A large international study found that 99% of heart attacks, strokes, and heart failure cases were preceded by at least one measurable risk factor, meaning these events are rarely random and often develop over years.
It's worth mentioning the importance of having a blood test for lipoprotein(a), commonly known as Lp(a), which is a particle similar to LDL cholesterol (the "bad" cholesterol), but with a key structural difference: it has an additional protein called apolipoprotein(a) attached to it. This particular structure makes it an independent and highly specific cardiovascular risk factor. Below, I'll explain why it's relevant and how it behaves in the body.
Unlike conventional LDL, Lp(a) increases cardiovascular risk through three main mechanisms: Like LDL, it accumulates in the walls of arteries, promoting the formation of atherosclerotic plaques (fatty deposits). Apolipoprotein(a) transports oxidized phospholipids that irritate the arterial wall, accelerating vascular damage. Its structure is very similar to plasminogen (a molecule that helps dissolve blood clots). Lp(a) "tricks" the body by competing with plasminogen, making it harder to eliminate clots and increasing the risk of heart attacks or strokes. Lp(a) levels are 90% genetically determined.
Unlike total cholesterol or triglycerides, what you eat or how much you exercise has little effect on its concentration. Levels tend to remain constant throughout life. Therefore, current medical guidelines recommend measuring it at least once in a lifetime for adults, especially if there is a family history of premature cardiovascular disease.
A person can have very low and healthy LDL cholesterol but high Lp(a), which maintains a residual risk of heart problems that often goes undetected in routine blood tests.
The current medical approach is to aggressively control all other risk factors (blood pressure, glucose, LDL) to compensate for the genetic risk of Lp(a).
The impact of Lp(a) on the heart valves is one of the most important discoveries of the last decade in cardiology. Unlike common LDL cholesterol, which primarily affects the coronary arteries, Lp(a) has a special affinity for valve tissue, especially the aortic valve.
1. Calcified Aortic Stenosis
The strongest association is with aortic stenosis, which is the narrowing of the valve that allows blood to flow from the heart to the rest of the body. Infiltration: Lp(a) is a small, dense particle that easily penetrates the layers of the aortic valve. Inflammation and Oxidation: Once inside, the oxidized phospholipids carried by Lp(a) activate cells called fibroblasts, transforming them into something similar to bone cells (osteoblasts). Calcification: This process causes the valve, which should be flexible like a thin tissue, to fill with calcium deposits, become rigid, and be unable to open properly.
Since Lp(a) is difficult to lower with current drugs, valve protection focuses on keeping the "environment" as clean as possible to prevent Lp(a) from causing damage. Markers that help predict whether this process is active include: Marker Role in valve health Glucose and Insulin. Low levels (such as fasting insulin < 5 µIU/mL) reduce systemic inflammation that promotes calcification. Vitamin D3 and K2. K2 is crucial because it helps direct calcium to the bones and prevents it from being deposited in soft tissues such as the valves. Inflammation (CRP): A low C-reactive protein level indicates less "fire" in the system for Lp(a) to oxidize tissues, and all the other factors in Dr. Mercola's excellent report are relevant.
Imaging Tests: How to assess valve health? If we suspect Lp(a) is affecting the valves or arteries, blood tests are not enough. We need to "photograph" the tissue. The best tools are:
A. The "Calcium Score" (Coronary Calcium Score)
This is a quick, non-contrast CT scan that measures the amount of calcium in the arteries of the heart. Usefulness: It is the best predictor of actual cardiovascular risk. A score of 0 indicates that, despite having high Lp(a) or cholesterol, the body is not depositing calcium in the arteries. Limitation: It focuses primarily on the coronary arteries, not so much on the valves.
B. Color Doppler Echocardiogram
This is the gold standard test for heart valves. What it looks for: It measures the opening of the aortic valve, the speed at which blood flows, and whether there is stiffness (sclerosis). Advantage: It is completely harmless (ultrasound) and allows you to see the heart's function in real time.
C. Multidetector Cardiac CT (For Aortic Valve)
If the echocardiogram shows evidence of calcium, this test is much more accurate for quantifying the volume of calcium specifically in the valve. It is used to distinguish between a simply "old" valve and a valve actively calcified by inflammatory processes (such as those caused by Lp(a)).
Although Lp(a) levels don't decrease easily, their danger increases when combined with: high LDL cholesterol, vascular inflammation, insulin resistance, smoking, and hypertension. When Lp(a) and LDL cholesterol are present, the risk multiplies.
Plaque progresses much more slowly. Systemic inflammation is low. Lp(a) becomes more dangerous when there is: chronic inflammation, oxidative stress, and metabolic syndrome. Markers that increase risk include: high-sensitivity C-reactive protein (hs-CRP), IL-6, and TNF-α. When inflammation is low, Lp(a) has less effect on the arterial wall.
Some people have genetic variants that: reduce lipid oxidation, improve vascular repair, and decrease inflammation. Therefore, not all elevated Lp(a) levels carry the same risk.
Lp(a) is more dangerous in middle age. The greatest impact of Lp(a) occurs between 40 and 65 years of age. At this stage: it accelerates plaque development, increases the risk of early heart attack, and promotes premature coronary artery disease. Therefore, it is considered especially important in young people with early heart attacks.
After 70–75 years of age, the relative risk decreases. In advanced age, something curious occurs: many people with high Lp(a) have already had events; those who reach advanced age tend to be more biologically resistant. This is called "survivorship bias" in epidemiology. It means that those who reach 70–80 years of age with high Lp(a) likely have protective factors.
What values are considered worrisome in older adults? In people over 70 years of age: Lp(a) Interpretation < 30 mg/dL normal. 30–50 mg/dL moderate risk. 50–90 mg/dL increased risk.
Factors that matter more in advanced age: blood pressure, chronic inflammation, endothelial function, glucose and insulin levels, and physical activity. A marker that many cardiologists consider more accurate than LDL cholesterol is Apolipoprotein B (ApoB).
Each lipid particle that can cause atherosclerosis contains one ApoB molecule. These particles are: LDL, VLDL, IDL, and Lp(a). ApoB measures the total number of atherogenic particles. Many small particles may carry little cholesterol, but they penetrate the arterial wall more easily.
Relationship between ApoB and Lp(a): Lp(a) also contains ApoB, therefore raising the ApoB value. This is why measuring ApoB helps to better assess risk when Lp(a) is high. ApoB <65 mg/dL is optimal, 65–80 mg/dL is good, 80–100 mg/dL is moderate, and >100 mg/dL is high. In people with high cardiovascular risk, a level <65 mg/dL is recommended.
Why many experts prefer ApoB: Because it is a better predictor of heart attack. Atherosclerosis and coronary heart disease. In fact, several studies show that ApoB predicts cardiovascular events better than LDL or total cholesterol.
GGT is an enzyme measured in blood tests and traditionally used to assess liver function. However, in recent years, many researchers also consider it a marker of oxidative stress and metabolic risk.
What GGT does in the body: GGT participates in the metabolism of one of the body's most important antioxidants: glutathione (GSH).
When GGT increases, it usually indicates: greater oxidative stress, a greater need to regenerate glutathione. Relationship with cardiovascular risk: Many epidemiological studies have found an association between elevated GGT and a higher risk of: myocardial infarction, atherosclerosis, metabolic syndrome, and type 2 diabetes.
It is believed to reflect: lipid oxidation and vascular inflammation.
GGT has even been found within atherosclerotic plaques. GGT also increases in conditions such as: fatty liver disease and insulin resistance. Visceral obesity, excessive alcohol consumption, and liver inflammation are all factors that can contribute to elevated levels of Lp(a), ApoB, and GGT. This is why GGT is considered a marker of liver metabolic health.
GGT doesn't just reflect liver function. It can also indicate systemic oxidative stress, metabolic risk, and vascular inflammation. Therefore, some physicians consider it an early metabolic marker.
Here are links to direct, peer-reviewed, and academically accessible scientific articles to delve deeper into the topics of Lp(a), ApoB, and GGT in relation to cardiovascular risk:
LP(A) IS STRONGLY ASSOCIATED WITH ATHEROSCLEROTIC RISK, INFLAMMATION, AND VALVULAR CALCIFICATION, AND IS AN INDEPENDENT GENETIC CAUSAL FACTOR OF CARDIOVASCULAR DISEASE.
APOB represents the total number of atherogenic lipoprotein particles and can better predict cardiovascular risk than LDL-C in many clinical settings.
Elevated GGT is consistently associated with a higher risk of cardiovascular disease, mortality, and adverse events, even after adjusting for classic factors.
Everyone's dehydrated so blood is too thick and sticky..solution is drink 2 liters of water a day approx and fast once a week one full day and another day only have a mid day meal..this will allow even more cel,veinl hydration,thin blood from start of issue...
It's worth mentioning the importance of having a blood test for lipoprotein(a), commonly known as Lp(a), which is a particle similar to LDL cholesterol (the "bad" cholesterol), but with a key structural difference: it has an additional protein called apolipoprotein(a) attached to it. This particular structure makes it an independent and highly specific cardiovascular risk factor. Below, I'll explain why it's relevant and how it behaves in the body.
Unlike conventional LDL, Lp(a) increases cardiovascular risk through three main mechanisms: Like LDL, it accumulates in the walls of arteries, promoting the formation of atherosclerotic plaques (fatty deposits). Apolipoprotein(a) transports oxidized phospholipids that irritate the arterial wall, accelerating vascular damage. Its structure is very similar to plasminogen (a molecule that helps dissolve blood clots). Lp(a) "tricks" the body by competing with plasminogen, making it harder to eliminate clots and increasing the risk of heart attacks or strokes. Lp(a) levels are 90% genetically determined.
Unlike total cholesterol or triglycerides, what you eat or how much you exercise has little effect on its concentration. Levels tend to remain constant throughout life. Therefore, current medical guidelines recommend measuring it at least once in a lifetime for adults, especially if there is a family history of premature cardiovascular disease.
Low risk: < 30 mg/dL (or < 75 nmol/L). High risk: > 50 mg/dL (or > 125 nmol/L).
A person can have very low and healthy LDL cholesterol but high Lp(a), which maintains a residual risk of heart problems that often goes undetected in routine blood tests.
The current medical approach is to aggressively control all other risk factors (blood pressure, glucose, LDL) to compensate for the genetic risk of Lp(a).
The impact of Lp(a) on the heart valves is one of the most important discoveries of the last decade in cardiology. Unlike common LDL cholesterol, which primarily affects the coronary arteries, Lp(a) has a special affinity for valve tissue, especially the aortic valve.
1. Calcified Aortic Stenosis
The strongest association is with aortic stenosis, which is the narrowing of the valve that allows blood to flow from the heart to the rest of the body. Infiltration: Lp(a) is a small, dense particle that easily penetrates the layers of the aortic valve. Inflammation and Oxidation: Once inside, the oxidized phospholipids carried by Lp(a) activate cells called fibroblasts, transforming them into something similar to bone cells (osteoblasts). Calcification: This process causes the valve, which should be flexible like a thin tissue, to fill with calcium deposits, become rigid, and be unable to open properly.
Since Lp(a) is difficult to lower with current drugs, valve protection focuses on keeping the "environment" as clean as possible to prevent Lp(a) from causing damage. Markers that help predict whether this process is active include: Marker Role in valve health Glucose and Insulin. Low levels (such as fasting insulin < 5 µIU/mL) reduce systemic inflammation that promotes calcification. Vitamin D3 and K2. K2 is crucial because it helps direct calcium to the bones and prevents it from being deposited in soft tissues such as the valves. Inflammation (CRP): A low C-reactive protein level indicates less "fire" in the system for Lp(a) to oxidize tissues, and all the other factors in Dr. Mercola's excellent report are relevant.
Imaging Tests: How to assess valve health? If we suspect Lp(a) is affecting the valves or arteries, blood tests are not enough. We need to "photograph" the tissue. The best tools are:
A. The "Calcium Score" (Coronary Calcium Score)
This is a quick, non-contrast CT scan that measures the amount of calcium in the arteries of the heart. Usefulness: It is the best predictor of actual cardiovascular risk. A score of 0 indicates that, despite having high Lp(a) or cholesterol, the body is not depositing calcium in the arteries. Limitation: It focuses primarily on the coronary arteries, not so much on the valves.
B. Color Doppler Echocardiogram
This is the gold standard test for heart valves. What it looks for: It measures the opening of the aortic valve, the speed at which blood flows, and whether there is stiffness (sclerosis). Advantage: It is completely harmless (ultrasound) and allows you to see the heart's function in real time.
C. Multidetector Cardiac CT (For Aortic Valve)
If the echocardiogram shows evidence of calcium, this test is much more accurate for quantifying the volume of calcium specifically in the valve. It is used to distinguish between a simply "old" valve and a valve actively calcified by inflammatory processes (such as those caused by Lp(a)).
https://pubmed.ncbi.nlm.nih.gov/36030913/
https://pubmed.ncbi.nlm.nih.gov/27040402/
https://www.ahajournals.org/doi/full/10.1161/ATV.0000000000000147
https://www.nejm.org/doi/full/10.1056/NEJMsa1906848
https://evidence.nejm.org/doi/full/10.1056/EVIDoa2200047
Although Lp(a) levels don't decrease easily, their danger increases when combined with: high LDL cholesterol, vascular inflammation, insulin resistance, smoking, and hypertension. When Lp(a) and LDL cholesterol are present, the risk multiplies.
Plaque progresses much more slowly. Systemic inflammation is low. Lp(a) becomes more dangerous when there is: chronic inflammation, oxidative stress, and metabolic syndrome. Markers that increase risk include: high-sensitivity C-reactive protein (hs-CRP), IL-6, and TNF-α. When inflammation is low, Lp(a) has less effect on the arterial wall.
Some people have genetic variants that: reduce lipid oxidation, improve vascular repair, and decrease inflammation. Therefore, not all elevated Lp(a) levels carry the same risk.
Lp(a) is more dangerous in middle age. The greatest impact of Lp(a) occurs between 40 and 65 years of age. At this stage: it accelerates plaque development, increases the risk of early heart attack, and promotes premature coronary artery disease. Therefore, it is considered especially important in young people with early heart attacks.
After 70–75 years of age, the relative risk decreases. In advanced age, something curious occurs: many people with high Lp(a) have already had events; those who reach advanced age tend to be more biologically resistant. This is called "survivorship bias" in epidemiology. It means that those who reach 70–80 years of age with high Lp(a) likely have protective factors.
What values are considered worrisome in older adults? In people over 70 years of age: Lp(a) Interpretation < 30 mg/dL normal. 30–50 mg/dL moderate risk. 50–90 mg/dL increased risk.
Factors that matter more in advanced age: blood pressure, chronic inflammation, endothelial function, glucose and insulin levels, and physical activity. A marker that many cardiologists consider more accurate than LDL cholesterol is Apolipoprotein B (ApoB).
Each lipid particle that can cause atherosclerosis contains one ApoB molecule. These particles are: LDL, VLDL, IDL, and Lp(a). ApoB measures the total number of atherogenic particles. Many small particles may carry little cholesterol, but they penetrate the arterial wall more easily.
Relationship between ApoB and Lp(a): Lp(a) also contains ApoB, therefore raising the ApoB value. This is why measuring ApoB helps to better assess risk when Lp(a) is high. ApoB <65 mg/dL is optimal, 65–80 mg/dL is good, 80–100 mg/dL is moderate, and >100 mg/dL is high. In people with high cardiovascular risk, a level <65 mg/dL is recommended.
Why many experts prefer ApoB: Because it is a better predictor of heart attack. Atherosclerosis and coronary heart disease. In fact, several studies show that ApoB predicts cardiovascular events better than LDL or total cholesterol.
GGT is an enzyme measured in blood tests and traditionally used to assess liver function. However, in recent years, many researchers also consider it a marker of oxidative stress and metabolic risk.
What GGT does in the body: GGT participates in the metabolism of one of the body's most important antioxidants: glutathione (GSH).
When GGT increases, it usually indicates: greater oxidative stress, a greater need to regenerate glutathione. Relationship with cardiovascular risk: Many epidemiological studies have found an association between elevated GGT and a higher risk of: myocardial infarction, atherosclerosis, metabolic syndrome, and type 2 diabetes.
It is believed to reflect: lipid oxidation and vascular inflammation.
GGT has even been found within atherosclerotic plaques. GGT also increases in conditions such as: fatty liver disease and insulin resistance. Visceral obesity, excessive alcohol consumption, and liver inflammation are all factors that can contribute to elevated levels of Lp(a), ApoB, and GGT. This is why GGT is considered a marker of liver metabolic health.
GGT doesn't just reflect liver function. It can also indicate systemic oxidative stress, metabolic risk, and vascular inflammation. Therefore, some physicians consider it an early metabolic marker.
Here are links to direct, peer-reviewed, and academically accessible scientific articles to delve deeper into the topics of Lp(a), ApoB, and GGT in relation to cardiovascular risk:
LP(A) IS STRONGLY ASSOCIATED WITH ATHEROSCLEROTIC RISK, INFLAMMATION, AND VALVULAR CALCIFICATION, AND IS AN INDEPENDENT GENETIC CAUSAL FACTOR OF CARDIOVASCULAR DISEASE.
APOB represents the total number of atherogenic lipoprotein particles and can better predict cardiovascular risk than LDL-C in many clinical settings.
Elevated GGT is consistently associated with a higher risk of cardiovascular disease, mortality, and adverse events, even after adjusting for classic factors.
https://pubmed.ncbi.nlm.nih.gov/PMC9989949/--
https://www.mdpi.com/2077-0383/11/20/6040----
https://pubmed.ncbi.nlm.nih.gov/40422940/--
https://pubmed.ncbi.nlm.nih.gov/34461734/---
https://pubmed.ncbi.nlm.nih.gov/39334349/--
https://pubmed.ncbi.nlm.nih.gov/35902283/---
https://pubmed.ncbi.nlm.nih.gov/39334349/---
https://pubmed.ncbi.nlm.nih.gov/28149843/---
https://pubmed.ncbi.nlm.nih.gov/29175647/--
https://pubmed.ncbi.nlm.nih.gov/28231268/---
https://pubmed.ncbi.nlm.nih.gov/26581592/--
Everyone's dehydrated so blood is too thick and sticky..solution is drink 2 liters of water a day approx and fast once a week one full day and another day only have a mid day meal..this will allow even more cel,veinl hydration,thin blood from start of issue...