Coronary Artery Calcium–Guided Prevention and Microbiome-Centered Nutrition: A Physician-Focused Review Integrating the Clinical Framework of William Davis, MD
Quick Summary
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CAC is most useful when you’re on the fence. In borderline/intermediate-risk patients—or when risk markers conflict—CAC can clarify preventive intensity and improve shared decision-making. [1-5]
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Don’t let CAC become the only scoreboard. Serial CAC is tricky: CAC is a powerful risk marker, but CAC change is not a clean surrogate, and plaque stabilization can increase calcification density. [11,19,20]
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Read beyond the score. CT scans often reveal actionable context (especially epicardial adipose tissue, plus extra-coronary calcification and incidental findings). [11,12]
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Vitamin D: correct deficiency, avoid over-promising event reduction. Davis targets higher 25(OH)D levels and reports CAC improvement clinically, but large RCTs/meta-analyses do not show consistent CV event reduction in broad populations. [15-19,21]
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Carnivore is a special case because it’s fiber-free. Short-term metabolic “wins” are common; longer-term risks are plausible via microbiome starvation, reduced SCFAs, barrier vulnerability, and endotoxemia pathways—supported by mechanistic and observational data. [9,20-27]
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Best counseling strategy: harm reduction. If patients insist on low-carb, steer toward fiber-aware low-carb and monitor apoB/LDL-P, BP, glycemic markers, and consider CAC when it will change management. [1-5,26,27]
Why this topic keeps showing up in clinic
CAC scoring exists for a simple reason: reduce “surprise” events by detecting atherosclerosis before it becomes symptomatic. Major guidelines support CAC as a risk-refining tool when standard risk estimation leaves uncertainty. [1-5]
At the same time, patients are increasingly adopting extreme dietary patterns—ketogenic and carnivore diets in particular. Many experience rapid improvements in weight, glucose, and triglycerides. That’s real, and it’s why adherence can be strong early on. The concern is what happens later, especially when the pattern is chronically fiber-free.
William Davis, MD has been consistent on two themes:
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use CAC (and related metrics) to measure risk more directly, and
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don’t ignore the gut microbiome—particularly when diets eliminate fermentable fibers for long periods. [6-12]
This review stays clinician-practical: how CAC fits prevention workflows, how to interpret claims about CAC “regression,” what you can responsibly say about vitamin D, and how to counsel fiber-free diets without turning the visit into a culture war.
1) CAC Scoring 101: what it measures and why it’s useful
Key bullets
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CAC is a direct marker of coronary atherosclerotic burden and improves risk discrimination over traditional factors in selected patients. [1-3]
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CAC is most helpful when it changes the conversation: “treat more aggressively” vs “hold and focus on lifestyle”. [1-5]
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Interpret CAC in context: CAC=0 ≠ zero risk, and CAC thresholds should inform (not dictate) intensity. [1-3]
Background: the “why” behind CAC
CAC scoring quantifies calcified coronary plaque via noncontrast CT (Agatston score). Clinically, it functions as a direct measure of subclinical atherosclerosis and predicts future events. [1-3] That’s why CAC is repeatedly positioned as a “risk adjudicator” when the usual tools (Pooled Cohort Equations, standard lipid panels, family history) don’t fully settle the preventive plan. [1-5]
A practical way to explain CAC to patients is: risk scores estimate probability; CAC helps reveal whether plaque is already present. Two people can have the same predicted 10-year risk; one has established subclinical disease and the other doesn’t. CAC helps separate them.
Guideline positioning: how CAC is meant to be used
The 2019 ACC/AHA primary prevention guideline supports CAC as a decision aid in adults at borderline/intermediate risk when uncertainty remains after clinician–patient discussion. [1,4] Global and specialty statements similarly support CAC for risk reclassification in selected scenarios. [2,3,5]
Common clinical anchors:
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CAC = 0: often lower near-term event risk (“power of zero”), but not risk-free—especially in smokers, diabetes, and strong family history. [1-3]
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CAC 1–99: supports up-classification depending on age and risk enhancers. [1]
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CAC ≥100 or ≥75th percentile: generally indicates higher risk and supports intensified prevention. [1-3]
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Very high CAC (often ≥300–400): frequently treated as a “very high risk” signal in scientific statements. [3,5]
Rescanning: when it helps (and when it’s reassurance medicine)
Serial CAC is more nuanced than the initial scan. Its value depends on whether a new result would change management. A commonly cited framework suggests for CAC=0, rescanning might be considered around 5–7 years (low risk), 3–5 years (intermediate risk), or about 3 years (high risk/diabetes) when it will affect decisions. [2,10]
Practical documentation tip (helps with overuse):
Before ordering a repeat CAC, document the clinical “fork in the road.” If the repeat result won’t change management, it’s probably reassurance medicine.
Mini Case Vignettes 
Where CAC changes the plan
Case 1: CAC = 0, but risk is not “zero”
Patient: 52-year-old with type 2 diabetes, BP controlled, LDL-C 92 mg/dL, non-smoker.
CAC: 0.
Clinical pitfall: over-reassurance.
How CAC helps: a CAC=0 supports a lower near-term event risk, but diabetes remains a high-risk condition; lifestyle and risk factor control remain non-negotiable. CAC=0 can help refine intensity discussions and adherence tactics, but it shouldn’t be used to “de-risk” diabetes away. [1-3]
Teaching point: “Zero calcium” is not “zero disease forever.” It’s a data point, not a permission slip.
Case 2: CAC is high with “okay” traditional numbers
Patient: 58-year-old, LDL-C 104 mg/dL, TG 110 mg/dL, no symptoms, “healthy eater,” strong family history.
CAC: 260.
How CAC helps: CAC moves this from theoretical risk to documented atherosclerosis. It often upgrades intensity—more assertive lipid and BP targets, consistent exercise, and a tighter dietary plan. [1-5]
Teaching point: CAC is how you catch the “normal labs, abnormal arteries” phenotype.
Case 3: Carnivore diet, improved glucose—but apoB spikes
Patient: 45-year-old with prediabetes; starts carnivore diet; A1c improves, TG falls, weight down 18 lb.
Lab surprise: LDL-C and apoB rise sharply (common in a subset).
How CAC helps: CAC may be appropriate if overall risk remains uncertain and the result would influence intensity and adherence. In the meantime, this is a harm-reduction counseling moment: keep carbs controlled, reintroduce fermentable fibers and unsaturated fats, and monitor apoB/LDL-P. [20-27]
Teaching point: a metabolic win doesn’t automatically mean an atherogenic win.
2) “Whole scan” value: CAC is a number, but the scan is more than the number
Key bullets
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Don’t reduce CT heart scans to a single Agatston score; context matters. [11]
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Epicardial adipose tissue (EAT) is one of the most actionable “extra” findings and is associated with adverse outcomes. [11,12]
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Extra-coronary calcification, aortic measures, and incidental findings can meaningfully influence counseling and follow-up. [11]
Background: why clinicians should care about “what else” is on the scan
Davis’s “read beyond the score” point is clinically strong because it’s practical. CT heart scans commonly contain additional information that can refine counseling. [11]
Examples:
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Epicardial adipose tissue (EAT): Davis highlights EAT as a cardiometabolic risk signal. [11] CT-measured EAT is associated with adverse outcomes in meta-analytic work. [12] EAT can function as a “visual proxy” for visceral adiposity and metabolic risk.
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Extra-coronary calcification: thoracic aorta/valves may reflect broader disease burden. [11]
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Thoracic aortic diameter: CT can detect dilation requiring surveillance. [11]
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Incidental pulmonary findings: clinically meaningful beyond cardiology. [11]
Recommended tweak: if you order CAC, request reporting (when available) that includes EAT and notable extra-coronary findings, or review the report with that lens.
3) CAC progression vs “regression”: where the discussion gets messy
Key bullets
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CAC is validated for risk stratification; CAC change is harder to interpret. [1-5,11]
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Some therapies can improve outcomes while CAC rises due to changes in plaque composition/density. [19,20]
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Davis reports CAC reduction in some patients within multi-component interventions; treat as hypothesis-generating, not universally reproducible. [10]
Background: CAC is a great risk marker, but a complicated endpoint
Davis argues CAC can decrease and presents clinical examples of reductions in Agatston and volumetric measures with intensive strategies. [10] Clinicians will reasonably ask about scan variability and the biology of calcification versus total plaque.
A major nuance: calcification dynamics are not identical to vulnerability dynamics. Some therapies (notably statins) may be associated with increased calcification while improving outcomes and stabilizing plaque. [19,20] This is often described as a shift toward denser calcification and fewer lipid-rich features—potentially a stabilization signature—even when CAC scores rise. [19,20]
Practical approach: treat CAC primarily as a tool to set intensity, motivate adherence, and contextualize risk. Interpret serial CAC—if you obtain it—alongside apoB/LDL-P, BP, glucose/insulin resistance markers, and symptoms.
4) Vitamin D: Davis’s target vs outcome trials (and how to present this honestly)
Key bullets
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Davis targets higher 25(OH)D levels (~60–70 ng/mL) and reports clinical CAC improvement after vitamin D repletion. [7,11,12]
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Large RCTs/meta-analyses do not show consistent CV event reduction with supplementation in broad populations. [15-19]
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Best clinician stance: correct deficiency, titrate with labs, and avoid implying proven event prevention. [15-19,21]
Background: what you can say, what you should avoid saying
Davis describes vitamin D repletion as a key intervention that coincided with CAC improvement in his clinical experience and recommends titration to a 25(OH)D of 60–70 ng/mL. [7,11] He emphasizes daily dosing, lab-guided titration, and supplementation nuances. [12]
But trial-level evidence matters for how we speak. VITAL did not show reduced major cardiovascular events with vitamin D supplementation in a broad cohort. [15,16] Meta-analyses similarly report no consistent reduction in major CV outcomes overall. [17-19]
Balanced physician phrasing:
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“If you’re deficient, replacement is appropriate and we’ll monitor levels.”
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“Vitamin D is not a proven heart-attack prevention pill for everyone.”
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“Some clinicians target higher levels and report imaging improvements, but definitive event-reduction evidence is lacking.”
Safety: avoid “more is better”
NIH ODS guidance emphasizes that excess vitamin D can lead to adverse effects (primarily via hypercalcemia), typically from supplement overuse. [21] If pursuing higher targets, monitoring calcium/renal function is prudent in selected patients.
“What I order” panel
(Practical labs + imaging)
Baseline risk work-up (common, high-yield)
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ApoB (or LDL-P if available), plus standard lipid panel
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A1c and fasting glucose (± fasting insulin/HOMA-IR if you use it)
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Blood pressure (home readings if possible)
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Renal function/electrolytes (esp. if supplement-heavy or low-carb extreme)
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25(OH)D when deficiency risk is present
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Optional/phenotype-dependent: hsCRP, Lp(a), TSH, ALT/AST
When I consider CAC
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Borderline/intermediate 10-year risk and uncertainty about statin/intensity
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Discordant signals (e.g., “normal LDL-C” but metabolic syndrome, high apoB, strong family history)
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Patient motivation/adherence is a major issue and an objective measure may help
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Not routinely for low-risk patients when it won’t change management [1-5]
When I re-check CAC
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Only if the result will change management; avoid “score chasing.” [2,10]
5) The fiber-free diet problem: carnivore-style patterns and cardiometabolic risk
Key bullets
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Carnivore diets are fiber-free by design; this is mechanistically distinct from “low carb.” [9]
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Higher dietary fiber intake is consistently associated with lower all-cause and cardiovascular mortality. [20-23]
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Mechanistic literature supports plausible pathways: fiber → SCFAs → barrier integrity → lower endotoxin exposure; endotoxemia is linked to atherothrombotic risk. [24,25]
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Low-carb patterns differ by sources: animal-based versions have been associated with higher mortality than plant-forward versions. [26,27]
Background: why this matters more than constipation
Patients often start carnivore for appetite control, weight loss, glycemic changes, or symptom relief. Early improvements can be dramatic. Davis’s warning is that the absence of fermentable substrate changes gut ecology over time in ways that may increase inflammatory and cardiometabolic risk—even if the patient feels better initially. [6-9]
Fiber supports SCFA production and mucus barrier integrity; reduced fiber can contribute to dysbiosis and barrier vulnerability. [24] Gut-derived endotoxemia is plausibly linked to vascular inflammation and atherothrombotic risk. [25]
Outcome context clinicians should respect:
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Fiber intake repeatedly associates with lower mortality and CV risk. [20-23]
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Animal-based low-carb patterns have been associated with higher mortality compared with plant-forward low-carb patterns. [26]
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ACC commentary has cautioned against long-term ketogenic patterns emphasizing animal sources. [27]
6) Carnivore-style diets in real practice: counseling, monitoring, harm reduction
Key bullets
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Expect short-term metabolic wins; plan for longer-term monitoring.
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Watch apoB/LDL-P and LDL-C closely; some patients spike.
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Offer fiber-aware low-carb rather than “go back to carbs.”
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Use CAC strategically when risk is uncertain and management could change. [1-5]
Background: how to keep the patient and still reduce risk
A harm-reduction model works best.
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Validate early wins.
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Explain time horizon (microbiome/barrier).
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Offer a concrete low-carb alternative that restores fermentable fibers.
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Put guardrails around monitoring and revisit decisions based on objective markers.
If the patient refuses to change, you can still improve safety by steering fat quality toward unsaturated sources, introducing tolerated fiber gradually, and tracking apoB and BP.
Fiber-aware low-carb starter list
(Practical, stepwise)
Goal: keep glycemic control while feeding the microbiome.
“Start low and go slow” strategy (to improve tolerance)
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Add one fermentable fiber source every 3–7 days
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Start with small portions; titrate based on symptoms
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If IBS/SIBO is suspected, adjust dose, consider gut-directed evaluation, and avoid “all at once” fiber loading
High-yield options (often tolerated)
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Legumes in small amounts (lentils, chickpeas) if tolerated
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Alliums (onion/garlic) in modest doses (or infused oils if sensitive)
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Resistant starch sources in controlled portions (e.g., cooled potatoes/rice in small amounts for non-keto low-carb; or green banana flour in micro-doses)
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Fermentable fiber supplements (e.g., inulin, GOS/FOS, PHGG) introduced gradually
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Low-net-carb vegetables with fermentable components (as tolerated)
“If the patient insists on carnivore”
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Consider a compromise: “mostly animal-based” plus targeted fiber/prebiotic add-on (even 5–10 g/day initially)
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Recheck apoB/LDL-P, BP, and symptoms after 6–12 weeks of adjustments
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Reassess sustainability and risk trade-offs using objective markers
(This aligns with Davis’s emphasis on “the right kind of fiber” rather than generic high-fiber advice.) [8,9]
7) Patient-safety signals from popular health practices (brief but important)
Key bullets
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Cold-water immersion can trigger arrhythmias early; don’t reduce risk to hypothermia alone. [28,29]
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Heavy metals in bone broths have been measured; high-frequency use deserves counseling. [30]
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Electrolyte loads in ketone salts/supplements can be clinically relevant; potassium excess is not benign. [31]
Background: why this belongs here
Clinicians increasingly see patients experimenting with cold plunges, high-dose supplements, ketone products, and aggressive “biohacks.” A short safety section is risk literacy, not fearmongering. It also helps physicians anticipate adverse events that otherwise look “out of nowhere.”
Clinical Pearls
(Physician Quick Hits)
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Physician-Focused Summary
CAC helps you see risk; diet quality determines whether risk drivers improve or quietly worsen.
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CAC is best used when it changes decisions. In borderline/intermediate-risk or discordant biomarker patients, CAC improves risk reclassification and supports more rational preventive intensity. [1-5]
-
The scan is more than the score. Whole-scan features—especially EAT—can meaningfully reshape counseling targets and urgency. [11,12]
-
Serial CAC is not a simple endpoint. Interpret CAC change cautiously, especially because plaque stabilization can coincide with rising calcification density and scores. [11,19,20]
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Vitamin D should be framed responsibly. Correct deficiency and monitor; avoid claiming proven event prevention in broadly selected populations. Davis’s higher-target strategy remains hypothesis-generating. [7,12,15-19,21]
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Carnivore diets are a special case because they eliminate fiber. Short-term metabolic wins are real; long-term microbiome and barrier concerns are plausible and supported by mechanistic and observational literature. [9,20-27]
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The practical solution is not “ban low-carb.” It’s “make low-carb microbiome-compatible,” monitor objective risk signals, and use CAC when clinically useful. [1-5]
Patient Handout for After-Visit Notes (Physician Copy/Paste)
After-Visit Summary: CAC Scan + Diet Guidance (Patient-Friendly)
1) What your CAC (coronary calcium) score means
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The CAC scan looks for calcium in the heart arteries. Calcium is a marker of plaque (atherosclerosis).
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A higher score usually means more plaque and higher future heart risk.
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A score of 0 often means low short-term risk, but it does not mean “zero risk,” especially with diabetes, smoking, or strong family history.
2) What we do with your result
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We use CAC to decide how aggressive we should be with prevention (nutrition, exercise, blood pressure, cholesterol treatment).
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CAC helps personalize your plan rather than guessing.
3) Important note about repeat scans
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Repeat CAC scans are not always helpful. We only repeat them if the result would change your treatment plan.
4) Vitamin D
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Vitamin D is important for overall health. If your level is low, we will replace it and recheck it.
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Vitamin D supplements have not been proven to prevent heart attacks in everyone, so we use it mainly to correct deficiency and support general health.
5) Diet and heart health (especially “carnivore” or very low-carb diets)
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Many people feel better quickly on very low-carb or carnivore diets.
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The main concern with carnivore-style diets is that they are fiber-free. Fiber helps support healthy gut bacteria and the gut barrier.
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Over time, lack of fiber may increase inflammation and other risk factors related to heart health.
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If you want to stay low-carb, we recommend a fiber-aware low-carb plan (low sugar/refined carbs, but includes safe sources of fiber and plant foods you tolerate).
6) What we will monitor
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We will follow your blood pressure, cholesterol (sometimes including apoB), blood sugar markers, and symptoms over time.
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If you choose a restrictive diet, we may monitor more closely.
7) Next steps
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Continue: ___ (exercise plan / BP plan / medication plan)
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Nutrition plan: ___
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Labs to recheck: ___
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Follow-up appointment in: ___
References: 
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Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease. Circulation. 2019;140(11):e596-e646.
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Golub IS, Termeie OG, Kristo S, et al. Major Global Coronary Artery Calcium Guidelines: Key Points and Clinical Applications. JACC Cardiovasc Imaging. 2023;16(1):98-117.
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Orringer CE, Blaha MJ, Blankstein R, et al. The National Lipid Association scientific statement on coronary artery calcium scoring. J Clin Lipidol. 2021;15(1):33-60.
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American College of Cardiology. 2019 ACC/AHA Primary Prevention Guideline—Key Points. 2019.
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Choi HYJ, et al. Coronary artery calcium scoring for prevention of cardiovascular disease. Am Fam Physician. 2022;106(1).
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Davis W. The Keto Trap. DrDavisInfiniteHealth.com. 2017.
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Davis W. 30+ Years of Coronary Calcium Scores: Lessons Learned About Vitamin D. DrDavisInfiniteHealth.com. 2025.
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Davis W. Prebiotic fibers: the RIGHT kind of high-fiber. DrDavisInfiniteHealth.com. 2020.
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Davis W. The disastrous microbiome consequences of fiber deficiency. DrDavisInfiniteHealth.com. 2025.
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Davis W. Yes, you can reduce your coronary calcium score. DrDavisInfiniteHealth.com. 2025.
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Davis W. 10 Things You Probably Didn’t Know About CT Heart Scans and Coronary Calcium Scores. DrDavisInfiniteHealth.com. 2025.
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Davis W. The finer points of vitamin D supplementation. DrDavisInfiniteHealth.com. 2024.
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National Lipid Association/related summaries on CAC=0 and risk (see statement in Ref 3).
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Major global CAC guidance synthesis (see Ref 2).
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Manson JE, Cook NR, Lee IM, et al. Vitamin D Supplements and Prevention of Cancer and Cardiovascular Disease. N Engl J Med. 2019;380(1):33-44.
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Manson JE, Bassuk SS, et al. VITAL trial—principal results and subsequent analyses. Ann Intern Med. 2020.
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Pei YY, et al. Vitamin D supplementation and cardiovascular events: meta-analysis. Nutrients. 2022.
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Nudy M, et al. Vitamin D supplementation and cardiovascular outcomes: meta-analysis. Trends Cardiovasc Med. 2020.
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BMJ meta-analytic summaries on vitamin D and major cardiovascular events. BMJ. 2023.
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Reynolds A, et al. Carbohydrate quality and human health: systematic review and meta-analysis. Lancet. 2019.
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NIH Office of Dietary Supplements. Vitamin D—Health Professional Fact Sheet. Updated 2025.
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Ramezani F, et al. Dietary fiber intake and mortality: systematic review/meta-analysis. Clin Nutr. 2024.
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Kim Y, et al. Dietary fiber intake and cardiovascular mortality: meta-analysis. Clin Nutr. 2016.
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Bailey MA, et al. Dietary fiber and SCFAs/barrier implications. Am J Physiol Gastrointest Liver Physiol. 2023.
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Violi F, et al. Gut-derived low-grade endotoxaemia, atherothrombosis and cardiovascular risk. Nat Rev Cardiol. 2022.
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Seidelmann SB, et al. Dietary carbohydrate intake and mortality: cohort study/meta-analysis. Lancet Public Health. 2018.
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American College of Cardiology. Very-low-carbohydrate/ketogenic diets and cardiometabolic risk. 2020.
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Shattock MJ, Tipton MJ. Autonomic conflict during cold water immersion. J Physiol. 2012.
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American Heart Association. Cold plunge risks and cold shock response (public guidance). 2022.
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Hsu D, et al. Essential and toxic metals in animal bone broths. Food Addit Contam Part B. 2017.
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NIH Office of Dietary Supplements. Potassium—Health Professional Fact Sheet. 2022.
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