any study, limitations must be acknowledged. In this study, we acknowledge that the results may not be generalisable to a larger population and that participants&#x2019; characteristics, such as age, comorbidities, environment, and adherence, may also influence the findings. In addition, because of the small sample size (<italic>n</italic> = 1), there is no control, and therefore, it cannot account for the placebo effect or other natural disease progressions. Finally, the duration of this case report was 36 months, which does not allow for the definition of long-term outcomes in terms of safety, sustainability, or durability.</p>
<p>Despite the limitations of a single case report, the 3-year duration revealed sustained positive outcomes. While nutritional studies often face challenges with dietary tracking and compliance, we mitigated this by monitoring daily glucose and ketone levels to confirm nutritional ketosis and by obtaining weekly dietary tracking reports provided by the participant. Weight loss may have contributed to improvements in MetS, IR, and biomarkers, independent of the LCK intervention. Given the multifactorial nature of these interventions, isolating their individual impact on BMD remains complex.</p>
</sec>
</sec>
<sec id="s0020">
<title>Conclusion</title>
<p>The case report examines a 65-year-old postmenopausal woman with MetS, IR, and POP, illustrating the effects of sequential, multimodal interventions. Intervention A, an LCK diet, improved MetS and IR markers but failed to prevent BMD loss. Intervention B added progressive PRT, which modestly increased BMD and shifted classification from osteoporosis to osteopenia. Intervention C combined algae-based calcium supplementation with diet and training, producing the most significant BMD gains. Overall, the findings suggest that integrated metabolic, nutritional, and exercise approaches may help to manage POP, although larger studies are needed to confirm these results.</p>
</sec>
</body>
<back>
<ack>
<title>Acknowledgements</title>
<sec id="s20021" sec-type="COI-statement">
<title>Competing interests</title>
<p>The authors declare that they have no financial or personal relationships that may have inappropriately influenced them in writing this article.</p>
</sec>
<sec id="s20022">
<title>CRediT authorship contribution</title>
<p>Melanie M. Tidman: Conceptualisation; Formal analysis; Investigation; Methodology; Project administration; Resources; Supervision; Writing - original draft; Writing - review &#x0026; editing. Mona Fazzina: Methodology; Resources; Writing - original draft; Writing - review &#x0026; editing. Dawn R. White: Resources; Writing - original draft; Writing - review &#x0026; editing. Tim A. White: Resources; Writing - original draft; Writing - review &#x0026; editing. All authors reviewed the article, contributed to the discussion of results, approved the final version for submission and publication, and take responsibility for the integrity of its findings.</p>
</sec>
<sec id="s20023" sec-type="data-availability">
<title>Data availability</title>
<p>The data that support the findings of this study are available on request from the corresponding author, Melanie. M. Tidman.</p>
</sec>
<sec id="s20024">
<title>Disclaimer</title>
<p>The views and opinions expressed in this article are those of the authors and are the product of professional research. They do not necessarily reflect the official policy or position of any affiliated institution, funder, agency, or that of the publisher. The authors are responsible for this article&#x2019;s results, findings, and content.</p>
</sec>
</ack>
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<fn><p><bold>How to cite this article:</bold> Tidman MM, Fazzina M, White DR, White TA. Synergistic management of metabolic syndrome with postmenopausal osteoporosis: A retrospective case report. J. metab. health. 2026;9(1), a128. <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.4102/jmh.v9i1.128">https://doi.org/10.4102/jmh.v9i1.128</ext-link></p></fn>
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