Many people don’t realize this, but across the world, cardiovascular disease death rates have been falling dramatically [1].
And today, we have the tools to virtually eliminate it completely.
But there are two pieces of the puzzle that remain controversial. This causes a lot of confusion when it comes to the practical steps we can take to lower our risks. And that’s a problem. This article will give you the data you need to know how to move forward.
Table of Contents
- What’s Uncontroversial
- Diet and Heart Disease
- The Saturated Fat Controversy
- The Cholesterol Controversy
- Practical Implications
- References
What’s Uncontroversial
Here’s what’s not controversial: we know that five things are powerful protectors of heart health.
1. Exercise — ideally with a mixture of cardio and weight training to get the unique benefits of each [2]. Even if we’re pushed for time, short bursts or “exercise snacks” can still make a meaningful impact.
2. Avoid smoking and limit alcohol intake — both contribute significantly to cardiovascular mortality. Smoking and secondhand smoke account for more than 30% of coronary heart disease deaths [3]. Binge drinking or regularly consuming ≥3 alcoholic drinks a day is also consistently linked to worse outcomes in every type of cardiovascular disease studied [4].
3. Sleep and stress — prioritizing good sleep and managing stress effectively both have critical roles in supporting cardiovascular health [5][6].
4. Blood pressure — keeping it within an optimal range, ideally around 120/80 mmHg, without causing dizziness or side effects, especially in older patients [7].
5. Healthy weight — achieving and maintaining this through diet and exercise is important. In some cases, medications like tirzepatide can support these goals [8].
Diet and Heart Disease
So what exactly is meant by a good diet? This is where the controversy begins.
Back in the 1950s, researcher Ancel Keys believed he knew the answer and launched a groundbreaking study to test his hypothesis.
At the time, heart disease had risen to public attention. In England, researchers documented a 15-fold increase in deaths from heart disease between 1921 and 1945 [9]. The same pattern emerged in the U.S., where heart disease went from rare in 1900 to the leading cause of death by midcentury [10].
When President Eisenhower had a heart attack in 1955, the nation was gripped by the question: what causes heart disease? Keys’ ideas were suddenly thrust into the national spotlight.
There was early evidence that elevated cholesterol was a key factor — particularly the low-density forms, which were more closely linked to heart disease [11].
Keys proposed that saturated fat raised LDL cholesterol, which in turn raised heart disease risk. To test this, he compared populations with different dietary fat intakes. He found a strong link between dietary fat and blood cholesterol levels [12].
He expanded this work into the Seven Countries Study, tracking 12,770 men from 16 cohorts in 7 countries [13]. The results supported his hypothesis: saturated fat intake was linked to higher cholesterol, and that was linked to heart disease [14].
A 25-year follow-up confirmed this relationship [15].
This became the foundation for what is known as the diet-heart hypothesis: saturated fat increases LDL cholesterol, which raises heart disease risk.
The Saturated Fat Controversy
But this is where controversy enters the picture.
The U.S. Department of Health and Human Services (HHS) recently published new dietary guidelines. While they still recommend limiting saturated fats to 10% of daily calories, the presentation seems more permissive. For example, a graphic from the guidelines features a steak prominently displayed [16].
Meanwhile, online debate continues: should we avoid animal-sourced saturated fats like red meat and full-fat dairy, or is the concern overblown?
Recently, a meta-analysis reviewed 9 trials with about 13,000 participants. It found no statistically significant difference in cardiovascular events between those who reduced saturated fat and those who didn’t [17].
But other meta-analyses, like the 2020 Cochrane review, did find benefit — a 17% relative risk reduction in cardiovascular events [18].
Why the discrepancy?
It often comes down to which studies are included. Many trials are old, and some suffer from serious flaws. One notable example is the Minnesota Coronary Survey, the largest study included in the first meta-analysis. It was excluded from the Cochrane review — and for good reason:
- The study lasted just over a year on average — too short to see meaningful cardiovascular outcomes [19].
- Most participants were under 30 — a group with an inherently low risk of heart attacks, regardless of diet [20].
- The intervention diet included margarine, which at the time contained trans fats — now known to be worse for heart health than saturated fats [21].
- Participants came and went from the hospital, and were only on the diet while institutionalized, meaning the intervention was inconsistently applied [22].
In short: garbage in, garbage out. Meta-analyses that include flawed studies like this one may not show a link between saturated fat and heart disease.
Cochrane reviews, however, apply strict quality criteria — for example, only including studies lasting 2 years or more — and show the relationship more clearly [18].
And we know this: consuming saturated fat raises LDL cholesterol, a well-established risk factor for heart disease.
The Cholesterol Controversy
This brings us to a second point of contention: Does LDL cholesterol really matter?
Some claim that low LDL is dangerous and point to studies showing a U-shaped curve — where both very high and very low LDL levels are linked to higher mortality [23].
But this can be misleading.
We often see this U-shaped pattern in other areas too — such as BMI in older adults [24] and blood pressure [25]. But this doesn't mean that being overweight or hypertensive is protective.
Here’s what’s going on:
People with very low cholesterol often fall into two categories:
- The elderly, who may lose weight and appetite as they age
- The chronically ill, with conditions like liver disease or cancer, which lower cholesterol levels and increase mortality risk
Additionally, patients recovering from heart attacks or strokes are often on aggressive LDL-lowering medications. Their cholesterol may be low, but their underlying disease means they still carry higher risk.
When studies adjust for age, malnutrition, and chronic illness, the U-shaped curve often disappears.
For example, a large cohort study of 41,000 patients showed this exact pattern. Initially, low non-HDL cholesterol was associated with higher death rates. But after adjustment, higher cholesterol levels correlated clearly with greater mortality [26].
Observational studies are helpful, but we also need to look at interventional evidence.
A consensus statement from the European Atherosclerosis Society, reviewing over 200 studies (RCTs, Mendelian studies, and prospective cohorts involving more than 2 million people), concluded clearly:
LDL causes atherosclerosis and heart disease [27].
What about people who are otherwise healthy?
Some argue that if you're lean, with good insulin sensitivity and blood pressure, you don't need to worry about cholesterol.
But the PESA study answers that. It showed that even in people with “optimal” values for all other cardiovascular risk factors, atherosclerosis developed when LDL levels exceeded 50–60 mg/dL. Each 10 mg/dL increase was linked with greater artery plaque buildup [28].
And there’s more:
- Statin trials show that lowering LDL reduces the risk of heart attacks, strokes, and all-cause mortality — even in people without prior cardiovascular events [29].
- Mendelian randomization studies, where genetic variations naturally lead to lifelong lower LDL levels, show substantially lower heart disease risk [30].
These studies act like natural experiments — giving us strong causal evidence.
None of this means LDL is the only risk factor. Not everyone with high LDL will get heart disease. But if we want to reduce risk, the evidence supports lowering saturated fat and LDL cholesterol.
Practical Implications
So what does all this mean for how we eat?
1. Minimize Saturated and Trans Fats
This doesn’t mean we should avoid all fats. In fact, early “low-fat” guidelines backfired — leading many to increase refined carb intake, which also raises cardiovascular risk.
Instead, we want to focus on unsaturated fats from foods like:
- Extra-virgin olive oil
- Nuts
- Fatty fish
A recent meta-analysis found that higher olive oil consumption reduced heart disease risk by 15% and all-cause mortality by 17% [31].
2. Increase Potassium
Unless you have severe kidney disease, prioritize potassium-rich foods such as:
- Leafy greens
- Beans and lentils
- Bananas
- Avocados
Potassium helps lower blood pressure. A meta-analysis found:
- A 3.49 mmHg reduction in systolic BP on average
- A 7.16 mmHg drop when intake hit 3,500–4,700 mg/day [32]
3. Target 1.2g of Protein/kg of Bodyweight
Higher protein intake supports weight loss and reduced cardiovascular risk. But the benefit seems strongest for plant-based protein like:
- Chickpeas
- Lentils
- Beans
These foods are also high in fiber and potassium, offering added benefits [33].
4. Prioritize Fiber
A massive meta-analysis published in The Lancet showed that higher fiber intake was associated with a 15–30% decrease in:
- All-cause mortality
- Cardiovascular disease
- Stroke [34]
Note: If you have IBS or IBD, speak with your doctor — high fiber may not be appropriate.
5. Eat Whole, Minimally Processed Foods
This ensures you're getting full nutrient density — with all the fiber, vitamins, and minerals that get stripped out of processed alternatives.
At the clinic, I work with patients to reduce saturated fat, lower LDL-cholesterol and ApoB levels, and transition to a diet rich in unsaturated fats, potassium, plant proteins, and fiber.
References
1. https://ourworldindata.org/cardiovascular-deaths-decline
2. https://pmc.ncbi.nlm.nih.gov/articles/PMC11460131/
3. https://pmc.ncbi.nlm.nih.gov/articles/PMC7399440/
4. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001341
6. https://www.nature.com/articles/s41569-024-01024-y
7. https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.119.14240
8. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000973
9. https://pmc.ncbi.nlm.nih.gov/articles/PMC503641/?page=19
10. https://pubmed.ncbi.nlm.nih.gov/24811552/
11. https://www.ahajournals.org/doi/epdf/10.1161/01.CIR.5.1.119
12. https://pmc.ncbi.nlm.nih.gov/articles/PMC441692/
13. https://pmc.ncbi.nlm.nih.gov/articles/PMC9794145/
14. https://www.cabidigitallibrary.org/doi/full/10.5555/19711403775
15. https://pubmed.ncbi.nlm.nih.gov/7644455/
16. https://cdn.realfood.gov/DGA.pdf
17. https://pmc.ncbi.nlm.nih.gov/articles/PMC12095860/
18. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD011737.pub3/full
19. https://www.ahajournals.org/doi/abs/10.1161/01.atv.9.1.129
20. https://www.ahajournals.org/doi/epdf/10.1161/01.ATV.9.1.129
21. https://www.ahajournals.org/doi/epdf/10.1161/01.ATV.9.1.129
22. https://www.ahajournals.org/doi/epdf/10.1161/01.ATV.9.1.129
23. https://www.nature.com/articles/s41598-021-01738-w
24. https://www.sciencedirect.com/science/article/pii/S0002916523050244#f2
25. https://www.sciencedirect.com/science/article/pii/S0735109714029088
26. https://www.sciencedirect.com/science/article/pii/S0261561422000371
27. https://pubmed.ncbi.nlm.nih.gov/28444290/
28. https://www.sciencedirect.com/science/article/pii/S0735109721051159?via%3Dihub
29. https://jamanetwork.com/journals/jama/fullarticle/2795522
30. https://pubmed.ncbi.nlm.nih.gov/23083789/
31. https://pmc.ncbi.nlm.nih.gov/articles/PMC9623257/
32. https://www.bmj.com/content/346/bmj.f1378.long
