You’ve Had a Heart Attack at a Young Age: Which Diet Could Have Prevented It and Which is Best Now?

As a cardiologist focused on prevention my goal is to see patients before they have a heart attack (myocardial infarction or MI). If I can assess risk and start appropriate lifestyle and pharmacologic treatments early in their life, even the highest risk patients can live their entire lives free of MI and without cardiac interventions like stents and bypass operations.

But what about those patients who have already had an MI at a young age. Although I’ve seen a fair number of patients have their first MI in their 40s, and a lot in their fifties it is rare to have it at age 37 as one reader (who we will call Arthur) described in an email to me.

Patients like Arthur are rightfully quite anxious about their heart health and typically have lots of really good questions about the cause of their early disease, the best treatments and lifestyle changes, and their long-term prognosis. There is often a sense that drastic or draconian diet changes are needed.

In preventing future cardiac problems for Arthur, we are engaged in “secondary prevention.” But what of pre-MI Arthur? Pre-MI Arthur had silently developed atherosclerotic plaques in his coronary arteries that were at high risk for rupturing or fissuring and causing his MI. With his first MI, he could have dropped dead.

Thus, pre-MI Arthur, who is totally free of any symptoms of significance would benefit equally from the diet, lifestyle changes, and medications we recommend for post-MI Arthur.

What follows are selections from my reader’s email with my accompanying comments.


Dear Dr Pearson, first off a big thanks to you for your efforts in providing up-to-date and scientifically grounded musings on cardiovascular-related topics in your blog, which is accessible while shying away from oversimplifying or being condescending towards the reader.

Thank you! It is encouraging words like this that motivate me to continue this pro bono project.

I’m writing to you because a couple of years ago, right around my 37th birthday, I had the dubious pleasure of being surprised by a massive heart attack from a 99% blockage in the LAD artery. After several days of struggles in the hospital (most of which I fortunately was not conscious for) I pulled through thanks to a stent, with perhaps surprisingly not too much apparent damage to the muscle, and a normal ejection fraction. 

Readers may have gotten the impression that I am philosophically opposed to stents in patients with coronary artery disease but the this young man’s history exemplifies the precise presentation for which stents work wonderfully-an acute heart attack. 

The heart muscle supplied by the LAD (left anterior descending) coronary artery (aka the widow maker) begins to die within minutes of a 100% blockage  but if the LAD is opened with a stenting procedure within 90 minutes of the onset of the blockage the death of muscle is interrupted. Thus, one can emerge from this process without damage to the main pumping chamber of the heart (left ventricle), typically measured by the percentage of blood ejected from the left ventricle (aka the ejection fraction.)

Premonitory Symptoms?

Arthur goes on to reveal some background information on his case

I don’t want this email to devolve into a lengthy dissertation on the background of this incident, let’s suffice it to say that while I had suffered some odd symptoms in the form of sustained palpitations during the days before this happened, and while my labs/vitals were not necessarily “perfect”, I didn’t suffer from hypertension, hyperlipidemia, diabetes (non-smoker) and I exercised regularly. But of course non of this offers a “guarantee” as you’ve certainly touched upon in posts on your blog.

It is not uncommon for patients to recall symptoms in the days or weeks leading up to their first heart attack. If the symptom is a briefer, less intense version of the main symptom that prompted them to call EMS for their MI it is likely these were true warning symptoms.

But palpitations are so common and typically benign that they are not a useful harbinger of an MI.

As I discussed here , absence of the standard risk factors despite an exemplary lifestyle and diet does not protect you from our reader’s fate.

The High Fat Diet? Safe or Not

Now my question: I mentioned that quick background to note some things that are encouraging: a high level dose of atorvastatin has helped get my LDL down to 40-50. Metropolol has helped keep my systolic blood pressure controlled, and during the catheterization (or in conjunction), my cardiologist didn’t really notice much more build up than in the area mentioned above (I’m aware though that this “might” also be typical in very premature cases). The only area where I feel I somewhat deviate from the guidance I have received, is in terms of my diet. Before, I wasn’t necessarily splurging on red meat, but I was certainly more relaxed about consuming saturated fat than I am today. For a long time, I have been eating in a way that perhaps most closely resembles the Mediterranean diet, but perhaps with more emphasis on foods high in unsaturated fats. These days, I might consume a diet of around 7% of total calories from saturated fat (mostly dairy) and as much as 45% of total calories from fat stemming from (mainly) a variety of nuts, but also meat alternatives like avocado.

The diet you are describing is excellent for a patient with premature coronary artery disease as long as 1) you are maintaining a good body weight 2) getting lots of fruit and vegetables and 3) you enjoy it and find it sustainable for the rest of your life.

Unfortunately, there is no evidence that changing to a vegan or vegetarian diet will lower your risk of repeat MI.  Those who promote the EsselstynPritikin or Ornish type diets claim to “reverse heart disease” and to be science-based but, as I’ve pointed out (see here) the science behind these studies is really bad.

Some individuals just inherit the risk and must learn to deal with the cardiovascular cards they’ve been dealt. Although proponents of very low fat consumption (both saturated and unsaturated fats or oils) like Esselstyn ( see my debunking of the incredibly bad science behind his dietary recommendation here) claim their diets reverse coronary atherosclerosis this is a false claim.

The PREDIMED study published in 2013 in the New England Journal of Medicine was a landmark primary prevention study that demonstrated that a higher fat diet,with a lot of that fat unsaturated, is superior to a low-fat diet in reducing cardiac events.

Participants were randomized to one of three diets: a MED supplemented with extra-virgin olive oil,  MED supplemented with mixed nuts or a control diet (advice to reduce dietary fat). Participants received quarterly individual and group educational sessions and either free provision of olive oil, mixed nuts or small nonfood gifts.

The high extra virgin olive oil group ingested an average of 3.6 tablespoons/day (51 grams/day equal to 459 calories/day) of olive oil with 98% of it being extra virgin olive oil.

The high nut group ate 8.2% of their total daily calories in the form of nuts, including an additional approximately one-ounce packet of nuts (15g of walnuts, 7.5 g of almonds, and 7.5g of hazelnuts) provided by the study coordinators.

7447 persons were enrolled (ages 55 to 80 years) for an average 4.8 years.

Those persons following the MED diet (either supplemented with olive oil or nuts) were 30% less likely to have  a major cardiovascular event (heart attack, stroke or death from cardiovascular causes.) There was a statistically significant reduction in stroke rate (≈39%) when considered as an isolated endpoint.

We don’t know exactly what components of the MED are the most beneficial.  This trial suggests that olive oil and nuts are at least two of the key ingredient so it makes sense to increase your consumption of these foods.

As I’ve discussed (?ad nauseam) in other posts, full-fat dairy and eggs, although banned by most “heart-healthy diets”, have not been shown to increase heart disease risk.  Fermented dairy consumption, in particular, in the form of plain full-fat yogurt (not adulterated with sugar) and full-fat cheese is consistently associated with a lower risk of coronary heart disease. Plain full-fat yogurt and full-fat cheese (from goat milk) were consumed by the inhabitants of Crete, the Greek Island on which the original MED was based.
It has to be emphasized that within this pattern of eating you want to be consuming real foods, not processed products of the industrial food industry which have been manipulated to appear healthy due to being “low-fat” or “low cholesterol.”

The Mediterranean diet is a pattern of eating which is varied, interesting and sustainable. It is a diet that can last a lifetime.

This Table summarizes dietary recommendations for those on the Mediterranean diet versus those on the Low-Fat diet.

Details of the food recommendations. Sofrito, EVOO, and nuts.

The vast majority of evidence in cardiac nutrition shows that unsaturated fat consumption when replacing carbohydrates, especially refined carbohydrates, is beneficial.

Secondary Prevention: the CORDIOPREV trial

PREDIMED was a primary prevention trial; patients had not experienced MIs, stents, bypasses, or strokes. Arthur is now considered a case of secondary prevention.

There is a similar ongoing trial of secondary prevention, The CORDIOPREV study (Coronary Diet Intervention With Olive Oil and Cardiovascular Prevention) with the primary objective of comparing the effect of 2 healthy dietary patterns (low-fat rich in complex carbohydrates versus a Mediterranean diet rich in extra virgin olive oil) on the incidence of cardiovascular events.

Last November, the results of one secondary outcome of the CORDIOPREV study were published. At baseline, subjects underwent ultrasonic evaluation of their carotid arteries to assess the intima-media thickness of both common carotid arteries (IMT-CC.) In addition, researchers measured carotid plaques (number and height), at the beginning of the study and after 5 and 7 years of dietary intervention. I’ve utilized IMT-CC (aka vascular age) and early carotid plaque to identify subclinical atherosclerosis in the youngish.

IMT-CC significantly decreased at 5 and 7 years compared to baseline in the Med diet group but did not decrease in the control, low-fat group.

The maximal height of carotid plaques significantly decreased in the Med diet group whereas it increased in the control group.

We are awaiting the long-term outcome data from CORDIOPREV but these data showing regression of carotid plaque height and decline in IMT are very encouraging that the higher fat Med diet can cause regression of atherosclerosis (in conjunction with modern pharmacologic CAD therapy).

Mediterranean-style Ketogenic Diets

A randomized controlled trial published in the journal Obesity a year ago demonstrated superior weight reduction with a high-fat Mediterranean diet compared to a low-fat diet with similar levels of LDL-C at the end. The high-fat dieters utilized the Keyto device and app which I’ve written about (I Am A Keto-Friendly Cardiologist And I Love Keyto) and as described below focuses on unsaturated fats from plants.

The Mediterranean-style ketogenic diet app, paired with a breath acetone biofeedback device, uses a traffic light system to recommend consumption of foods (ad libitum, cautiously, avoid) according to the amount of net carbohydrates based on nutritional information gathered from the United States Department of Agriculture food database. The app emphasizes avoidance of refined carbohydrates, and priority is placed on fats from plant- (e.g., olive oil, avocado, nuts) and fish-based (e.g., salmon) sources that fit the Mediterranean guidelines

Arthur is not eating a ketogenic diet but my point is that even if you upped your fat consumption to ketogenic levels with mostly unsaturated fats you would not be increasing your cardiovascular risk.

I would also be fine with Arthur liberalizing his saturated fat content. For those who choose the ketogenic diet under my care, we carefully watch biomarkers including the LDL-C and advanced biomarkers I mention below.

I am happy with how this diet makes me feel during the day, and it seems to help me with weight management. But I’m of course aware of how my relaxed attitude towards total fats (as % of calories) deviates from most of the standard advice for my situation. Here I take some comfort in that my cholesterol (and triglycerides) seems to fall within a good range. But my question is if this is a naive way to view my dietary choice? Are there other mechanisms/channels suggested by the research whereby a high-fat (even if not heavy in saturated fat) diet might contribute to continued atherosclerosis?

It is wonderful that you have found a diet you are so happy with.

The major thing right now that is putting your LDL-C in such a low range (and lowering your risk of future cardiac problems) is the high-dose statin that you are taking. There is no evidence that lowering your unsaturated fat intake would further lower that. More importantly, there is nothing to suggest that changing the macronutrient composition of your current diet will lower your risk of further events.

With the LDL-C in its current range (assuming no smoking or uncontrolled diabetes) you will have regression of any plaque and minimal cardiac events. Your prognosis is excellent.

Thoughts on Patients with very Premature CAD

Just to note, I’m also aware that the isolated focus on macronutrients may be misplaced as well. But of course I can’t help but notice areas that I have control over where I might deviate somewhat.

Finally, of course I’m curious what your thoughts might be around premature cases. Even though my understanding is that the prognosis is typically not “great”, are there some things the research has pointed to in terms of contributing to (relatively) successful outcomes for very premature CAD? Or perhaps the opposite – mistakes often made in treatment of premature cases (for any number of reasons) that might exacerbate the risks?

I talk about premature CAD a lot on this blog. I’m a big proponent of the early detection of advanced or premature asymptomatic CAD. About a year ago I summarized the optimal approach.

Depending age we utilize either coronary artery calcium screening or vascular screening to detect subclinical atherosclerosis for primary prevention.

For those with advanced subclinical atherosclerosis, a strong family history or a history like my reader of early heart attack, stent, bypass or stroke I check three key biomarkers that are not in the standard lip panel

  1. Lipoprotein (a) (a highly atherogenic, inherited marker that is not measured in standard lipid panels)
  2. Apolipoprotein B (apoB, now recognized as our single best measure of atherogenic dyslipidemia)
  3. High-sensitivity CRP (the most studied and useful measure of inflammation)

You didn’t mention lipoprotein (a) but this has to be checked. In patients like you with such early onset of symptomatic CAD with fairly unremarkable standard risk factors , I find the majority have elevated lipoprotein (a).

Once risk markers are identified we are going to have very aggressive goals for lowering apo B, LDL-C and CRP. These will be accomplished by statins as tolerated with help of other lipid-lower agents known to reduce cardiovascular risk including ezetimibe and PCSK9inhibitors.

Skeptically Yours,


N.B. Since I started writing this and shortly before I published this the final results of the CORDIOPREV trial were published (

This did show a reduction in major cardiac events with the high fat Med diet compared to the low fat diet! I will examine this in more detail and report back.

h/t Marilyn Mann


23 thoughts on “You’ve Had a Heart Attack at a Young Age: Which Diet Could Have Prevented It and Which is Best Now?”

  1. Thank you to Arthur for so thoroughly sharing his story and Dr. Pearson for this superb, informative, science-based, and practical post which stands head and shoulders above the usual internet fare. There is a dearth of information about secondary prevention and far too much quackery. My experience parallels Arthur’s. I’m a longtime runner, non-smoker who (at least for the last 2 decades) has generally avoided many of the foods in the Standard American Diet, but I had lifelong high LDL (~ 145-165), family history (albeit two hard drinking, chain smoking grandfathers who died from heart failure by 60). My annual bloodwork came back consistently low on all other risk factors so I never, to my never-ending regret, got on a statin. Nor was I put on one. In fact the primary care doctors seemed agnostic about whether I needed a statin. In hindsight, I did. At 54, I had an MI due to a 90% LAD blockage, treated with PCI within about two hours and my EF is now back to what it had been prior to MI. Like Arthur, thanks to high dose atorvastatin and hard work, I have gotten my LDL down to 40-45 from the high level, during my MI/ER visit, of 180 (!) I have finally shed 25 extra pounds that I’d carried for decades. Like Arthur, since the MI, I have struggled with what to eat. I have erred too far in the direction of the mostly vegetables and fruit/non-fat diet this past year. The information laid out here by Dr. Pearson is a relief. It confirms what my cardiologists have also told me, so this post has been triply reassuring. I also appreciate the info on the three other risk factors. My CRP levels are low. My question: having read a recent New York Times article about a celebrity trainer who had an MI possibly due to high lipoprotein (a) I brought up the latter test to my cardiologist (he has 30 + years in the field) and he said it’s not needed. I believe he said that, in part because, as far as I know, there is no evidence I have a high level of it, or perhaps it isn’t covered by insurance, and/or, also, unless I am mistaken, there is currently no available clinical intervention to mitigate that lipoprotein (a) factor. Or am I wrong?Thanks again for the cogent overview of the clinical studies on the Med. diet.

  2. Thank you for this wonderful post Dr. Pearson. I would love to see an updated post on Zetia sometime, when/if you are able. I am already on Crestor 10mg as higher doses gave me elevated liver enzymes. I have since added Zetia as my Apo(B) level was a little over 100. I am eagerly waiting to see what the combination of Crestor and Zetia does!

    I also really enjoy your discussion of diet. I am just over 40 years old and went on the Dr. Fuhrman diet a few years ago. I admit that I lost 20 – 30 pounds, but quite frankly found it unsustainable in the long term. My wife and I now consume the Mediterranean diet as you recommend on this site. The hardcore vegan diets like Fuhrman or Esselytn are not sustainable in the long run in my opinion.

    Thank you very much for this website and this discussion. I have benefited greatly from it, and am grateful.

  3. Dr. Pearson, Thank you for the information you so well present in your blog posts. I am learning a lot about my cardiac issues and care. May you love long and prosper!

    • Arnold,
      Don’t advise daily ice cream intake. But to be honest I have a weakness for Ben and Jerry’s Americone Dream. Every 2 weeks or so I give into that weakness and eat some. The major issues from a health standpoint would be the calories should one eat it frequently and the high sugar. The dairy fat component is OK.
      Dr P

  4. Very interesting . I managed to drop 30 lbs in 2 years and reduce my A1C from 7.7to 6.3 by following a Mediterranean/ keto diet . I stopped consuming white flour, ( my husband makes flour for a living ?), white bread and actually most breads, pastas, sugar,potatoes. I do use mct oil in my coffee with stevia . I eat an occasional sweet potato , snack on nuts ,eat lots of avocados, fresh berries ,fiber wraps and chicken . I also eat local farm eggs, grass fed beef , pastured pork and poultry , all raised within15 miles of my home . I can my own veggies , pickles , sauerkraut. I use evoo ,real butter and home rendered lard . I believe I have also halted my nafld which had progressed to nash . With a stent in my mid LAD , I feel better now than I have in many years. All my numbers are well within normal limits . Here’s to hoping I have no cardiovascular events in the near future . I should also add my father died at 48 of a massive heart attack but he was also a smoker and a drinker of hard liquor . My mother is a triple bypass survivor at age 70 . I am currently 56.

  5. I am 67 years young and very healthy in good shape, exercise more than most my age, and eat a “good” diet even though there is so much contradictory information on the net which is confounding. Being Italian born but living in the USA I often reference my relatives in Italy. They are slimmer and healthier than most Americans I know and most live into their nineties with fewer health issues it seems. Their diet is “Mediterranean” but they certainly do eat sugar, pasta, fatty meat and other processed supposedly unhealthy food choices but perhaps not in the amounts I see eaten here in the USA.So I wonder if the “pure” Meditereanean diet really exists anymore as it did in the past.Being at the age I am, I worry about heart disease but can’t take statins because of serious side effects . I’ve never had a heart attack and I had great cholesterol numbers taking ezetimbe for years but my Doc took me off of it because he said “It doesn’t do anything”. Sorry for a long post which I could have said it better with just this: I just want to thank-you for your wonderful blog and posts. You help me more than my doctors ever have with useful information. You rock!!

      • Dr Pearson ,Is Zetia (ezetimibe) good as a stand alone? I was thinking about bringing this up next time with my new Doc. and starting it up again as my LDL is now 115. I did well while on it with no side effects.My LDL dropped to 70 while on it.I know in some past blog you wrote you only use it as a last resort. Has anything changed?

        • It is good as a stand alone. I need to update my zetia blog post as I use it quite frequently now since good outcome data has emerged and it became generic.
          dr P

  6. Great article, as always, Dr. Pearson. I

    wholeheartedly agree with identifying whether Lp(a) was playing a factor in his “early onset” CAD. It would be interesting to know more about his family history and genetic clues to early onset CVD events.

    Quantitative cardiac CTA (with Cleerly™️, etc.) might have a role here to better define and quantify the burden of asymptomatic vulnerable lesions and could also be used as a direct method to determine the response to lifestyle and pharmacotherapy. Alas, CIMT, at the individual level, is insensitive to determine the small changes in plaque that occur with therapy and even then only tells one about the cerebrovascular bed and not the coronary circulation.

    Thanks again for you insights, Dr. Pearson!

    • John,
      thank you.
      Do you have experience with Quantitative cardiac CT with Cleerly in a clinica population.?
      It would be fantastic to have a reliable noninvasive tool to assess vulnerable plaque burden.
      I currently tell my patients that tool does not exist.
      Can’t use coronary calcium. Merely ordering serial CCTA (unless you have a research lab focused on quantitation ) would not qualify.
      Dr. P

  7. I read this post with much interest. . I have survived 4 heart attacks and had a triple bypass surgery. Currently in CHF with two of my grafts closed, I have been following mostly vegan diet. I would like to know what diet to follow in order to live a bit longer and avoid any more events?

    • Thank you for all the great information you provide. Are you familiar at all with the work of dr. Ford Brewer? He rarely uses high-dose statins and only prescribes rosuvastatin or Livalo for any of his patients. His focus is on inflammation insulin resistance and prediabetes as being the main risk factors and not high LDL. I would never go on a high dose statin for any reason. I take Crestor 5 mg every other day due to a 500 calcium score five years ago at age 55. I’m very fit and athletic and never have had high cholesterol. Your thoughts please and thank you very much!

      • Bart,
        I took a quick look at Brewer’s website and saw several red flags of quackery.
        Under the “Products” section I see he is promoting/selling a device to lower BP and numerous useless, expensive supplements.
        Such activity I consider the #1 Red Flag of Quackery. Beware in such situations that the entire enterprise is pseudoscientific and just geared to separate the gullible from their money.
        In your case given the very high CAC score, I would advise checking for a high lipoprotein (a) level.
        Dr P

        • Dr. Brewer trained at Johns Hopkins and many of his patients have improved their health greatly with his approach. The device you speak of is FDA-approved although I don’t use it. I had lpa checked as part of an NMR lipid panel about 5 years ago and it was 50. Thank you for your response and I respect your opinion but I certainly don’t consider him a quack by any means and I also respect your knowledge and approach. If possible could you do a future discussion on the different statins recommended dosages etc thank you!

          • Bart,
            I can’t tell without the unit designation (?mg or nm/l) whether your lipo a is high.
            A post on the different statins is a good idea and I’ll try to write something as time allows.
            Dr P

            • Thank you for your quick response sir. I just pulled out the old lab result sheet from 2015 right after my calcium score and after on a statin for only a couple weeks at that time. The measurement says nmol/L and my number was actually 68. The optimal range on this sheet says below 75 but I know that varies with different Labs Etc thank you and much respect!

              • Bart,
                So your lipo a is at upper limits of normal and doesn’t explain your advanced CAC score for age.
                On Brewer, perhaps we could create a post in which you present your arguments in favor of Brewer’s program and legitimacy and I’ll outline my issues with them.
                you can email me “pro” arguments at
                dr P

                • I’m guessing due to my high cac score but with normal standard lipid panel all my life I may have insulin resistance or prediabetes but my doctor doesn’t seem to be interested in digging deeper. Wish I could find a cardiologist here in South Jersey who I can establish a relationship and who will work with me.
                  I’ll consider your suggestion on the pros but please don’t think I was trying to push his approach on you. I have followed and enjoyed your contents as well as dr. Brewer for quite a while and will continue to do so. I’ve learned much from both of you and much appreciated! Thank you so much for the interaction. I look forward to more interesting topics.

      • I have terrific blood sugar, no signs of diabetes, no family history of diabetes, and my triglycerides have always been fine. I have been an avid runner, weight-lifter, and non-smoker since my teens. What I do have is well over a decade of elevated LDL and a strong family history of heart disease on both sides. Earlier this year, at age 46, when I thought I was in as good a shape as I was in my twenties, I got a CAC score of 106, which puts me in the top 3% of people my age…not a top 3% you want to be in. That was almost certainly entirely due to years of bad cholesterol that did not respond at all to being an avid athlete who maintained a fairly healthy diet. Again, there is nothing in my lab work to suggest even a remote hint of diabetes, nor has there ever been, but there is nearly two decades of high cholesterol. I’m very happy to have finally been put on a high dose statin regimen and feel I should have been on one MUCH earlier.


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