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Cardiovascular System
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In one pass The heart is a pump that never stops for a lifetime, and it has to eat and drink too: it needs a steady supply of energy, a few minerals, and oxygen to keep contracting, beat after beat. Not this — Aspirin 60+ for primary cardiovascular prevention — The US Preventive Services Task Force withdrew its recommendation for people 60 and over in 2022: the bleeding risk outweighs the heart and blood-vessel benefit, a net harm.
Educational content, not medical advice — consult a clinician.
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Chapter 1
The pump
The heart is a pump that never stops for a lifetime, and it has to eat and drink too: it needs a steady supply of energy, a few minerals, and oxygen to keep contracting, beat after beat.
Each beat starts when potassium, sodium, magnesium, and calcium, all charged minerals, move in and out across the membrane of the heart-muscle cells and spark the electrical signal to contract (this coordination is called excitation-contraction coupling). Almost all the energy a contraction burns is made by the mitochondria, and the oxygen reaches the heart muscle carried by the iron in your blood. If any one of these runs short for long, the heart is among the first to lose strength.
Know the warning sign of a cardiac emergency: crushing pain or tightness in the chest that lasts several minutes without easing may be a heart attack, so call your local emergency number immediately.
Each beat starts when potassium, sodium, magnesium, and calcium, all charged minerals, move in and out across the membrane of the heart-muscle cells and spark the electrical signal to contract (this coordination is called excitation-contraction coupling). Almost all the energy a contraction burns is made by the mitochondria, and the oxygen reaches the heart muscle carried by the iron in your blood. If any one of these runs short for long, the heart is among the first to lose strength.
Know the warning sign of a cardiac emergency: crushing pain or tightness in the chest that lasts several minutes without easing may be a heart attack, so call your local emergency number immediately.
Numbers · How much work the heart does
The heart never rests for a lifetime, and laying out the numbers shows how much it depends on nutrition:Heart rate: 60–80 beats a minute at rest, about 100,000 beats a day, and about 3 billion beats in a lifetime.Output: about 5 L a minute at rest and up to 25 L during exercise, or about 7000 L a day.Oxygen use: blood flow through the coronary arteries (the vessels that supply the heart muscle itself) is only about 5% of cardiac output, yet the heart muscle uses about 10–15% of the body's oxygen at rest. Per unit of weight, that is more than the brain.Fuel: healthy heart muscle gets about 60–70% of its from burning fatty acids (beta-oxidation), 20–30% from glucose, and 5–10% from lactate and ketones. Heart muscle mainly burns fat.Coronary blood flow: about 70 ml a minute for every 100 g of heart muscle at rest.
One key weak point: the muscle of the left ventricle gets its blood supply mainly while the heart relaxes, because the contracting muscle squeezes the coronary arteries. So a heart rate that stays too fast (above 150 beats a minute), or a relaxation phase that gets cut too short, can leave the heart muscle itself short of oxygen. That is one reason people who already have coronary heart disease tend to get angina (chest pain from a starved heart muscle) when the heart races.
So when a beta-blocker slows the heart rate, it is not just making the heart comfortable; it also buys the heart muscle time to take in its own oxygen.
Chapter 2
Vessels relax on their own
A blood vessel is not a lifeless pipe. It relaxes or tightens on its own in response to blood flow, and exercise trains exactly that skill.
The innermost layer of a vessel is a thin sheet of cells called the endothelium. When blood rushes across it, the endothelium senses the push and releases a small molecule, nitric oxide (). Nitric oxide tells the muscle in the vessel wall to let go, the vessel widens, and blood flows more easily. Regular aerobic exercise sets off this process again and again, which amounts to rehearsing this make-way response.
So exercise does not only train your heart rate; it also trains how your vessels respond.
The innermost layer of a vessel is a thin sheet of cells called the endothelium. When blood rushes across it, the endothelium senses the push and releases a small molecule, nitric oxide (). Nitric oxide tells the muscle in the vessel wall to let go, the vessel widens, and blood flows more easily. Regular aerobic exercise sets off this process again and again, which amounts to rehearsing this make-way response.
So exercise does not only train your heart rate; it also trains how your vessels respond.
Mechanism · How nitric oxide relaxes vessels
Nitric oxide () was the first gas signaling molecule discovered in the body (Furchgott, Ignarro, and Murad won the 1998 Nobel Prize for it).It is made by endothelial nitric oxide synthase (eNOS): L-arginine plus oxygen yields nitric oxide and L-citrulline. The reaction needs tetrahydrobiopterin (BH4) and (a coenzyme that supplies reducing power in the cell) as helpers.
There are three main triggers. The first is shear stress, the force of blood flowing along the vessel wall, which rises sharply during exercise; it is the core reason aerobic training improves blood vessels. The second is acetylcholine. The third is bradykinin, which is part of how ACE inhibitor blood-pressure drugs work.
What happens next: nitric oxide enters the smooth muscle of the vessel wall and switches on guanylate cyclase, which makes cGMP, so the smooth muscle relaxes and the vessel widens. Nitric oxide also holds back platelet clumping and white blood cells sticking to the wall, and both of these are linked to slowing atherosclerosis.
What raises nitric oxide: regular aerobic and strength training; and the nitrate in leafy greens and beets. Bacteria in the mouth first turn nitrate into nitrite, and the body then turns that into nitric oxide, a route that does not go through eNOS. In the by Siervo and colleagues (2013), nitrate or beetroot juice lowered systolic blood pressure in the short term by an amount on the order of 3–5 mmHg. Enough sleep and not smoking also help.
What lowers nitric oxide: long-term high blood sugar and insulin resistance; sitting for long hours; and antiseptic mouthwash. In the trial by Kapil and colleagues (2013), killing the mouth bacteria that reduce nitrate cut off this nitrate-to-nitrite route, and blood pressure rose slightly.
Endothelial dysfunction means too little nitric oxide is made, or it is broken down too fast. It is thought to be the earliest step in atherosclerosis, coming before plaque and symptoms, and at this step it can still be reversed.
Chapter 3
Plaque cascade
Heart attacks and ischemic strokes together are the leading cause of death worldwide, and the disease behind both is atherosclerosis. It is not the simple picture of fat clogging a pipe; it is a chronic inflammatory process that runs for decades.
Seeing this chain of cause and effect is what shows exactly which step each measure blocks, whether it is diet, statins, exercise, or quitting smoking.
The last link in the chain is a plaque that suddenly ruptures and a clot that blocks the vessel. If crushing chest pain or tightness lasts several minutes without easing, or one side of the face suddenly droops, an arm or leg on one side turns weak, or speech becomes slurred, it may be a heart attack or a stroke. Call your local emergency number immediately.
Seeing this chain of cause and effect is what shows exactly which step each measure blocks, whether it is diet, statins, exercise, or quitting smoking.
The last link in the chain is a plaque that suddenly ruptures and a clot that blocks the vessel. If crushing chest pain or tightness lasts several minutes without easing, or one side of the face suddenly droops, an arm or leg on one side turns weak, or speech becomes slurred, it may be a heart attack or a stroke. Call your local emergency number immediately.
Mechanism · Six steps from injury to rupture
Step 1: The endothelium is injured (this can start as early as age 10–20)Long-standing high blood pressure, high blood sugar, smoking, and oxidative stress reduce the nitric oxide the endothelium makes and make the vessel wall leakier. There are no symptoms yet, but the inner wall of the vessel is already scraped.
Step 2: gets in and is oxidized
LDL particles (especially the small, dense kind, sdLDL) pass through the damaged endothelium, stay in the layer beneath it, and are oxidized into oxidized LDL (ox-LDL). The immune system treats it as a foreign threat that must be cleared.
Step 3: Macrophages swallow it and become foam cells
Monocytes from the blood are drawn in beneath the endothelium, turn into macrophages, and swallow large amounts of oxidized LDL through scavenger receptors (CD36 and SR-A). This pathway does not shut off when the cell has had enough, so the macrophages keep swallowing until they bloat into foam cells and die.
Step 4: Fatty streaks
Foam cells and lipid outside the cells pile up into yellow streaks you can see with the naked eye. They already appear in childhood. This step can still be reversed: if the endothelium recovers and less LDL gets in, the streaks can fade.
Step 5: Fibrous plaque and calcification
Smooth muscle cells move into the inner layer of the wall and secrete collagen, forming a fibrous cap over the lipid core. Calcium starts to build up. The plaque begins to narrow the vessel, and angina appears, or leg pain that comes on after walking a certain distance and eases with rest (intermittent claudication).
Step 6: The plaque ruptures and a clot forms
The critical turning point is usually not a vessel slowly closing up, but the fibrous cap suddenly tearing. The lipid core is exposed, platelets clump instantly, clotting switches on, and an acute clot blocks the vessel completely. The result is a heart attack (myocardial infarction) or an ischemic stroke.
Rupture is often triggered by inflammation plus a sudden surge in the force of blood flow (getting up in the morning, or intense emotional stress). In the observational study by Muller and colleagues (1985), heart attacks clustered between 6 a.m. and noon.
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In practice · Which step each measure blocks
Knowing which step each measure blocks is what shows why some things matter a lot and others matter less:Quitting smoking blocks step 1 (it protects the endothelium). Quitting lowers cardiovascular risk, and the benefit starts soon after you quit. It is one of the cheapest single changes with the biggest payoff.Lowering (statins, diet, exercise): LDL-C is low-density lipoprotein cholesterol, often called bad cholesterol. Lowering it blocks step 2 (fewer LDL particles get into the vessel wall). Statins lower LDL-C by 30–50%. The Cholesterol Treatment Trialists' (CTT) Collaboration pooled 26 randomized trials in 2010: every 1 mmol/L drop in LDL-C cut major cardiovascular events by about 22%.Lowering blood pressure blocks steps 1 and 6 (less force pounding the vessel wall, and a lower risk that a plaque ruptures). The more systolic pressure comes down, the more stroke risk falls.Omega-3 fats ( and ): by mechanism they would act at steps 5 and 6 (stabilizing plaque, calming inflammation, and reducing heart-rhythm problems). But in trials, healthy people taking ordinary fish oil to prevent heart disease mostly saw no benefit.Exercise blocks step 1 (it helps the endothelium make more nitric oxide), and it also improves whole-body metabolism and calms inflammation.Low-dose aspirin blocks step 6 (it holds back platelet clumping). People who have already had a heart attack, a stroke, or peripheral artery disease (PAD), which is secondary prevention, usually take it long term, as their doctor decides. For people without these conditions (primary prevention), the US Preventive Services Task Force (USPSTF) advised in 2022 that people aged 60 or older should not start it for this purpose (the bleeding risk outweighs the benefit), and that people aged 40–59 with higher cardiovascular risk should decide individually with their doctor.Controlling blood sugar blocks step 1 (fewer advanced glycation end products, or AGEs, which form when sugar sticks to proteins, and less inflammation).
Do not underestimate:
Periodontitis (gum disease) and other chronic infections: body-wide inflammation drives damage to the endothelium, and gum health is linked to cardiovascular events (an observed association).Routinely sleeping less than 6 hours: it is linked to worse blood pressure, inflammation, insulin resistance, and balance of the autonomic nervous system.
Do not overestimate:
Taking fish oil on its own for primary prevention has weak evidence; prescription doses (3–4 g a day) help only when are very high.High-dose antioxidant supplements do not help, and some do harm. In the HOPE trial, 400 of vitamin E a day did not reduce heart attacks, strokes, or cardiovascular deaths. In the ATBC trial, male smokers given beta-carotene had more lung cancer, not less. One explanation is that they cannot block the oxidized-LDL step precisely and end up disturbing the body's other redox signals.
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Chapter 4
Particles that carry fat in blood
The fat you eat changes how many of the small fat-carrying particles there are in your blood. The one to watch most closely is (low-density lipoprotein cholesterol, often called bad cholesterol). The more of it there is, the easier it is for it to slip into the vessel wall, get oxidized, and build up into plaque.
Different fats push it in different directions. Trans fat is the one to avoid most. The effect of saturated fat depends on what you replace it with. Omega-3 fats mainly act on and inflammation.
Different fats push it in different directions. Trans fat is the one to avoid most. The effect of saturated fat depends on what you replace it with. Omega-3 fats mainly act on and inflammation.
Clinical · Which lipid numbers to read
Is your cholesterol high? is too blunt a question. What tracks cardiovascular events most closely is how many artery-clogging particles are in your blood (the particle count), plus a special, gene-driven particle called . Total cholesterol on its own tells you little.Lipoproteins that drive atherosclerosis (each particle carries one ApoB-100 protein on its surface):
: the main actor. It gets into the vessel wall, is oxidized, and sets off plaque.VLDL and IDL: the precursors of LDL, rich in .Lp(a): an LDL particle with a long apo(a) tail attached. It is set mainly by the LPA gene (an estimated 90% of it is inherited) and is hardly moved by diet or statins. People with high levels have a higher risk of early coronary heart disease.
Lipoproteins thought to be protective (carrying ApoA-I):
: it carries cholesterol from the rest of the body back to the liver (reverse cholesterol transport). But the idea that higher HDL is always better is wrong. A Mendelian randomization study (Voight 2012, which uses gene variants that naturally raise HDL as a kind of natural randomization) found that those variants did not lower heart-attack risk. Raising HDL is not the same as being protected.
How to read the panel today:
LDL-C: the starting point. How low it should go is not one number for everyone; it depends on your overall risk tier, and the higher the risk, the stricter the target.ApoB: counts the particles directly, and is more accurate than LDL-C in people with high triglycerides, diabetes, or obesity.Lp(a): testing once in a lifetime is enough (it barely changes), yet many people have never been tested. A commonly used cutoff for high is above 50 mg/dL (about 125 nmol/L), and people above it should get their other risks under control earlier.The triglyceride-to-HDL ratio: a more sensitive marker when looking at metabolic syndrome.
How much diet can move (without medication):
Cutting out trans fat, replacing saturated fat with polyunsaturated fat, and eating more viscous fiber (such as the beta-glucan in oats) and plant sterols each lower LDL-C somewhat. The American Heart Association's 2017 presidential advisory concluded that in randomized trials that replaced saturated fat with polyunsaturated vegetable oil, cardiovascular disease fell by about 30%, similar to the effect of statins.High doses of and (3–4 g a day) mainly lower triglycerides; LDL-C stays the same or rises slightly.
Statins lower LDL-C by 30–50%. The Cholesterol Treatment Trialists' (CTT) Collaboration pooled 26 randomized trials in 2010: every 1 mmol/L drop in LDL-C cut major cardiovascular events by about 22%. That is the part diet cannot replace.
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Chapter 5
Blood pressure
Blood pressure is not set by the heart alone. The kidneys regulate the body's sodium and water, potassium intake affects how much sodium is excreted and how relaxed the vessels are, and body weight, sleep, stress, and exercise all play a part.
So a blood-pressure-lowering diet is not about one single thing. It is a whole way of eating, plus moving more, sleeping enough, and keeping weight in check.
So a blood-pressure-lowering diet is not about one single thing. It is a whole way of eating, plus moving more, sleeping enough, and keeping weight in check.
Evidence · DASH and other lifestyle changes
DASH (Dietary Approaches to Stop Hypertension) comes from a funded by the US National Institutes of Health and published in 1997 (Appel 1997), and it is still the benchmark for a blood-pressure-lowering diet.It differs from a typical American diet in a few places: twice as much fruit and vegetables (8–10 servings a day); clearly more whole grains, low-fat dairy, legumes, and nuts; and clearly less red meat, sugary food, and sodium. The trial menu provided about 4.7 g of potassium a day. That is the design amount of the trial diet, not a target for everyone.
The effect shows within 4 weeks. In people with hypertension, systolic pressure fell by 11.4 mmHg on average and diastolic pressure by 5.5 mmHg, comparable to the usual drop from a single blood-pressure drug. A separate trial, DASH-Sodium (Sacks 2001), cut sodium further on the DASH diet: going from about 3.5 g to about 2.3 g a day lowered systolic pressure by only 1.3 mmHg more, and going on down to about 1.2 g lowered it by another 1.7 mmHg. In people with normal blood pressure the effect was much smaller (systolic down 3.5 mmHg, diastolic down 2.1 mmHg). It is one of the best-supported examples of a nutrition intervention.
Here are the common lifestyle measures for hypertension, with each one's rough effect on systolic pressure. They are listed roughly from largest to smallest; weight loss is counted per kilogram, so the more you lose, the larger the drop, and it does not slot neatly into the order:
1. DASH diet (about -11 mmHg)
2. Regular aerobic exercise (150 minutes a week, about -5 to -8 mmHg)
3. Cutting sodium (about -4 to -6 mmHg)
4. Raising potassium (about -4 to -5 mmHg)
5. Limiting or stopping alcohol (about -3 mmHg)
6. Losing weight (for people with a body mass index, , above 25: about 1 mmHg for every 1 kg lost)
These figures come from different studies and compare only roughly. Done together, the measures' effects partly add up, but not as a simple sum. A combined drop of 15–25 mmHg in systolic pressure when all of them are in place is a rough estimate. For some people with early hypertension, that may be enough to put off medication for now; whether to take medication is for a doctor to decide, based on overall risk.
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Chapter 6
Pattern over single nutrient
Heart and blood-vessel nutrition has no single-supplement answer. The steadier foundation is a whole way of eating and living: high-fiber foods, enough potassium, little trans fat, and sodium kept in check, plus regular exercise, enough sleep, and medical care when it is needed.
A single nutrient or supplement rarely carries a cardiovascular benefit on its own in trials; most of the evidence is for whole eating patterns.
A single nutrient or supplement rarely carries a cardiovascular benefit on its own in trials; most of the evidence is for whole eating patterns.
Evidence · What PREDIMED found
PREDIMED (Estruch 2018, NEJM) is one of the weightiest trials in cardiovascular nutrition: 7,447 adults in Spain at high cardiovascular risk but without cardiovascular disease when they enrolled, followed for a median of 4.8 years.Three groups were compared: a Mediterranean diet plus extra-virgin olive oil (about 50 ml a day); a Mediterranean diet plus mixed nuts (about 30 g a day); and a control group advised to eat a low-fat diet.
Results (the primary endpoint was heart attack, stroke, and cardiovascular death combined): the event rate was 3.8% in the Olive Oil group, 3.4% in the nut group, and 4.4% in the control group. The adjusted were 0.69 and 0.72, a about 30% lower (31% and 28%). Broken down, strokes fell more clearly than heart attacks.
The trial has a history that has to be told. The paper first published in 2013 was retracted because some participants had not been randomized as the protocol required, and it was republished in 2018 with analyses that do not rely entirely on randomization; the results were similar. So it is no longer a clean randomized trial, and its evidence should be discounted a little.
The core diet has several features in common: plenty of fruit, vegetables, whole grains, legumes, and fish; olive oil as the main cooking fat; as little red meat, processed meat, and sugary food as possible. It does not need to be deliberately low in fat; total fat can reach 40% of energy, as long as it is mostly monounsaturated and polyunsaturated. The traditional Mediterranean diet includes a little red wine with meals (about 1 glass a day), but the World Health Organization's 2023 position is that no level of alcohol is safe for health and less is better. PREDIMED did not show that drinking helps either, so people who do not drink should not start for their health.
Compared with a Western low-fat diet, the Mediterranean diet is not low in fat; it is about good fat. That is one of the most important shifts in nutrition science over the past 20 years: from eating less fat to eating the right fat.
On a Chinese table, the usual swaps are: camellia seed oil or rapeseed (canola) oil instead of olive oil (both are low in saturated fat); sea bass, salmon, or black carp instead of sardines and anchovies; black beans, soybeans, or adzuki beans instead of chickpeas and lentils. The wine does not need to be copied, and should not be.
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References · 16
- National Institutes of Health, Office of Dietary Supplements. (2021). Potassium — Fact Sheet for Health Professionals. ods.od.nih.gov/factsheets/Potassium-HealthProfessional
- National Institutes of Health, Office of Dietary Supplements. (2022). Magnesium — Fact Sheet for Health Professionals. ods.od.nih.gov/factsheets/Magnesium-HealthProfessional
- National Institutes of Health, Office of Dietary Supplements. (2024). Calcium — Fact Sheet for Health Professionals. ods.od.nih.gov/factsheets/Calcium-HealthProfessional
- National Institutes of Health, Office of Dietary Supplements. (2024). Iron — Fact Sheet for Health Professionals. Fact sheet (updated September 4, 2025; Wayback snapshot 21 September 2026): RDAs 8 mg/day for men and for women 51+, 18 mg women 19-50, 27 mg pregnancy; UL 45 mg/day from age 14; bioavailability about 14%-18% from mixed diets with meat, seafood and vitamin C and 5%-12% from vegetarian diets; serum ferritin below 30 mcg/L suggests iron deficiency and below 10 mcg/L IDA, but inflammation can raise ferritin; supplemental iron of 45 mg/day or more may cause nausea and constipation; people with hereditary hemochromatosis are at risk of iron overload (fact sheet). Heme vs nonheme: heme iron (lean meat and seafood are the richest sources) has higher bioavailability than nonheme iron, and other dietary components affect it less; calcium might reduce the bioavailability of both forms; heme iron is about 10%-15% of total iron intake in western populations. The sheet gives no separate heme and nonheme absorption percentages (fact sheet, Wayback 2026 snapshot). ods.od.nih.gov/factsheets/Iron-HealthProfessional
- U.S. Department of Health and Human Services. (2018). Physical Activity Guidelines for Americans (2nd ed.). health.gov/paguidelines/second-edition/pdf/Physical_Activity_Guidelines_2nd_edition.pdf
- Siervo, M., Lara, J., Ogbonmwan, I., & Mathers, J. C. (2013). Inorganic nitrate and beetroot juice supplementation reduces blood pressure: a systematic review and meta-analysis. The Journal of Nutrition, 143(6), 818-826. Dietary nitrate modestly lowered blood pressure (effect strongest from beetroot/leafy-green nitrate). 10.3945/jn.112.170233
- Kapil, V., Haydar, S. M. A., Pearl, V., Lundberg, J. O., Weitzberg, E., & Ahluwalia, A. (2013). Physiological role for nitrate-reducing oral bacteria in blood pressure control. Free Radical Biology and Medicine, 55, 93-100. 10.1016/j.freeradbiomed.2012.11.013
- Libby, P., Ridker, P. M., & Hansson, G. K. (2011). Progress and challenges in translating the biology of atherosclerosis. Nature, 473(7347), 317-325. 10.1038/nature10146
- Ross, R. (1999). Atherosclerosis — an inflammatory disease. The New England Journal of Medicine, 340(2), 115-126. 10.1056/NEJM199901143400207
- Sacks, F. M., Lichtenstein, A. H., Wu, J. H. Y., Appel, L. J., Creager, M. A., Kris-Etherton, P. M., et al. (2017). Dietary fats and cardiovascular disease: A presidential advisory from the American Heart Association. Circulation, 136(3), e1-e23. Coconut oil is ~82% saturated; the AHA advises against its use because it raises LDL-C with no known offsetting favorable effect, and recommends replacing saturated with unsaturated fat. 10.1161/CIR.0000000000000510
- Cholesterol Treatment Trialists' (CTT) Collaboration. (2010). Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet, 376(9753), 1670-1681. 26 randomised trials, about 170,000 participants: per 1.0 mmol/L LDL reduction, major vascular events RR 0.78 (0.76-0.80), all-cause mortality RR 0.90 (0.87-0.93), mainly from fewer coronary deaths; no effect on stroke death, cancer death or cancer incidence; more versus less intensive statins lowered LDL a further 0.51 mmol/L and major vascular events a further 15%; no threshold seen within the range studied (abstract, PMID 21067804). 10.1016/S0140-6736(10)61350-5
- Mozaffarian, D., & Wu, J. H. Y. (2011). Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events. Journal of the American College of Cardiology, 58(20), 2047–2067. 10.1016/j.jacc.2011.06.063
- National Academies of Sciences, Engineering, and Medicine. (2019). Dietary Reference Intakes for Sodium and Potassium. National Academies Press. The PubMed book abstract (PMID 30844154) gives no reference values; it says the report updates the sodium and potassium DRIs with an expanded model that adds chronic-disease endpoints (the Chronic Disease Risk Reduction Intake). The numeric AIs and CDRRs were not re-read for this note (abstract). www.ncbi.nlm.nih.gov/books/NBK538102
- Appel, L. J., Moore, T. J., Obarzanek, E., Vollmer, W. M., Svetkey, L. P., Sacks, F. M., et al. (1997). A clinical trial of the effects of dietary patterns on blood pressure (DASH). New England Journal of Medicine, 336(16), 1117-1124. 459 adults with SBP below 160 and DBP 80-95 mmHg, 3-week run-in, then 8 weeks of control, fruit-and-vegetable or combination (DASH) diet, with sodium and body weight held constant. Combination diet lowered SBP/DBP 5.5/3.0 mmHg more than control; in the 133 with hypertension 11.4/5.5, in the 326 without 3.5/2.1 (abstract, PMID 9099655). 10.1056/NEJM199704173361601
- U.S. Department of Agriculture & U.S. Department of Health and Human Services. (2020). Dietary Guidelines for Americans, 2020-2025 (9th ed.). www.dietaryguidelines.gov/sites/default/files/2020-12/Dietary_Guidelines_for_Americans_2020-2025.pdf
- World Health Organization. (2023). No level of alcohol consumption is safe for our health. The Lancet Public Health, 8(1), e6-e7. www.who.int/europe/news/item/04-01-2023-no-level-of-alcohol-consumption-is-safe-for-our-health