New Cholesterol Guidelines

Ann: Recognizing that it's cholesterol particles that cause heart disease and that if we get them low, we can prevent it, we finally have a public conversation about "lower is better." The medical community has failed to break through against the misinformation that you need cholesterol for your brain to function and that statins are evil. Finally, we've broken through that, and I think that is huge and has done a ton of good.

Brent: Welcome to the Life Lab by Death Clock. I'm your host, Brent Franson. The mission of Death Clock is to help 100 million people live ten years longer. Today, we speak with Dr. Anne Marie Navarre about the new recommendation from the American College of Cardiology and American Heart Association for when people should think about taking statins—at what age and when they should start trying to lower cholesterol in their blood, specifically LDL cholesterol.

Brent: Dr. Navarre is an associate professor in the departments of Internal Medicine and Population and Data Sciences at UT Southwestern Medical Center and is a member of the Division of Cardiology. Dr. Navarre serves as an associate editor of JAMA Cardiology, is a board member of the American Society for Preventive Cardiology, and was on the committee at the American College of Cardiology that wrote these new guidelines.

Brent: She's a wonderful guest. I hope you enjoy.

Brent: Dr. Anne Marie, welcome to the show.

Ann: Thanks for having me.

Brent: We've talked a lot about heart health on the show, and some of the guidelines around recommendations for statins have recently changed. You were on the committee that wrote those recommendations, so I'm excited to talk statins and understand these new changes. Before we do that, can you give us a sense of your background and a little bit of your bio?

I'm a preventive cardiologist at UT Southwestern Medical Center in Dallas. I also have a PhD in public health that framed a lot of my initial training. I spend some of my time in clinic running a preventive cardiology clinic. I also take care of patients in the cardiac intensive care unit at our big county hospital, Parkland.
So I'm a preventive cardiologist. I'm at UT Southwestern Medical Center in Dallas. I have a PhD, also in public health that framed a lot of my initial training. I spent some of my time in clinic. I have a preventive cardiology clinic. I also take care of patients in the cardiac intensive care unit at our big county hospital, parkland.

And then the rest of my time I spend doing research around cardiovascular prevention. I also help lead clinical trials of new cholesterol-lowering therapies.
And then the rest of my life I spend doing research around cardiovascular prevention. I help also lead clinical trials of new cholesterol lowering therapies.

Brent: Okay. Could you tell us a little bit about the committees that write these guidelines? This is a guideline from the American College of Cardiology, and there's some relationship to the American Heart Association. Can you give us a sense of what those two groups are, how these committees are formed, and what they are tasked with?

Ann: This guideline specifically for lipids is often referred to as the American Heart Association/American College of Cardiology Multi-Society Guideline because it involves several other national societies focused on cardiovascular health, such as the American Society for Preventive Cardiology and the Preventive Cardiovascular Nurses Association. Each organization nominates its own set of experts who then must be vetted.

Ann: The final writing group consists of experts in dyslipidemia, cardiology, and primary care. We have pharmacists on the guidelines, as well as a patient representative. The committee meets once a week for well over a year. We review all the evidence that has come out since the last guideline, formulate the best recommendations, and then vote on the final criteria and recommendations for each specific section.

Brent: Okay. People are most familiar with the American Heart Association, but it is important to characterize this recommendation. To clarify, this is not a fringe recommendation or the view of just one isolated society.

Brent: This recommendation effectively represents the American medical establishment's view on statins and their role in preventing heart disease, right?

Ann: That's correct. A couple of important points to add: although this is an American guideline, if you compare it to European or Asia-Pacific guidelines, we generally agree on the vast majority of management. It is all focused around the same evidence base, with slight nuances in final interpretation.

Ann: Generally speaking, the strategy is global. To get into the guideline, a very high level of evidence is required. You can see the guideline as an encyclopedia of the minimum evidence-based standard.

Ann: However, many practitioners go beyond the guidelines in clinical practice based on further interpretation of evidence. We don't cover every possibility in the guidelines because we are constrained to where we have the most robust clinical trial evidence.

Brent: So it functions like a meta-analysis: evaluating all the robust research on a topic to see what can be stated definitively with a high standard for evidence.

Ann: Correct. To achieve our highest level of recommendation, randomized trials are required. For any therapy, we need placebo-controlled trials demonstrating that the treatment accomplishes the intended goal, such as preventing a heart attack or stroke.

Brent: The age for considering statins was dropped fairly substantially, surprising a lot of people.

Brent: Could you tell us what that change was?

Ann: For certain groups of people, we've always recommended statins regardless of age. If you had a heart attack in your 20s, or if you have familial hypercholesterolemia where your LDL cholesterol is 190 or above, age doesn't matter.

Ann: Your risk of heart disease is very high, and there have long been recommendations for treating that group. Where we made a bigger expansion was recommending evaluating risk starting around age 30. We now recommend screening for high cholesterol starting in childhood. Once you reach 30, the recommendation is to evaluate your global risk factors, calculate your risk of heart disease over the next 10 to 30 years, and treat accordingly.

Ann: If you are 30 and your LDL cholesterol is over 160, you should be on cholesterol-lowering medication because your long-term risk of heart disease is high. If you are young and have a greater than 10% chance of a heart attack or stroke over the next 30 years, we recommend getting your LDL cholesterol below 100.

Brent: How are we measuring that risk? A standard lipid panel gives LDL, HDL, and triglycerides. You can also get a scan to look for calcified plaque buildup in the heart.

Brent: Someone might look at lipoprotein(a) or apolipoprotein B (ApoB). If someone is 30 years old and doesn't know their 10-year or 30-year risk, what should they do first to understand it?

Ann: Those risk percentages come from a specific equation derived from thousands of people, called the PREVENT risk equation. You can search for the ASCVD PREVENT equation online. You input parameters including smoking status, diabetes, blood pressure, and lipid panel results.

Ann: That gives you an estimate of your risk. However, it doesn't include some other important risk enhancers that increase risk, such as lipoprotein(a), which isn't picked up on a regular lipid panel. If it's high, you're at increased independent risk for heart disease.

Ann: In those cases, we recommend more aggressive treatment. Other risk enhancers include pregnancy complications, South Asian ancestry, and inflammatory diseases. The risk equation alone underestimates risk for those individuals. Most people should start with the risk equation, and around age 45 or 50, consider coronary artery calcium (CAC) testing.

Ann: It takes time to build up cholesterol in heart arteries and for it to calcify. For most people in their 30s, a CAC score isn't very helpful because even if cholesterol is present, it isn't calcified yet.

Ann: For people in their 40s or 50s who are on the fence, coronary calcium testing moves you from calculated guesswork to directly determining if you already have cholesterol buildup in your heart arteries.

Ann: From there, the amount of plaque present guides how low your cholesterol should be treated. The risk score becomes less important once we know how much plaque is already building up.

Brent: LDL and HDL correlate with heart disease, but are not heart disease in themselves. A phenotypic measurement like a CAC scan shows whether you actually have calcified plaque buildup in your arteries.

Brent: A CT coronary angiogram shows soft plaque buildup. Someone could be an older woman with very high LDL cholesterol and no plaque in her arteries, or vice versa.

Brent: You can have great biomarkers and a lot of plaque, but having high LDL when younger increases the odds of developing plaque later in life, though it's not definitive.

Ann: Biomarkers correlate with heart disease, but LDL is more than that. ApoB-containing lipoproteins—VLDL, LDL, and Lp(a) particles—each have a single ApoB protein. Measuring ApoB tells us how many bad cholesterol particles are floating in your blood.

Ann: Those particles get trapped in artery walls, leaving cholesterol behind that builds up and causes heart disease. LDL is causal, not just correlated. Some people with high cholesterol never get heart disease, while others with normal cholesterol do.

Ann: Other factors determine how likely particles are to get trapped and build up. Above an LDL of about 100, the degree and duration of exposure function like pack-years of smoking, increasing long-term risk.

Ann: While we talk about risk calculators and CAC, lowering cholesterol remains foundational to preventing heart disease.

Brent: Say someone is 30 or 35, listening to this, and wants to pay more attention to their health. The first step is understanding current risk factors.

Brent: If someone is at risk, what are the recommendations, and how do they determine their risk?

Ann: It's easy: get a lipid panel ordered through your primary care doctor or a clinic, know your blood pressure, and use the online PREVENT equation to find your 10-year risk.

Ann: If you are under 60, it provides a 30-year risk comparison. If your LDL is over 160, your risk of developing plaque is high. Even if calculated risk seems low, if you want to live a long, healthy life, treatment is recommended regardless of that calculated score.

Brent: Say I'm 35, my LDL is above 160, and I don't have calcified plaque. What is the recommendation? Should I take a statin every day and talk to my doctor?

Brent: What is the recommendation? I'm going and I'm taking a stat in every day. I'm talking to my doctor about statins.

Ann: Yes. I tell my 35-year-old patients to get LDL below 100. Once heart disease is present, LDL needs to be below 55 to stabilize and regress plaque. Preventing plaque formation is much easier than regressing it.

Ann: If you're young, use enough statin to get LDL below 100, ensure blood pressure is controlled, don't smoke, eat well, and exercise. Diet and exercise are pivotal for heart disease prevention, but they work independently of cholesterol levels.

Ann: Adopting a Mediterranean diet and exercising regularly may drop LDL by only 15% to 20%. If starting at 160, lifestyle alone won't reach 100. These strategies are complementary, but people often feel like they failed when lifestyle isn't enough.

Ann: If your LDL is over 160, genetics—rather than lifestyle—is likely driving it that high, which is why therapy is recommended.

Brent: Is this recommendation specific to statins, or to overall cholesterol levels? Other drugs exist, like ezetimibe or PCSK9 inhibitors.

Brent: Is the recommendation specific to statins or it's specific to cholesterol levels?

Ann: Statins are inexpensive ($3–$5/month), highly effective, and the most well-studied option, supported by decades of clinical trials in hundreds of thousands of patients proving they prevent heart disease. We recommend starting with statins due to this strong evidence base and accessibility.

Ann: It wouldn't make sense to recommend a PCSK9 inhibitor to a low-risk young person, as they haven't been studied in that population. Evidence shows that what matters most is how low you get your LDL or ApoB, regardless of how you achieve it.

Ann: For most people, LDL and ApoB track together. Whether achieved through ezetimibe, PCSK9 inhibitors, or statins, the benefit corresponds to the reduction in LDL. Guidelines start with statins due to cost and trial evidence.

Ann: If someone cannot tolerate statins, ezetimibe is a great alternative. Some patients experience 30% to 40% LDL reduction with ezetimibe, while others get only 15%, requiring non-generic options that cost several hundred dollars a month.

Brent: If recommendations account for cost, I prefer focusing purely on clinical effectiveness. Is the statin recommendation primarily due to evidence quality, or would PCSK9 inhibitors be recommended if cheaper?

Brent: PCSK9 inhibitors haven't been studied as extensively in young people, which is why recommendations center on statins.

Ann: Without clinical trials showing benefit in young people, we would be extrapolating to assume equal benefit. Even if costs were equal, I would still start with statins because they have been studied in hundreds of thousands of people over decades. We understand their risks, benefits, and drug interactions thoroughly.

Ann: It's the robust evidence base, not just cost, that dictates starting with statins.

Brent: How much pushback do you receive regarding over-medication vs. focusing on lifestyle? You noted high LDL levels often can't be resolved with diet and exercise alone.

Brent: I assume there is commentary pushing back against pharmaceuticals, advocating for natural approaches instead.

Brent: How prevalent is that pushback, and how do you respond?

Ann: The worst scenario for Big Pharma would be everyone in their 30s taking generic statins to lower LDL. No one is getting rich off statins; they are loss leaders. Pharmacies and grocery stores sell them under $10 a month to bring customers inside.

Ann: Services like Mark Cuban Cost Plus Drugs offer a three-month supply of statins and ezetimibe for under $10. Pharma profits far more when patients develop full heart disease. Ischemic heart disease remains the leading cause of death in the US.

Ann: If everyone maintained optimal physical activity, consumed whole foods, and avoided pollution, secondhand smoke, and microplastics, fewer people would need statins. But that doesn't reflect real-world population epidemiology.

Ann: We are not claiming everyone must take a statin. Rather, if you want to lower your risk of a heart attack or stroke, starting early is the most effective tool.

Ann: Over half of US adults take vitamins despite a lack of outcome data showing cardiovascular benefit. Randomized trials show fish oils don't prevent events, yet 20% of people take them for heart health. The public is motivated to prevent disease.

Ann: I view statins as a preventive tool with proven efficacy. The longer you take them, the greater the benefit. I'd love a world free of heart disease where medications weren't needed, but that isn't our current reality.

Ann: We have effective tools to combat the cardiovascular epidemic; we just need to use them.

Brent: That's a great point. While there is a narrative about Big Pharma, supplement and wellness spaces often operate with far less oversight. Pharmaceutical guidelines undergo strict scrutiny, data evaluation, and conflict-of-interest checks.

Brent: Unregulated supplements and off-label compounds lack those rigorous checks, so consumers should remain discerning regarding unverified health claims.

Brent: Established organizations like the American Heart Association operate within strict regulatory and legal oversight structures.

Ann: Supplements are regulated similarly to food items rather than pharmaceuticals. The safety monitoring system for supplements is reactive rather than proactive, with no requirement to prove efficacy before marketing products for "heart support."

Ann: Structure-function claims do not require proof of disease prevention. Consumers assume over-the-counter availability implies safety, but regulation is minimal.

Ann: There is no standard dosing enforcement for supplements, and issues like oxidation or heavy metal contamination occur in fish oils. Supplement manufacturers often promote anti-statin narratives to sell expensive monthly packs that lack proven benefits.

Brent: What about concerns that statins cause dementia? That claim appears frequently online. What does the evidence show?

Ann: Multiple randomized trials and meta-analyses demonstrate that statins do not cause dementia or worsen existing dementia. While rare individual patients report cognitive side effects that resolve upon switching medications, trials show no population-level link.

Ann: Statins prevent strokes, which are a primary cause of vascular dementia. Protecting brain health requires preventing arterial cholesterol buildup over a lifetime.

Ann: Studies also show potential improvements in erectile function with statin use. Regarding safety, statins carry a slight risk of accelerating diabetes onset in predisposed individuals.

Ann: In individuals with normal glucose levels and healthy weight, statins do not induce diabetes. In pre-diabetic or obese individuals, statins may bring forward a diabetes diagnosis by several weeks.

Ann: Given that heart disease is the leading cause of death in diabetic patients, statin therapy paired with lifestyle modifications remains crucial for overall prevention.

Ann: Statins do not directly cause diabetes in healthy populations.

Brent: Brain health is closely linked to heart health. Protecting cardiovascular health is foundational to protecting cognitive function.

Brent: Where does the concern about cognitive issues originate?

Ann: It isn't observed in clinical trial data, though anecdotally a few patients report it. The most common concern is muscle aches. Severe muscle breakdown (rhabdomyolysis) occurs in roughly 1 in 10,000 cases.

Ann: That effect is obvious, bilateral, and resolves upon stopping medication. It was more common with simvastatin, which is rarely used now, and occurs far less at lower doses.

Ann: In general population surveys, 1 in 3 people report general aches. In statin trials, muscle ache complaints occur at equal rates in the placebo and treatment groups.

Ann: Discontinuation rates due to side effects are identical between statin and placebo groups across trials. This points to a "nocebo" effect, where anticipation of a side effect causes a real physical perception.

Ann: Switching to a different statin type usually resolves the issue.

Brent: I experienced muscle aches when taking statins, so I switched to a PCSK9 inhibitor. It's interesting how expectation can influence symptoms.

Brent: So it's in your head, Brent.

Ann: I listen to my patients' reported experiences. Everyone responds individually. My father, a retired physician, experienced muscle weakness while taking statins.

Ann: We added CoQ10 supplementation, and he is now on a maximum statin dose without side effects.

Brent: He takes CoQ10 alongside the statin and no longer experiences side effects?

Ann: Yes. We tailor treatment to the individual—adjusting dosages, trying different statins, or utilizing alternative options like oral PCSK9 inhibitors or bempedoic acid if intolerance persists.

Ann: If statin intolerance occurs, alternative therapeutic avenues remain available.

Brent: Do you take a statin yourself?

Ann: My baseline LDL cholesterol is around 60, so I do not. However, if my LDL were above 100, I would take one.

Brent: If statins are highly effective with low risk, why not take one universally?

Ann: Epidemiological studies show that low-risk individuals with optimal lipid profiles, normal Lp(a), healthy habits, and no family history of heart disease generally do not require medication when LDL is naturally below 100.

Ann: With a low baseline risk profile, pharmacotherapy isn't indicated.

Brent: If your LDL rose above 100, you would start treatment immediately?

Ann: Absolutely. If my LDL exceeded 100, I would start right away. Long-term studies, such as the West of Scotland Coronary Prevention Study (WOSCOPS), followed participants given statins vs. placebo over five years.

Ann: Even after the formal trial ended and crossover occurred, long-term follow-up revealed persistent cardiovascular protection in the original statin group.

Ann: Early LDL lowering helps prevent initial plaque formation and promotes favorable arterial remodeling, producing a legacy protective effect.

Ann: Starting statin therapy in your 30s or 40s compounds benefits over time, reducing lifetime risk. Starting early prevents heavy disease burdens later that would require multiple high-dose drugs.

Ann: It compounds over time and blunts long-term risk of heart disease.

Brent: What are your thoughts on ApoB becoming prominent relative to LDL? Is there a significant practical distinction between the two markers?

Brent: How do you evaluate their clinical importance?

Ann: I've used ApoB clinically for a decade. While framed as a new trend online, it is simply a refined marker of atherogenic particle concentration.

Ann: LDL cholesterol measures the mass of cholesterol contained within LDL particles. For most people, LDL mass correlates with total particle number. However, risk is driven by the total number of atherogenic particles entering artery walls rather than particle mass alone. Each atherogenic particle carries one ApoB molecule.

Ann: Fractionated particle testing provides little added value once ApoB and Lp(a) are known. ApoB and Lp(a) provide the most comprehensive risk assessment.

Ann: While LDL and ApoB track together for most individuals, discordance occurs in a minority. For example, some young women present with elevated LDL-C (120–130) but low ApoB (80–90), indicating cholesterol-rich particles without an unsafe particle count.

Ann: Conversely, others have normal LDL-C but elevated ApoB. Generally, target values correspond directly: an LDL target of 70 aligns with an ApoB target of 70 mg/dL.

Ann: For primary prevention in low-risk individuals, aiming for an ApoB below 90 mg/dL—or below 70 mg/dL for optimal protection—is reasonable.

Brent: Lp(a) is an important genetic risk marker. Commercial lipid particle subfractionation tests exist, based on the concept that smaller, denser particles penetrate arterial walls more easily.

Brent: However, cardiologists note that particle size testing rarely alters clinical management beyond standard lipid panels, ApoB, and Lp(a).

Brent: Standard panels, ApoB, and Lp(a) provide all the necessary information.

Ann: Correct. Lp(a) represents a specific class of LDL particles carrying an additional apolipoprotein(a) moiety that makes particles stickier and more atherogenic. Roughly 15% to 20% of the population has high Lp(a) levels.

Ann: Lp(a) concentration is predominantly genetically determined, reaching adult levels in childhood. Elevated Lp(a) is a major driver of early cardiovascular events in families without other traditional risk factors, inheriting in an autosomal dominant pattern.

Ann: If an individual has high Lp(a), first-degree relatives have a 50% chance of inheriting elevated levels. This explains strong family histories of early heart disease.

Brent: So someone can have elevated total LDL cholesterol genetically while maintaining normal Lp(a)?

Ann: They are distinct. The gene regulating Lp(a) expression is independent of polygenic pathways governing overall LDL metabolism. While monogenic conditions like familial hypercholesterolemia exist, common polygenic high cholesterol involves many small-effect variants.

Ann: Lp(a) levels remain stable throughout life, except for modest increases during menopause. Testing is generally needed only once. If high, clinical management involves lowering overall LDL targets.

Ann: If a patient's baseline LDL goal is 100 mg/dL, an elevated Lp(a) prompts lowering the target to 70 mg/dL to offset overall cardiovascular risk.

Ann: Guidelines advise intensifying therapy when Lp(a) is high. Until targeted Lp(a)-lowering therapeutics become available, reducing overall atherogenic particle burden remains the key strategy.

Brent: Are you optimistic about emerging targeted therapies designed to lower Lp(a) directly?

Ann: I am currently leading major cardiovascular outcome trials for these agents. Initial Phase 3 trials evaluate antisense oligonucleotides (monthly injections) and siRNAs (quarterly injections) in established cardiovascular disease populations.

Ann: A third drug, lepodisiran, administered every six months, is being evaluated in primary prevention trials for high-risk Lp(a) individuals. Epidemiology strongly supports causal risk reduction if Lp(a) is lowered substantially (by 80%–90%).

Ann: Sufficient reduction magnitude is required to produce clear clinical benefits. While biology suggests success, clinical science requires rigorous trial verification.

Ann: HDL therapeutics serve as a historical warning: despite strong epidemiological links between high HDL and lower heart risk, drugs designed to raise HDL failed to reduce cardiovascular events in randomized trials.

Ann: We await definitive outcome trial results, though preliminary mechanism data remains encouraging.

Brent: What are your thoughts on tadalafil (Cialis) being promoted online for general cardiovascular health in middle-aged individuals?

Brent: Should someone in their 40s consider tadalafil solely for heart health benefits?

Ann: There is no compelling clinical trial evidence supporting PDE5 inhibitors for primary cardiovascular prevention. Side effects include blood pressure drops. Taking it for erectil dysfunction is fine, but not for cardiovascular prevention.

Brent: What is the biological rationale proposed for its potential benefit?

Ann: Mechanistic and animal studies show positive effects on endothelial function, vascular reactivity, or cellular signaling pathways. Compelling biological narratives can be constructed around many compounds.

Ann: However, medical practice requires randomized clinical outcome trials demonstrating clear human efficacy and safety, as unexpected adverse events frequently arise when moving from theory to human testing.

Ann: We have proven, underutilized tools for cardiovascular prevention. Effective risk reduction consists of avoiding smoking, exercising regularly, maintaining physical activity, managing blood pressure, and lowering LDL cholesterol.

Ann: Unproven experimental therapies are unnecessary when core risk factors can be managed effectively. For aggressive protection, target LDL below 70 mg/dL or 55 mg/dL.

Ann: No guidelines or trials support off-label PDE5 inhibitor use for long-term cardiovascular prevention.

Brent: How have health influencers impacted public understanding? Popular books and media have increased interest in preventative health and educated the public on basic lipid biology.

Brent: This engagement has made many individuals more proactive regarding their personal health management.

Brent: Conversely, some online narratives promote unverified claims that outpace clinical evidence, encouraging self-experimentation with unproven compounds.

Brent: Self-experimentation with compounds like unstudied peptides poses risks. Some commentators advocated early statin use prior to updated consensus statements. What is your overall assessment of the "Medicine 3.0" movement's impact?

Brent: While some influencer recommendations align with clinical consensus, others exceed evidence boundaries.

Ann: A major positive is raising public awareness that atherogenic particles cause heart disease and that lower levels prevent events. Public messaging around "lower is better" has countered long-standing anti-statin misinformation.

Ann: That shift has been beneficial. However, formal clinical guidelines maintain strict evidence standards compared to individual clinical practice, where preventive cardiologists have advocated early risk interventions for years.

Ann: Guidelines require conservative threshold data to maintain public trust and medical credibility. Individualized clinical decisions can go beyond minimum guideline baselines when clinically indicated.

Ann: My primary concern with some health commentators is the tendency to undermine mainstream medicine to build audience trust, despite practicing principles derived from academic research and epidemiology.

Ann: Extrapolating preliminary data without acknowledging missing long-term safety data can be misleading. Discrediting the broader medical community is unnecessary when discussing advanced interventions.

Ann: Broad online access to prescription compounds without supervision is concerning. Commentators should present evidence transparently without disparaging standard medical practice.

Ann: Preventive cardiologists have emphasized ApoB and early intervention long before these concepts were popularized in mainstream books. Less adversarial framing would benefit public health.

Ann: In reality, clinical experts and health advocates agree on core preventative goals.

Brent: Undermining public trust in medical consensus around major cardiovascular diseases can have real-world consequences if patients decline proven, life-saving therapies based on unverified claims.

Brent: Human health guidance carries significant responsibility.

Ann: Public health literacy is critical, but consuming media podcasts is distinct from conducting primary scientific research. Media literacy helps individuals become informed patients, but shouldn't replace primary evidence evaluation.

Ann: Selectively interpreting literature to fit specific media narratives risks creating unnecessary division between patients and evidence-based clinical medicine.

Ann: Cardiologists share the goal of reducing atherogenic cholesterol and preventing early heart attacks. The primary requirement is engaged patients taking action on foundational preventive steps.

Brent: Dr. Anne Marie Navarre, thank you for your time, insight, and research efforts.

Ann: Thank you for having me.

Brent: The Life Lab by Death Clock is recorded in Boulder, Colorado, and San Francisco, California. Produced by Patrick Godinho, music by Patrick Lee, and hosted by Brent Franson, founder and CEO of Death Clock.