Welcome back to another exciting journey through the labyrinth of health science! Today, we're switching gears from gut health and sugar to the heart of the matter – cardiovascular disease (CVD). After immersing myself in as many papers on the subject as I could stomach and as many hours listening to podcasts that my beautiful wife would allow, I’ve uncovered some pivotal insights about ApoB and LPa that are too valuable not to share.
What the Hell are ApoB and LPa, Anyway?
First up, let's demystify these acronyms. Apolipoprotein B (ApoB) and Lipoprotein(a) [LPa] are like the covert operatives in your blood, playing critical roles in cholesterol transport and plaque formation. Understanding them is crucial because, unlike the usual cholesterol suspects (I'm looking at you, LDL and HDL), these guys give us the real scoop on CVD risk.
Let’s break down an analogy that I’ve heard Dr. Attia make several times to help us understand these compounds better.
Picture your lifespan as a race from point A to point B, where point B is, well, the end of the road (death). In this race, you've got two pedals: the accelerator and the brake. Now, imagine factors like ApoB and LPa as forces acting on these pedals.
ApoB is like having a heavy foot on the gas. It speeds up your journey towards heart disease, the metaphorical cliff. But here's the twist: you can ease off the gas and hit the brakes. Dietary changes and medications can effectively slow down this race, giving you more time on the track.
But what about LPa? This guy is a bit trickier. It's like a subtle, constant pressure on the accelerator, determined by the luck of the genetic draw. High LPa means your car is naturally faster, inching you closer to that cliff edge without you even realizing it. Unlike ApoB, where you can slam on the brakes, LPa requires a more nuanced approach. It's about keeping an eye on the speedometer and making adjustments as needed.
Peter Attia beautifully encapsulates this with his analogy: "We have a car that we can't stop, but we can slow down to a very slow pace." This is the essence of managing ApoB and LPa. It's not about halting progress but controlling the speed, understanding the factors at play, and making informed choices to manage the risks.
Why Your Cholesterol Test Might Be Missing the Mark
We've all been there – getting those cholesterol numbers and thinking we've got the full picture. But here's the kicker: traditional metrics can be deceiving. They often overlook the nuanced roles of different lipoproteins in heart health. It's like judging a book by its cover without reading the chapters that matter. Traditional tests typically measure total cholesterol, HDL (high-density lipoprotein), and LDL (low-density lipoprotein) cholesterol. However, they miss out on crucial details. ApoB, for instance, gives a more accurate count of the particles that can deposit cholesterol into the artery walls, leading to atherosclerosis. Similarly, LPa, a subtype of LDL, is a unique risk factor for cardiovascular disease. Elevated LPa levels are associated with increased risk, regardless of other cholesterol levels. Hence, these traditional cholesterol numbers might not fully reflect your cardiovascular risk.
Cholesterol: The Body's Enigma
Our bodies are indeed cholesterol-crafting machines, intricately linked to what we consume. However, unraveling this mystery isn't straightforward. Although dietary cholesterol's impact on blood levels is often discussed, the reality is more complex. The liver, our primary cholesterol factory, adjusts its production based on dietary intake. Eating high amounts of cholesterol-rich foods doesn't necessarily cause a spike in blood cholesterol levels. Conversely, reducing dietary cholesterol doesn't always lead to lower blood cholesterol levels. This intricate dance between dietary intake and the body's cholesterol production is influenced by individual genetics, lifestyle factors, and the types of fats consumed. It's a delicate balance that varies greatly from person to person, underscoring the importance of personalized approaches to cholesterol management.
The type of fat we consume does in fact play a role in determining our cholesterol levels. Saturated fats, found in foods like red meat and dairy products, can increase LDL cholesterol, often labeled as 'bad' cholesterol. But even this seems to depend on the individual. In contrast, unsaturated fats, present in foods like fish, nuts, and olive oil, are considered heart-healthy. They can increase HDL cholesterol, the 'good' cholesterol, and may even lower LDL levels. The most interesting paper I came across on this subject was published in The American Journal of Clinical Nutrition. The paper reviews the impact of dietary saturated fat on cardiovascular disease (CVD) risk. Clinical trials replacing saturated fat with polyunsaturated fat almost unanimously showed reduced CVD events. The authors concluded that replacing saturated fat with polyunsaturated fat can lower CVD risk. The authors also suggest that dietary recommendations should focus more on reducing excess adiposity (fat), rather than strictly reducing saturated fat intake.
Additionally, trans fats, commonly found in processed foods, are particularly harmful as they both raise LDL cholesterol and lower HDL cholesterol. This variation in fat types means that our choices of fats can significantly influence our cholesterol levels and overall heart health.
It's also crucial to note that the body's response to dietary cholesterol is highly individualized. For some, consuming high-cholesterol foods has minimal impact on their blood cholesterol levels, as their bodies compensate by reducing internal cholesterol production. However, others might see significant changes in their blood markers with even modest intake of cholesterol-rich foods. This variability can be attributed to genetic factors, metabolic differences, and overall lifestyle. It serves as a reminder that dietary guidelines are not one-size-fits-all, highlighting the growing importance of personalized nutrition in health management.
Familial Hypercholesterolemia: When Genetics Loads the Gun
For some, the battle against high cholesterol is a hereditary challenge. Familial Hypercholesterolemia (FH) is a genetic disorder that affects millions worldwide. In FH, the body's ability to remove LDL cholesterol from the blood is impaired, leading to elevated cholesterol levels from a young age. This condition significantly increases the risk of developing heart disease early in life. While lifestyle changes like diet and exercise may help, they often aren't enough to manage FH effectively. Medications, particularly statins, play a crucial role in controlling cholesterol levels for those with FH. These drugs help reduce the production of cholesterol in the liver and increase the liver's ability to remove LDL cholesterol from the blood, making them vital in the management of this genetic condition.
Statins: The Heart's Guard
The life-saving impact of statins is well-documented and significant. While specific numbers can vary depending on the population studied and the context, research has consistently shown that statins substantially reduce the risk of cardiovascular events and death, particularly in those at high risk. For example, a study involving over 6,000 men who had high levels of cholesterol were given statins and followed for 20 years. The study showed these men, even after 20 years, were 25% less likely to die of a heart attack. This highlights the crucial role of statins in reducing mortality, especially in populations at greater risk.
Additionally, broader research indicates that statins are effective in preventing heart attacks and strokes, leading to a substantial decrease in mortality rates among those with high risk of coronary heart disease. It's clear from these studies that statins play a significant role in cardiovascular health management and have contributed to saving countless lives over the years.
These findings underscore the importance of statins as not just another medication, but a critical tool in the fight against cardiovascular disease, providing significant protection for the heart and extending lives.
Ignoring High ApoB and LPa: A Risky Game
Here's where things get real. Ignoring elevated ApoB and LPa levels is like playing Russian roulette with your heart health. I'll delve into why taking these markers seriously is not just smart – it's a lifesaver.
A comprehensive study published in Nature has shown that individuals with elevated lipid profiles, characterized by high levels of total cholesterol (TC), triglycerides, ApoB, and a high ApoB/ApoA-I ratio, are at a significantly increased risk of cardiovascular mortality. Specifically, in individuals aged 39–59, high total cholesterol was associated with increased all-cause mortality. Notably, high triglycerides and high ApoB were consistently linked to a higher risk of mortality, irrespective of age. This data underscores the critical importance of not overlooking elevated ApoB and LPa levels, as they are key indicators of cardiovascular health risks. In the simplest explanation possible, having high levels of Lp(a) and Apo(B) makes it more likely that you will die. The higher these numbers, the higher your risk of death. BUT, this also works the other way. The lower you can keep your Apo(B) and LP(a), the less likely you will die of heart disease. By the way, you can order these tests for around $40 from any Quest labs site. Clearly, a worthwhile investment.
Exercise And CVD:
As we delve into the complexities of cholesterol and its implications for heart health, understanding the nuanced roles of ApoB and LPa provides a critical foundation. Yet, recognizing the power of lifestyle changes, particularly exercise, in influencing our cardiovascular destiny is equally vital. Exercise stands as a formidable ally in the battle against CVD. Regular physical activity not only influences traditional CVD risk factors like insulin resistance, hypertension, dyslipidemia, and obesity but also exerts profound effects on cardiorespiratory fitness (CRF), which is a stronger predictor of CVD risk than physical activity levels alone. A paper published in The Journal Of The American College of Cardiology concluded: “Exercise volumes that meet or exceed the current physical activity guidelines of 150 to 300 minutes of moderate-intensity or 75 to 150 minutes of vigorous-intensity aerobic exercise each week are associated with significant reductions in CVD and all-cause mortality.”. By embracing an active lifestyle that meets or surpasses recommended guidelines, individuals can markedly diminish their CVD risk, illustrating that alongside genetic and biochemical markers, our daily habits hold substantial sway over our cardiovascular health.
As we conclude this discussion on ApoB and LPa, it's essential to emphasize the significance of understanding and monitoring these biomarkers for heart health. The knowledge about ApoB and LPa levels can indeed be the key to unlocking a healthier future and achieving longevity with a thriving heart.
Here's why this knowledge is crucial:
Early Detection: Elevated ApoB and LPa levels can be silent threats to heart health. By monitoring these markers, individuals and healthcare providers can detect potential risks early on, allowing for timely intervention.
Personalized Care: Recognizing your ApoB and LPa levels enables personalized heart health management. It allows healthcare professionals to tailor interventions, such as medication or lifestyle changes, to your specific needs. Please, for the love of god, listen to your doctor rather than the social media influencers.
Prevention: Knowledge is power when it comes to preventing heart disease. Understanding the role of ApoB and LPa in cholesterol metabolism empowers individuals to make informed choices about diet, exercise, and other lifestyle factors that influence these markers.
Lifesaving Interventions: For those with genetic predispositions or high-risk profiles, understanding the significance of ApoB and LPa can be a lifesaver. Medications and interventions can be prescribed when necessary to mitigate the risk of cardiovascular events.
Be Weary
There are many advantages to “rebelling” against conventional wisdom, in particular, when it comes to nutrition. If you’re an influencer, it’s much easier to get attention if you make claims that counter the norm. On top of that, we all have our own biases towards the foods we enjoy. Most of us love the taste of a buttered steak. Wouldn’t it be amazing if that butter smeared steak would also increase our life and health span!? Of course it would. But often, what appears to be to good to be true, in fact, is. Here’s a quote directly from Dr. Peter Attia that I feel sums this up quite well: “The “cholesterol paradox” holds a certain surface-level glamor. It plays on our natural fascination with mystery and desire to question convention. Wouldn’t it be revolutionary if it were true that high cholesterol had no impact on mortality – or was even potentially protective?
But upsetting conventional wisdom takes more than an appealing idea, particularly when convention is backed by reams of research ranging from countless human randomized clinical trials to Mendelian randomizations to (literally) millions of patient-years of epidemiology. With its significant shortcomings, the Rozanski et al. study simply doesn’t come close to providing a convincing argument against the long-held and well-supported wisdom that low LDL levels are associated with reduced risk of CVD and mortality. In the end, the “cholesterol paradox” appears to be little more than a flashy name for a fictitious phenomenon.”.
In conclusion, the message is clear: let's not merely go through life; let's actively work to outlive our expectations. By embracing knowledge about ApoB and LPa, making informed choices, and collaborating with healthcare professionals, we can embark on a journey towards a heart-healthy and fulfilling life. It's a commitment to not just an increase in lifespan, but an increase in health span.
Until next time,
Jake Louro
Louro Training
Some of my references:
https://www.bhf.org.uk/what-we-do/our-research/research-successes/statins-save-lives
https://www.nature.com/articles/s41598-021-03959-5
https://www.sciencedirect.com/science/article/pii/S0002916523016702?via=ihub
https://www.ahajournals.org/doi/10.1161/ATVBAHA.120.315291
https://www.sciencedirect.com/science/article/pii/S0735109722055401?via=ihub#sec8