Periodontal Disease and Other Adverse Health Outcomes Share Risk Factors, including Dietary Factors and Vitamin D Status
Abstract
:1. Introduction
- Review the history of associations between periodontitis or PD and other adverse health outcomes and determine whether PD is a causal risk factor for those adverse health outcomes, such as CVD, diabetes, and respiratory diseases;
- Review the role of dietary risk factors for PD and other adverse health outcomes;
- Review the evidence that vitamin D reduces the risk of PD as well as other adverse health outcomes;
- Make recommendations regarding changes in dietary patterns and food groups and in serum 25-hydroxyvitamin D [25(OH)D] concentrations for reducing the risks of PD and other adverse health outcomes.
2. Associations between Periodontal Disease and Other Adverse Health Outcomes
3. Dietary Risk Factors for Periodontitis/Periodontal Disease and Other Adverse Health Outcomes
Disease | Variable | Population | Approach | Finding | Ref. |
---|---|---|---|---|---|
T2DM | Processed meat | 184 countries | Comparative risk-assessment model to estimate the effect of 11 dietary factors, separately and jointly, on absolute and proportional burdens of new T2DM cases among adults globally and by age, sex, education, urbanicity, world region, and nation, in 1990 and 2018. | Attributable burden 20.3% (95% CI, 18.3–23.5%) | [68] |
T2DM | Red meat | 184 countries | Cross-sectional study | Attributable burden 20.1% (95% CI, 19.0–21.2%) | [68] |
CHD, incident | Meat, sausages | Germany, 200 cases, 255 controls | Risk per 100 g/d | HR = 2.55 (95% CI, 1.14–5.68) | [118] |
IHD incident | Meat, 50 g/day; | Meta-analysis of 12 of 13 prospective studies, N = 1,427,989; cases, 32,630. Studies were conducted in Asia (n = 3), the US (n = 4), Australia (n = 1), Europe (n = 4), and for one multicountry cohort in the Americas, Asia, Africa, and Europe. | HR = 1.09 (95% CI, 1.06–1.22) | [119] | |
IHD incident | Processed meat, 50 g/day | Meta-analysis of 10 of 13 prospective studies, N = 1,427,989; cases, 32,630 | HR = 1.18 (95% CI, 1.12–1.25) | [119] |
Disease | Population | Approach | Finding | Ref. |
---|---|---|---|---|
Periodontitis | Harvard Health Professionals Follow-up Study 34,160 males aged 40–75, 2197 developed periodontitis | Prospective study, 1986–1998; Q1, 0.3 s/d; Q3, 1.3 s/d; Q5, 3.4 s/d | For Q5, mRR = 0.77 (95% CI, 0.66–0.89, ptrend < 0.001 | [71] |
4. Vitamin D Status Modifies Risk of Periodontitis/Periodontal Disease and Other Adverse Health Outcomes
- Measuring serum 25(OH)D concentrations for all prospective participants;
- Enrolling those with concentrations associated with increased risk for the expected outcome;
- Supplementing with vitamin D doses high enough to raise serum 25(OH)D concentration to maximize the effect of vitamin D;
- Normalizing all participants for potentially outcome-affecting variables not directly related to vitamin D, such as diet and vitamin A intake; and
- Measuring and analyzing results with respect to achieved 25(OH)D concentrations.
5. Discussion
6. Summary and Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Criterion | Meaning |
---|---|
Strength of association | OR or RR between 1 and 2 is considered weak, whereas >2.0 is considered strong. |
Consistency | Similar findings in different situations. |
Specificity | A factor influences specifically a particular outcome or population. |
Temporality | The causal agent should precede the incidence of an expected outcome. |
Biological gradient | A monotonically changing dose-response relationship. |
Plausibility | Mechanisms exist to explain the effect. |
Coherence | The interpretation should not seriously conflict with generally known facts of the natural history and biology of the disease. |
Experiment | RCTs are generally the strongest type of evidence. They should be for disease outcomes, not merely biological parameters related to diseases. In the absence of RCTs, prospective studies may be used. |
Analogy | Analogous exposures for demonstrated outcomes. |
Food Groups | Q1 Intake (Servings/Day) [90] | Q5 Intake (Servings/Day) [90] | rEDIH r [22] | rEDIP r [22] |
---|---|---|---|---|
Proinflammatory | ||||
French fries | −0.39 | −0.14 | ||
High-energy drinks | 0.20 ± 0.34 | 0.52 ± 0.75 | −0.20 | −0.25 |
Low-energy drinks | 0.33 ± 0.63 | 0.89 ± 1.54 | −0.21 | −0.17 |
Processed meats | 0.30 ± 0.32 | 0.55 ± 0.64 | −0.35 | −0.17 |
Red meat | 0.55 ± 0.40 | 0.81 ± 0.59 | −0.48 | −0.22 |
Refined grains | 0.96 ± 0.79 | 1.80 ± 1.52 | −0.04 | −0.22 |
Anti-inflammatory | ||||
Beer | 0.67 ± 1.13 | 0.11 ± 0.26 | 0.08 | 0.18 |
Coffee | 3.40 ± 2.14 | 0.94 ± 1.24 | 0.31 | 0.45 |
Fruit juice | 0.93 ± 1.15 | 0.67 ± 0.70 | 0.11 | 0.09 |
Leafy green vegetables | 0.95 ± 0.65 | 0.61 ± 0.51 | 0.20 | 0.29 |
Whole grains | 0.22 | 0.15 | ||
Wine | 0.65 ± 0.96 | 0.08 ± 0.17 | 0.27 | 0.22 |
Disease or Outcome | Variable | Population | Approach | Finding | Ref. |
---|---|---|---|---|---|
T2DM | Refined rice and wheat | 184 countries | Cross-sectional study | Attributable burden 24.6% (95% CI, 22.3–27.2%) | [68] |
T2DM | UPFs (Q1, <215 g/d; Q2, 215–323 g/d; Q3, >323 g/d) | Spain, 20,060 adults, 175 new cases | Prospective study, 12-yr follow-up | HR = 1.53 (95% CI, 1.06–2.22) | [100] |
Periodontitis, moderate/severe | UPFs | Southern Brazil, N = 537, 205 with initial, moderate, and severe periodontitis; results for moderate and severe periodontitis | Prospective study | Standardized coefficient = 0.11, standard error = 0.05, p = 0.02 | [101] |
Overweight/obesity | UPFs | 8451 middle-aged university graduates in Spain, followed up for a median of 8.9 yrs [102]; 11,872 civil servants in Brazil 35–74 yrs followed up for a mean of 3.9 yrs [103] | Two prospective observational studies | RR = 1.23 (95% CI, 1.11–1.36) | [104] |
IHD/cerebrovascular disease mortality | UPFs (14.6% vs. <6.6%) | Italy, 22,475 men, mean age 55 ± 12 yrs, 255 deaths | Prospective study, 8.2-yr follow-up | HR = 1.52 (95% CI, 1.10–2.09) | [105] |
CVD mortality | UPFs (14.6% vs. <6.6%) | Italy, 22,475 men, mean age 55 ± 12 yrs, 439 deaths | Prospective study, 8.2-yr follow-up | HR = 1.58 (95% CI, 1.23–2.03) | [105] |
CVD incidence/mortality | UPFs | Three prospective observational studies | Meta-analysis | RR = 1.29 (95% CI, 1.12–1.48) | [104] |
All-cause mortality rate | UPFs (14.6% vs. <6.6%) | Italy, 22,475 men, mean age 55 ± 12 yrs, | Prospective study, 8.2-yr follow-up | HR = 1.26 (95% CI, 1.09–1.46) | [105] |
All-cancer incidence | UPFs (Q1, 8.5 ± 2.5%; Q2, 14.3 ± 1.4%; Q3, 19.8 ± 1.9%; Q4, 32 ± 9.8%) | France, adults, median age 42.8 yrs, 2228 cases | Prospective study, 2009–2017 | For Q4 vs. Q1, HR = 1.23 (95% CI, 1.08–1.40, ptrend = 0.001) | [106] |
Outcome | Mechanisms | Ref. |
---|---|---|
Autoimmune diseases | Regulates adaptive immunity so that the body does not attack its own tissues | [139] |
Bone health | Regulates calcium and phosphorus absorption and metabolism | [137] |
Cancer | Reduces incidence by affecting cellular differentiation, proliferation, and apoptosis; reduces mortality by reducing angiogenesis around tumors and metastasis; many other mechanisms | [140] |
CVD | Vitamin D deficiency activates renin-angiotensin-aldosterone system; serum 25(OH)D upregulates nitric oxide concentrations, reduces oxidative stress and regulates inflammatory pathways | [141] |
Infectious diseases | Induces production of antimicrobial peptides such as human cathelicidin; reduces risk of cytokine storm | [142,143] |
Infectious diseases | Inhibits expression of proinflammatory cytokines through blocking the TNF-induced NF-κB1 signaling pathway; and initiates expression of ISGs for antiviral defense program through activating the IFN-α-induced Jak-STAT signaling pathway | [144] |
Inflammation | Shifts production of cytokines from Th1 (proinflammatory) to Th2 (anti-inflammatory) | [145] |
Insulin resistance | Maintains pancreatic β-cell function; increases insulin sensitivity in insulin-responsive tissue; reduces serum concentrations of parathyroid hormone; regulates renin-angiotensin-aldosterone system; exerts positive effects on hepatic lipogenesis and gluconeogenesis; reduces formation of reactive oxygen species | [146] |
Muscle health | Regulates oxygen consumption rate, maintains mitochondrial function, reduces risk of muscle atrophy | [147] |
Pregnancy outcomes | Most effects mediated by calcitriol, whose concentrations increase during pregnancy. Calcitriol regulates calcium absorption from the GI tract. Calcitriol produced in the placenta acts as an autocrine/paracrine regulator of immunity at the fetal-maternal interface for acceptance of the fetal allograft; calcitriol regulates estradiol and progesterone secretion in the placenta; calcitriol downregulates FLT1 and vascular endothelial growth factor gene expression, thereby reducing risk of preeclampsia. Calcitriol regulates immune function through effects on cytokine production | [148] |
Population | Intervention: Vitamin D Dose, Ca Dose | Baseline, Achieved 25(OH)D (ng/mL) | Outcome | Ref. |
---|---|---|---|---|
Michigan, USA, 40 patients with severe PD; all received open flap debridement surgery in one segment of the mouth | Half given teriparatide (20 µg) or placebo; all given 800 IU/d and 1000 mg from 3 days before surgery to 6 wks after | Deficient (N = 7): 17 ± 0; 6 wks, 26 ± 4; 6 mo, 20 ± 3 Sufficient (N = 13): 34 ± 3; 6 wks, 41 ± 6; 6 mo, 31 ± 2 | BL to 1 yr deficient vs. sufficient: CAL gain: −0.43 vs. 0.92 mm, p < 0.01 PPD reduction: −0.43 vs. 1.83 mm, p < 0.01 RLBG: not significant For teriparatide treatment, no significant effect of vitamin D on CAL and PPD, but IDR was better for vitamin D sufficient (2.05 mm) than vitamin D deficient (0.87 mm), p < 0.01 | [160] |
India, 96 adults 18–64, various stages of gingivitis | GpA, 2000 IU/d; GpB, 1000 IU/d; GpC, 500 IU/d; GpD, 0 IU/d | GpA, 22 ± 7; 52 ± 10; GpB, 27 ± 1; 44 ± 9; GpC, 24 ± 5; 37 ± 6; GpD, 28 ± 3; 29 ± 4 | BL to 3 m, GI; % reduction GpA: 2.4 ± 0.5, 62% ** GpB: 2.4 ± 0.6, 53% ** GpC: 2.2 ± 0.6, 38% ** GpD: 2.3 ± 0.6, 0 | [161] |
Egypt, 28 patients with CP treated with SRP | T: 10,000 IU/d, 5 d/wk, 12 wk | T: 14 ± 8; 38 ± 8 C: 17 ± 6; ? | BL to 3 m, Mean diff T, C GI: −19% * PI: −10% * PPD: −26% * CAL: −13% * | [162] |
China, 360 moderate-to-severe periodontitis patients | T1: 120, 2000 IU/d T2: 120, 1000 IU/d | T1, 2000 IU/d: 25 ± 2; 58 ± 2 T, 1000 IU/d: 41 ± 2; C: 26 ± 2 | AL (mm): T1, −0.3 ± 0.2; T2, −0.3 ± 0.2; C, −0.2 ± 0.1; p = 0.048 PPD (mm): T1, −0.1 ± 0.2; T2, −0.1 ± 0.2; C, −0.1 ± 0.1; p = 0.043 | [163] |
India, 27 healthy periodontitis patients | T: 25,000 IU/wk, 6 mo | T (N = 13): 17; 39 C (N = 14): 14; 23 | FMBS, NS; FMPS, NS; PPD, NS | [159] |
Russia, 110 patients with moderate generalized periodontitis, 40 controls, all given conventional periodontal treatment by day 14 | Gp1 (N = 55): 0 Gp2 (N = 55): 800 IU/d; 500 mg/d, 12 mo Gp3 (N = 40): 0 | Gp1: 15 ± 0; 17 ± 0 Gp2: 15 ± 0; 37 ± 0 Gp3: 44 ± 1; 45 ± 0 | BL, 12 m MI: Gp1, 2.6 ± 0.0; 2.1 ± 0.1 * Gp2: 2.7 ± 0.1; 1.1 ± 0.0 * Gp3: 2.5 ± 0.1; 1.3 ± 0.0 * PeI: Gp1: 5.4 ± 0.1; 4.7 ± 0.1 * Gp2: 5.4 ± 0.1; 3.7 ± 0.1 * Gp3: 5.3 ± 0.1; 3.6 ± 0.1 * PMA: Gp1: 53 ± 0; 33 ± 1 * Gp2: 52 ± 1; 22 ± 0 * Gp3: 53 ± 0; 19 ± 0 * SI: Gp1: 3.1 ± 0.0; 1.8 ± 0.1 * Gp2: 3.2 ± 0.1; 1.4 ± 0.1 * Gp3: 3.0 ± 0.1; 0.9 ± 0.0 * | [164] |
Country | Year Pub. | Sex | Population CP, N, Age (Mean, Range), Years | 25(OH)D (ng/mL) PD | Population Controls, N, Age (Mean, Range), Years | 25(OH)D (ng/mL) Controls | Ref. |
---|---|---|---|---|---|---|---|
India | 2023 | F, M | 50, 33 ± 6 | 13.6 ± 4.7 | 50, 31 ± 6 | 17.2 ± 6.9 | [183] |
USA | 2021 | F, M | 1437, 69 | 29.1 ± 12.3 | 625, 69 yrs | 33.2 ± 12.2 | [88] |
Italy | 2020 | F, M | 46, 53 ± 4 | 17.4 ± 5.2 | 43, 54 ± 5 | 29.9 ± 5.4 | [184] |
Norway (Nor) | 2019 | M | 21, 52 ± 13 | 19.2 ± 6.1 | 23, 50 ± 13 | 26.6 ± 7.4 | [185] |
Norway (Tam) | 2019 | M | 27 | 13.3 ± 5.0 | 21 | 13.9 ± 3.4 | [185] |
Turkey | 2018 | F, M | 55, 36 (30–47) | 16.1 ± 8.3 | 27, 39 (21–40) | 16.9 ± 6.4 | [186] |
USA | 2018 | 388 | 19.4 ± 1.0 | 9308 | 21.8 ± 0.5 | [187] | |
USA (Puerto Rico) | 2017 | F, M | 19, 48 ± 9 | 18.5 ± 4.6 | 19, 49 ± 8 | 24.2 ± 7.1 | [188] |
Turkey | 2017 | F, M | 18 | 14.6 ± 6.4 | 18 | 17.6 ± 9.7 | [189] |
Iran | 2016 | F | 30, 34 | 12.3 ± 8.4 | 30, 34 | 19.3 ± 10.1 | [190] |
India | 2016 | F, M | 50, 43 | 16.9 ± 5.5 | 48, 44 | 22.3 ± 5.7 | [191] |
Disease | Population | Intervention | Finding | Ref. |
---|---|---|---|---|
Asthma | 7 RCTs with 95 events for 518 participants in treatment arm, 526 controls with 133 events | Vitamin D supplementation | Reduction in rate of asthma exacerbation (RR = 0.73 [95% CI, 0.58–0.92], but only for patients with serum 25(OH)D <30 ng/mL). | [202] |
Autoimmune disease | 25,871 participants, USA, mean 25(OH)D in treatment group ~31 ng/mL | Half given 2000 IU/d vitamin D3, followed up for 5.3 years | 63 participants who received vitamin D and omega-3 fatty acids (HR = 0.69 [95% CI, 0.49–0.96]), 60 who received only vitamin D (HR = 0.68 [95% CI, 0.48–0.94]). Due mainly to rheumatoid arthritis. | [203] |
Cancer, all, incidence, mortality rates | 25,871 participants, USA, mean 25(OH)D in treatment group ~31 ng/mL | Half given 2000 IU/d vitamin D3, followed up for 5.3 years | Secondary analysis of an RCT for those with BMI <25 kg/m2: 25(OH)D increased from 33 to 46 ng/mL, HR = 0.76 (95% CI, 0.63–0.90). For all-cancer mortality after omission of the first 2 years of data HR = 0.75 (95% CI, 0.59–0.96). | [195] |
Cancer, all mortality rate | For total cancer mortality, five trials were included (1591 deaths; 3–10 years of follow-up; 22–54 ng/mL of achieved circulating 25(OH)D in intervention group) | Vitamin D supplementation | RR = 0.87 (95% CI, 0.79–0.96; p = 0.005) | [204] |
Cancer, colorectal, survival | 7 RCTs with 957 colorectal cancer patients | Vitamin D supplementation | Reduction in adverse outcomes, N = 815, HR = 0.70 (95% CI, 0.48–0.93); progression-free survival, N = 340, HR = 0.65 (95% CI, 0.36–0.94) | [205] |
Dental caries | 17 trials from 1926 to 1942, 660 participants, mean ages 4–12 yrs | Vitamin D3 supplementation, 300–1400 IU/d (one with 3050 IU/d) | Reduced risk of dental caries, pooled relative rate = 0.51 (95% CI, 0.40–0.65) | [206] |
Osteoporosis Review | Vitamin D deficiency symptoms are secondary hyperparathyroidism and bone loss, leading to osteoporosis and fractures; mineralization defects, which may lead to osteomalacia in the long term; and muscle weakness, causing falls and fractures. | [207] | ||
RTIs, acute | 25 eligible RCTs (total 11,321 participants, aged 0–95 years) were identified. IPDs obtained for 10,933 (96.6%) participants. | Vitamin D supplementation reduced risk of acute RTI among all participants (aOR = 0.88 [95% CI, 0.81–0.96]). In subgroup analysis, protective effects were seen in those receiving daily or weekly vitamin D without additional bolus doses (aOR = 0.8 [95% CI, 0.72–0.91]) | [208] |
Disease or Outcome | Population | Intervention | Finding | Ref. |
---|---|---|---|---|
Airway microbial activity | 40 participants in US, aged 18–60 yrs | 20 supplemented with 1000 IU/d of vitamin D3 in summer, 20 in winter, 20 with placebo in each season | Airway surface liquid had high antimicrobial (LL-37) activity in summer without vitamin D supplementation and in winter after vitamin D supplementation | [212] |
COVID-19 | All people ≥18 years old living in Barcelona-Central Catalonia (n = 4.6 million) | Those supplemented with cholecalciferol or calcifediol from April 2019 to February 2020 were compared with propensity score-matched untreated controls | Patients on cholecalciferol treatment achieving 25(OH)D levels ≥30 ng/mL had lower risk of SARS-CoV-2 infection, lower risk of severe COVID-19, and lower COVID-19 mortality than unsupplemented 25(OH)D-deficient patients (56/9474 [0.6%] vs. 96/7616 [1.3%]; HR = 0.66 (95% CI, 0.46–0.93), p = 0.02) | [213] |
COVID-19 | VA patients with Veterans Administration Corporate Data Warehouse electronic health records. 199,498 treated, controls | Those with at least one VA service or vitamin D3 prescription and at least one vitamin D lab test between 1 January 2019, and 31 December 2020 | For COVID-19 incidence: HR = 0.72 (95% CI, 0.65–0.79) For COVID-19 mortality: HR = 0.77 (95% CI, 0.55–1.06) | [214] |
Dementia | US, 12,388 participants National Alzheimer’s Coordinating Center dataset, followed up 1 yr | 1797 had calcium-vitamin D; 1046 had cholecalciferol only; 1283 had ergocalciferol only; and 511 had at least two supplements together, mostly ergocalciferol plus calcium-vitamin D (n = 268) and cholecalciferol plus calcium-vitamin D (n = 233). Age ~72 ± 8 yrs | For incident dementia, HR = 0.60 (95% CI, 0.55–0.65) Limitation: no information on serum 25(OH)D concentration available | [215] |
Prediabetes to T2DM | 3 RCTs included | Tested cholecalciferol, 20,000 IU (500 μg) weekly; cholecalciferol, 4000 IU (100 μg) daily; or eldecalcitol, 0.75 μg daily, vs. matching placebos | Among participants assigned to vitamin D group who maintained an intratrial mean serum 25(OH)D level of ≥50 ng/mL compared with 20–29 ng/mL during follow-up, cholecalciferol reduced risk for diabetes by 76% (HR = 0.24 [95% CI, 0.16–0.36]), with a 3-yr absolute risk reduction of 18.1% (95% CI, 11.7–24.6%). | [216] |
Hypertension | Open-label vitamin D supplementation to increase 25(OH)D concn to >40 ng/mL. | For hypertensives, this reduced systolic blood pressure by 18 mmHg and diastolic blood pressure by 12 mmHg and reduced prevalence of hypertension in 71%. | [217] | |
MI | Patients treated at Veterans Health Administration from 1999 to 2018 | Three groups: 25(OH)D <20 ng/mL; treated with vitamin D, 25(OH)D 20–30 ng/mL; treated with vitamin D, 25(OH)D >30 ng/mL. Among the cohort of 20,025 patients, risk of MI was significantly lower for >30 ng/mL vs. 20–30 ng/mL (HR = 0.65 [95% CI, 0.49–0.85]) and <20 ng/mL (HR = 0.73 [95% CI, 0.55–0.96]). | [218] | |
Preterm delivery | 1064 pregnant patients aged 18–45 yrs between September 2015 and December 2016 in South Carolina. 46% white, 37% African American, 11% Hispanic. | Serum 25(OH)D concn measured at first prenatal visit. Women counseled on how to achieve 25(OH)D >40 ng/mL and given bottles of 5000-IU vitamin D3 capsules. | Overall preterm birth rate was 13%. For preterm birth, comparing >40 ng/mL vs. <40 ng/mL, OR = 0.38 (95% CI, 0.23–0.62, ptrend = 0.0003). Result largely independent of race/ethnicity. | [219] |
Pregnancy outcomes: stratified randomized field trial in Iran | Iran, 900 pregnant women at screening site; 900 at nonscreening site. | Subjects with moderate deficiency I1: 50,000 IU of oral vitamin D3/wk for 6 wks I2: 50,000 IU of oral vitamin D3/wk for 6 wks and then maintenance dose of 50,000 IU/mo of vitamin D3 until delivery I3: Single dose of i.m. 300,000 IU of vitamin D3 I4: Single dose of i.m. 300,000 IU of vitamin D3 and then maintenance dose of 50,000 IU/mo of vitamin D3 until delivery Subjects with severe deficiency I5: 50,000 IU of oral vitamin D3/wk for 12 wks I6: 50,000 IU of oral vitamin D3/wk for 12 wks and then maintenance dose of 50,000 IU/mo of vitamin D3 until delivery I7: i.m. 300,000 IU of vitamin D3; 2 doses for 6 wks I8: i.m. 300,000 IU of vitamin D3; 2 doses for 6 wks, followed by maintenance dose of 50,000 IU/mo of vitamin D3 until delivery | After supplementation, only 2% of women in nonscreening (control) site had 25(OH)D >20 ng/mL vs. 53% of women in screening site. Adverse pregnancy outcomes, including preeclampsia, gestational diabetes mellitus, and preterm delivery, were decreased by 60%, 50%, and 40%, respectively, in screening (supplementation) site. | [220] |
Outcome | Population | Approach | Finding | Ref. |
---|---|---|---|---|
All-cause mortality rate | 307,601 unrelated UK Biobank participants of White European ancestry (aged 37–73 yrs at recruitment). 18,700 deaths during 14-yr follow-up. | Genetically predicted 25(OH)D estimated using 35 confirmed variants of 25(OH)D. 100 strata of 25(OH)D used. | Association of genetically predicted 25(OH)D with all-cause mortality was L-shaped (pnonlinear < 0.001), and risk for death decreased steeply with increasing concentrations until 20 ng/mL. Evidence for association also seen in analyses of mortality from cancer, CVD, and respiratory diseases (p ≤ 0.033 for all outcomes). | [225] |
AD | Data from International Genomics of Alzheimer’s Project (N = 17,008 AD cases and 37,154 controls). | SUNLIGHT Consortium identified 4 SNPs to be genomewide significant for 25(OH)D, which described 2.44% of variance in 25(OH)D in Canadian Multicentre Osteoporosis Study | A 1-SD decrease in natural log–transformed 25(OH)D (~10 ng/mL increased AD OR = 1.25 (95% CI, 1.03–1.51; p = 0.02). | [226] |
AD | 21,982 cases and 41,944 cognitively healthy controls of European descent from four consortia, including ADGC, CHARGE, EADI, and GERAD/PERADES | 6 loci including GC, NADSYN1/DHCR7, CYP2R1, CYP24A1, SEC23A, and AMDHD1 from a recent GWAS including 79,366 (all European descent) | For meta-analysis of results for each SNP OR = 0.62 (95% CI, 0.46–0.84). | [227] |
AD | UK Biobank. In this GWAS dataset, a proxy phenotype for AD case-control status was assessed via self-report. Participants asked to report “Has/did your father or mother ever suffer from Alzheimer’s disease/dementia?” Excluded participants whose parents were aged <60 yrs, dead before reaching age 60 yrs, or without age information. | 6 loci including GC, NADSYN1/DHCR7, CYP2R1, CYP24A1, SEC23A, and AMDHD1 from a recent GWAS including 79,366 (all European descent) | For meta-analysis of results for each SNP OR = 0.88 (95% CI, 0.73–1.06; p = 0.19). | [227] |
CVD | Nonlinear MR analysis conducted in UK Biobank with 44,519 CVD cases and 251,269 controls. Serum 25(OH)D concn instrumented using 35 confirmed genomewide significant variants. | We constructed a weighted genetic score (vitamin D-GS) consisting of 35 SNPs to instrument serum 25(OH)D concn. 100 strata of 25(OH)D used. | L-shaped association between genetically predicted serum 25(OH)D and CVD risk (pnonlinear = 0.007), where CVD risk initially decreased steeply with increasing concentrations and leveled off around 20 ng/mL. | [198] |
Pneumonia, bacterial | 116,335 randomly chosen white Danes aged 20–100 yrs from the Copenhagen City Heart Study and Copenhagen General Population Study | Plasma 25(OH)D decreasing genetic variants around CYP2R1 (rs117913124, rs12794714, and rs10741657), DHCR7 (rs7944926 and rs11234027), GEMIN2 (rs2277458), and HAL (rs3819817) | In genetic analyses, OR for bacterial pneumonia per 4-ng/mL lower plasma 25(OH)D was 1.12 (95% CI, 1.02–1.23) in Wald’s ratio, 1.12 (95% CI, 1.04–1.20) in inverse variance weighted, 1.63 (95% CI, 0.96–2.78) in MR-Egger, and 1.15 (95% CI, 1.05–1.26) in weighted median instrumental variable analysis. | [228] |
T2DM | 96,423 white Danes aged 20–100 yrs from 3 studies. 5037 had T2DM | Assessed effects of genetic variation in DHCR7 (related to endogenous production) and CYP2R1 (related to liver conversion) on plasma 25(OH)D concn | OR for T2DM for 8-ng/mL reduction in genetically determined plasma 25(OH)D concn was 1.51 (95% CI, 0.98–2.33). | [229] |
T2DM | Meta-analysis of 10 MR studies involving 58,312 cases and 370,592 controls | Genetic score using two 25(OH)D synthesis SNPs (DHCR7-rs12785878 and CYP2R1-rs10741657) | For 10-ng/mL increase in genetically determined 25(OH)D OR = 0.86 (95% CI, 0.77–0.97). | [230] |
Year | Country(ies) or Region | Organization | Target | 25(OH)D Concn (ng/mL) | Vitamin D Dose (IU/d) (40 IU = 1 µg) | Ref. |
---|---|---|---|---|---|---|
2010 | Western developed | Experts | General health | 30–100 | 800 | [235] |
2011 | USA | IOM | Bone health | >20 | 600–800 | [236] |
2011 | USA | Endocrine Society | Bone health | >30 | 1000–2000 | [237] |
2013 | Poland | EVIDAS | General health | 30–50 | Adults: 800–2000; obese adults: 1600–4000 | [238] |
2017 | 40 countries | Review | General health | >12 or >20 in most guidelines | Mostly 200–800 | [239] |
2018 | Poland | EVIDAS | General health | >30 | 200–2000 | [240] |
2018 | UAE and Gulf populations | Experts | General health | 30–50 | 400–2000, depending on age | [241] |
2018 | USA | Experts | Pregnancy | >40 | 4000–5000 | [231] |
2019 | Europe, Middle Eastern | ECTS | General health | >20 in most guidelines | Not given | [242] |
2022 | Central and Eastern Europe | Experts | General health | 30–50 | 800–2000; higher vitamin D doses (e.g., 6000 IU/d) may be used for the first 2–4 weeks | [243] |
2023 | Poland | EVIDAS | General health | 30–50 | 400–4000 depending on age | [244] |
2023 | KSA and UAE | Experts | General health | >30 | Up to 4000 | [245] |
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Grant, W.B.; van Amerongen, B.M.; Boucher, B.J. Periodontal Disease and Other Adverse Health Outcomes Share Risk Factors, including Dietary Factors and Vitamin D Status. Nutrients 2023, 15, 2787. https://doi.org/10.3390/nu15122787
Grant WB, van Amerongen BM, Boucher BJ. Periodontal Disease and Other Adverse Health Outcomes Share Risk Factors, including Dietary Factors and Vitamin D Status. Nutrients. 2023; 15(12):2787. https://doi.org/10.3390/nu15122787
Chicago/Turabian StyleGrant, William B., Barbara M. van Amerongen, and Barbara J. Boucher. 2023. "Periodontal Disease and Other Adverse Health Outcomes Share Risk Factors, including Dietary Factors and Vitamin D Status" Nutrients 15, no. 12: 2787. https://doi.org/10.3390/nu15122787