Cardiovascular disease remains the leading cause of death in developed countries and is increasing in countries undergoing epidemiological transition; the good news is that it is probably the chronic disease where prevention has the greatest scope and where the… Read more.
67 factors with evidence, ordered from highest to lowest effectiveness. Information, not medical advice.
*⏱ 2 min read
A myocardial infarction, commonly known as a heart attack, is a critical and often life-changing event that strikes suddenly, but whose underlying causes develop over time; when blood flow to a part of the heart is blocked, the heart muscle is deprived of oxygen, cells are forced to switch from aerobic to anaerobic metabolism, harmful metabolic byproducts accumulate and reactive oxygen species are produced, triggering an inflammatory cascade that can lead to cell death and long-term heart failure.
The most significant risk factors for premature heart attack in men aged 18 to 55 and women aged 18 to 65 are mostly modifiable: diabetes increases the risk 4-5 times; smoking increases it more than 4 times; dyslipidemia almost 3 times; obesity with a BMI over 30, 1.5 times; total cholesterol above 200 mg/dL and HDL below 60 mg/dL increase the risk 2-3 times; and elevated triglycerides above 150 mg/dL are associated with higher risk even with mild elevations.
A recent study showed that practicing 16:8 time-restricted eating during the 6 months after a heart attack produced robust improvements in cardiac function that were not seen in patients who kept their usual meal schedule; just one month after the heart attack, participants assigned to 16:8 fasting experienced a 6.6% increase in left ventricular ejection fraction, versus only 1.5% in the regular diet group, and this improvement not only persisted but kept increasing until it reached 10.3% at 6 months.
The most surprising thing about these results is that the magnitude of the improvement in cardiac function with fasting was comparable to that of established clinical interventions such as stem cell therapy, which improves pumping efficiency by 8.5% at 4 months, stem cell injection directly into the heart, which produces a 4.3% improvement, and empagliflozin, an SGLT-2 inhibitor drug that improves pumping efficiency by 4.7% at 6 months; this means that 6 months of 16:8 TRE matched or exceeded pharmacological and experimental treatments.
*⏱ 2 min read
Small vessel disease is a condition that causes blood vessel dysfunction related to aging and contributes to the development of cardiovascular disease, dementia, and stroke; small vessel disease in the brain, called cerebral small vessel disease, contributes to approximately 50% of dementia cases worldwide, including Alzheimer's, Parkinson's, and other common neurodegenerative diseases, making it both one of the most overlooked and one of the most important causal factors of cognitive decline.
The blood-brain barrier is formed by a layer of endothelial cells supported by astrocytes and pericytes that form tight junctions that regulate which substances can pass from the bloodstream into the brain; small vessel dysfunction compromises this barrier, allowing the entry of inflammatory and toxic molecules that would normally be excluded, which triggers neuroinflammation and contributes to protein misfolding, the formation of amyloid plaques and tau tangles characteristic of Alzheimer's, and the loss of dopaminergic neurons in the case of Parkinson's.
The most recent research shows that the burden of small vessel disease has a greater effect on cognition in people with dementia than the burden of amyloid-beta and tau, which represents a change in how scientists and clinicians should investigate and diagnose Alzheimer's; modifiable risk factors include hypertension, diabetes, chronic inflammation, smoking, and a sedentary lifestyle, and aggressive blood pressure management from early in life can significantly reduce the risk of developing small vessel disease.
Protective strategies include vigorous aerobic exercise, which improves small vessel density and endothelial function; omega-3 fatty acids, especially DHA, which improves blood-brain barrier integrity; vitamin D, which regulates vascular inflammation; and strict glycemic control, since diabetes and prediabetes accelerate small vessel dysfunction; caloric restriction and intermittent fasting have also been associated with improvements in cerebral vascular function, possibly through reduced inflammation and improved insulin sensitivity.
⏱ 2 min read
Cardiovascular disease remains the leading cause of death in developed countries and is rising in countries in epidemiological transition; the good news is that it is probably the chronic pathology where prevention has the greatest margin and where modifiable risk factors explain the vast majority of individual risk. Cardiovascular health is built over decades of sustained habits and benefits from interventions that act on multiple mechanisms in parallel.
High blood pressure: every 10 mmHg reduction in systolic pressure is associated with a 20% reduction in major cardiovascular events.
High LDL cholesterol: a robust causal factor demonstrated by Mendelian genetic studies and statin trials.
Diabetes and prediabetes: significantly increase cardiovascular risk.
Smoking: the modifiable factor with the greatest individual absolute impact; quitting tobacco dramatically reduces cardiovascular risk within years.
Obesity and sedentary lifestyle: independent and additive factors.
Diet: dietary quality is one of the most robust predictors.
Chronic stress and sleep deprivation: less visible but significant factors.
Untreated sleep apnea: a potent and frequently underdiagnosed cardiovascular factor.
Chronic inflammation: high-sensitivity CRP is a useful marker.
The PREDIMED trial showed that the Mediterranean diet supplemented with EVOO or nuts reduces major cardiovascular events by approximately 30% compared with a low-fat control diet in people at high cardiovascular risk. It is probably the dietary intervention with the best clinical backing for primary cardiovascular prevention. The key components: extra virgin olive oil as the main fat, oily fish 2-3 times a week, nuts daily, frequent legumes, plenty of fruits and vegetables, whole grains preferred over refined ones, and moderation or elimination of red and processed meats and ultra-processed foods.
Regular physical activity is probably the most effective "cardiovascular polypill": it reduces blood pressure, improves the lipid profile, improves insulin sensitivity, reduces inflammation, improves endothelial function, helps with weight control, and improves mental health. Recommendation: 150 minutes/week of moderate aerobic exercise or 75 minutes/week of vigorous exercise, plus 2-3 strength sessions per week.
Omega-3 EPA/DHA (1-4 g/day): especially with a high EPA concentration, with backing in secondary prevention.
CoQ10 (ubiquinol): in heart failure (Q-SYMBIO study) and in statin myopathy.
Vitamin K2 MK-7: with growing backing in arterial calcification and vascular stiffness.
Magnesium: subclinical deficiency linked to hypertension and arrhythmias.
Red yeast rice: an alternative to statins in mild dyslipidemia (with the same pharmacological precautions).
Berberine: improves the glycemic profile and has a modest effect on lipids.
Dietary nitrates (beetroot): improve endothelial function and blood pressure.
Cocoa polyphenols: improve endothelial function.
Hawthorn (Crataegus): with backing in mild-to-moderate heart failure.
In people at high or very high cardiovascular risk: - Statins: first-line treatment to reduce LDL. - Antihypertensives: when blood pressure is not controlled with lifestyle. - Low-dose aspirin: in secondary prevention; nuanced risk-benefit balance in primary prevention. - SGLT-2 inhibitors and GLP-1 agonists in diabetes: with documented cardiovascular benefit.
Cardiovascular prevention is one of the areas where the combination of healthy habits (Mediterranean diet, regular exercise, not smoking, healthy weight, adequate sleep, stress management) with pharmacological control when appropriate (blood pressure, cholesterol, diabetes) produces large reductions in mortality. There are no "magic bullets," just the sustained sum of good decisions over decades.
⏱ 2 min read
Cardiovascular disease remains the leading cause of death in developed countries and is rising in countries in epidemiological transition; the good news is that it is probably the chronic pathology where prevention has the greatest margin and where modifiable risk factors explain the vast majority of individual risk. Cardiovascular health is built over decades of sustained habits and benefits from interventions that act on multiple mechanisms in parallel.
High blood pressure: every 10 mmHg reduction in systolic pressure is associated with a 20% reduction in major cardiovascular events.
High LDL cholesterol: a robust causal factor demonstrated by Mendelian genetic studies and statin trials.
Diabetes and prediabetes: significantly increase cardiovascular risk.
Smoking: the modifiable factor with the greatest individual absolute impact; quitting tobacco dramatically reduces cardiovascular risk within years.
Obesity and sedentary lifestyle: independent and additive factors.
Diet: dietary quality is one of the most robust predictors.
Chronic stress and sleep deprivation: less visible but significant factors.
Untreated sleep apnea: a potent and frequently underdiagnosed cardiovascular factor.
Chronic inflammation: high-sensitivity CRP is a useful marker.
The PREDIMED trial showed that the Mediterranean diet supplemented with EVOO or nuts reduces major cardiovascular events by approximately 30% compared with a low-fat control diet in people at high cardiovascular risk. It is probably the dietary intervention with the best clinical backing for primary cardiovascular prevention. The key components: extra virgin olive oil as the main fat, oily fish 2-3 times a week, nuts daily, frequent legumes, plenty of fruits and vegetables, whole grains preferred over refined ones, and moderation or elimination of red and processed meats and ultra-processed foods.
Regular physical activity is probably the most effective "cardiovascular polypill": it reduces blood pressure, improves the lipid profile, improves insulin sensitivity, reduces inflammation, improves endothelial function, helps with weight control, and improves mental health. Recommendation: 150 minutes/week of moderate aerobic exercise or 75 minutes/week of vigorous exercise, plus 2-3 strength sessions per week.
Omega-3 EPA/DHA (1-4 g/day): especially with a high EPA concentration, with backing in secondary prevention.
CoQ10 (ubiquinol): in heart failure (Q-SYMBIO study) and in statin myopathy.
Vitamin K2 MK-7: with growing backing in arterial calcification and vascular stiffness.
Magnesium: subclinical deficiency linked to hypertension and arrhythmias.
Red yeast rice: an alternative to statins in mild dyslipidemia (with the same pharmacological precautions).
Berberine: improves the glycemic profile and has a modest effect on lipids.
Dietary nitrates (beetroot): improve endothelial function and blood pressure.
Cocoa polyphenols: improve endothelial function.
Hawthorn (Crataegus): with backing in mild-to-moderate heart failure.
In people at high or very high cardiovascular risk: - Statins: first-line treatment to reduce LDL. - Antihypertensives: when blood pressure is not controlled with lifestyle. - Low-dose aspirin: in secondary prevention; nuanced risk-benefit balance in primary prevention. - SGLT-2 inhibitors and GLP-1 agonists in diabetes: with documented cardiovascular benefit.
Cardiovascular prevention is one of the areas where the combination of healthy habits (Mediterranean diet, regular exercise, not smoking, healthy weight, adequate sleep, stress management) with pharmacological control when appropriate (blood pressure, cholesterol, diabetes) produces large reductions in mortality. There are no "magic bullets," just the sustained sum of good decisions over decades.