February 27, 2013

Metabolic disease

Is a Mediterranean diet best for preventing heart disease?

by Peter Attia

Read Time 8 minutes

This week an article titled Primary Prevention of Cardiovascular Disease with a Mediterranean Diet was featured in the New England Journal of Medicine. The study received a considerable amount of attention, including an article in the NY Times.

Study design

The objective of this study, as its name suggests, was to study the impact of a Mediterranean Diet on the primary prevention of CVD.  Primary prevention of X implies looking at patients (ideally those susceptible to X) who have not yet had X to see if your intervention prevents X. Such trials are more difficult (i.e., larger and more expensive) than secondary prevention trials because in secondary prevention trials you start with patients who have already had X and are therefore at much greater risk of having X again.

Let’s use a relevant example.  A primary prevention trial for CVD would study subjects who have never had a heart attack or stroke, and look for which treatment (e.g., a drug like a statin) reduces the number of such events (sometimes called MACE – Major Adverse Cardiac Events).  A secondary prevention trial would study subjects who have already suffered some MACE and look at interventions to prevent a recurrence.

This study, a primary prevention trial, enrolled about 7,500 patients who were at high risk for CVD, but who had not suffered any MACE, and randomized them to one of three diets – two variants of a Mediterranean Diet, and a low fat diet.  Table 1 shows the dietary targets.  The two variants of the Mediterranean Diet were (i) one that emphasized extra virgin olive oil (EVOO) and (ii) another that emphasized nuts.

(As an aside, my 40th birthday is coming up soon and my wife suggested to my daughter that they make me a cake for my birthday.  My daughter – who loves cake, of course – objected immediately by saying, “Mommy, we can’t do that…Daddy hates sugar!”  A few minutes later she came back to my wife and said, “Mommy, wait, I have a great idea…we can make Daddy a nut cake!”  Those of you who read this post may recall the last point I made.  Suffice it to say, if I were in this study, I would have done really well on the nuts arm, though I think I eat closer to 5 or 6x the amount they were recommended per day.) 

Table 1

As you can see all three arms were discouraged from consuming bakery goods, sweets, pastries, red meat, processed meats, and spread fats.  The authors report compliance data, but not biomarkers (if I wasn’t so short on time, I’d go back and read the other publications of this study which likely show biomarkers – e.g., insulin, glucose, HDL-C, and triglycerides – which are pretty good for confirming compliance, especially HDL-C).

So, macro point #1 is this:

Everyone in this study, almost by necessity, was consuming a very healthy diet relative to their baseline diet (if you believe most folks were on a “standard” diet, or worse yet, a poor diet, prior to enrollment, which I do).  I’ll come back to this point later, but it’s worth remembering this as you read on.

Table 2, below, shows you the baseline characteristics of the subjects in each arm.  I must admit, before I saw the results of trial, but knew it was going on, I was a bit surprised at how audacious the investigators were.  Primary prevention trials are really challenging!  However, as soon as I read the inclusion criteria and saw this table I realized this wasn’t really a garden variety primary prevention trial, per se.  Why do I say that?  Less than 10% of the subjects were of normal weight.  Less than 20% did not have high blood pressure.  50% had type 2 diabetes.  Less than 30% had normal lipid profiles (presumably defined by LDL-C and HDL-C cutoffs).  Over 40% were taking statins.  You get the point.  Virtually everyone enrolled in this study had metabolic syndrome.

This is not a criticism of the study, to be clear.  It’s merely a statement of why this study, I believe (and hopefully will make a case for), showed a treatment effect in the setting of primary prevention with a dietary intervention.  In fact, this is exactly what the authors sought in the enrollment.  They specifically looked for high risk patients who had not yet suffered a MACE.  In my humble opinion, this was a very good choice for two reasons:

  1. If they selected healthy subjects, they would have needed 5-10x the number of subjects, and
  2. This patient population is in desperate need of dietary intervention.

So, my only minor critique of this is the semantics of calling this a primary prevention trial.  It would be more accurate to call it a primary prevention trial of patients with diagnosed metabolic syndrome.

Table 2

One thing I always look for in dietary trials (and trust by now you’re also looking for) is something called performance bias, which is very common in dietary intervention trials. In fact, you’ll recall it was the main flaw of the meta-analysis I wrote about a while ago.  The authors of this particular study (you can read about this in the methods section) did a good job avoiding this.

This brings me to macro point #2.  This study would have been better if the “control” arm (in this study, the low fat arm), was actually a true control relative to the “standard” patient diet.  For example, this might look like the following 3 arms: standard fare diet vs. low-fat diet vs. Mediterranean diet (pick one of the 2 from this study).  The drawback of this approach is that patients in the “standard fare” would almost certainly have a performance bias working against them.  The other two groups would have a sizable intervention effect, while this (true) control arm would be left on their own.

The final point I want to make is more of a so-called teaching point. Broadly speaking, there are two (and an emerging third) types of studies in human nutrition:

  1. Efficacy studies – studies that elucidate (under the strictest most controlled conditions ever used to study humans) the mechanism of action of food.  In other words, these studies ask, “How does factor X or factor Y actually work at the mechanistic level in the body?”
  2. Effectiveness studies – studies that elucidate to what extent free-living people will adhere to a dietary change, and determine the long-term safety and effectiveness of that change. In other words, these studies ask, “Does this dietary intervention work over time, and what are the risks and benefits?”
  3. Econometric studies – studies that elucidate (under free-living conditions) how to change people’s behavior, by changing the defaults, the economic forces, and the cues. In other words, these studies ask, “How do we induce people to change behavior – to eat healthy — once the science provides definitive answers about what that behavior should be?”

Obviously, this study is in the second category, as virtually all “diet studies” are.  I mention this for the reason that while it’s tempting to speculate on a mechanism of action in this study, there was not a single design element in this study to elucidate such things.  So, at best, we are really looking at the difference between two dietary interventions.

What happened in this study?

Table 3 shows the outcome of the study and commensurate hazard ratios.  I won’t walk you through this table in its entirety, but I’ll show you how to read one row of each.

Consider the first row, the primary end point (recall: this was defined as a composite of myocardial infarction (MI, “heart attack”), stroke, and death from cardiovascular cause).  The first row shows the number of crude events.  Of course, to see this in an apples-to-apples fashion the number needs to be normalized to a common denominator, in this case events per 1,000 person-years.  So, the row that’s particularly important is the one that shows 8.1, 8.0, and 11.2 per 1,000 person-years.  (Note, one uses person-years to also normalize for and remove any impact of time in study.)  Next to each number I’ve listed above are two numbers in parentheses.  These are the 95% confidence intervals.  So, even though the first is listed as 8.1, you can be “95% sure” the actual number is between 6.6 and 9.9.

How can you tell if this is “statistically significant?”  Most of us don’t possess the ability to do this in our heads.  So, the authors do it for us in the last two columns.  The right-most column compares the control (low-fat) to the Med Diet (nuts), while the column to the left of that compares the control group to the Med Diet (EVOO).  The number shown, called a p-value, is defined as the probability the difference you’re seeing is due to chance.  The smaller the better, and generally a number below 0.05 is considered to earn the moniker “statistically significant.” (Not to be confused with “clinically significant,” which I’ll discuss below).

Before we go back to the other endpoints, let me comment quickly on the hazard ratio for this endpoint. A hazard ratio is essentially the probability of an event in the treatment group divided by the probability the same event occurs in the control group (hence, control groups have a hazard ratio of 1.0).

So, the hazard ratio of 0.70 means there was relative risk reduction of 30% for the Med Diet relative to the control diet.  This should not be confused with absolute risk reduction, which I’ll get to shortly.  For the sake of time and space, I will not go into the details of unadjusted and multivariate adjusted analyses.

But there was no difference in MI or death?

As you can see from Table 3, there was no statistically significant difference in death (CVD or otherwise) or MI across the three groups.  It’s very tempting to make the following mistake:

“Hey, none of this matters, because you won’t live longer.”

Remember that pesky little statistical thing called power.  This study was powered (at 80%) to detect a difference in the primary outcome, which it showed.  In fact, the intention-to-treat was greater than 7,500 because the authors expected no more than a 20% relative risk reduction.  But they saw a 30% difference, and the study was halted early.

So, we don’t actually know which of the following statements is correct:

  1. This dietary intervention does not result in a difference in MI or death; or
  2. It does, but this study was not large or long enough to detect it.

Very important distinction.  I can’t emphasize this enough.

Table 3

Back to absolute versus relative risk

Figure 1, below, shows the Kaplan-Meier estimates for the primary end point (A) and total mortality (B).  Each figure shows both the full y-axis (which always varies from 0 to 1) and, in the upper right corner, a zoomed view to show the difference.  The fact that the zoom view is necessary tells you something about the absolute risk reduction.  It’s small.

Here’s a quick calculator to determine the absolute risk reduction (ARR).  When you plug the numbers in from this study (I’ll just do it for the low-fat vs. EVOO group), you’ll see the ARR is 0.3065%.  The reciprocal of this number is 1/0.003065 = 326.  This is called the number needed to treat (NNT).  This means that 326 people would need to undergo this dietary intervention for about 4 or 5 years to prevent one “count” of the primary outcome.
Figure 1

Is this important? Or, to be more specific, is this “clinically significant” as I asked earlier?  Well, it depends on the intervention.  If this study were testing a drug with a 1% major toxicity rate, the answer would be emphatically, no.  Obviously, we could not justify treating 326 people to save 1, if 3.26 people (on average) will experience a major toxicity!

Conversely, if this study were testing a drug with a 1% minor toxicity rate (e.g., headache) and a 0.001% major toxicity rate (e.g., kidney failure), the answer is not so clear.  For perspective, most drugs fall into this second category (e.g., statins, aspirin).

I could go through the exact same argument using Quality-Adjusted Life Year (QALY) instead of toxicity. While this approach is not used in the United States (perhaps it should be), it is certainly the cornerstone of other healthcare systems, such as the NHS in the United Kingdom.

While it’s beyond the scope of what I wanted to write about today, the key to sorting through this grey zone is better defining patient susceptibility and outcomes in large clinical trials.  For example, I would argue that the data on statins could be much better if the treatment target was LDL-P or apoB instead of LDL-C, especially in high risk patients with metabolic syndrome, at least half of whom have discordant LDL-P and LDL-C.

So, what to make of the modest ARR in this study? Well, question 1 should be: what is the toxicity of a Mediterranean Diet?  Question 2 should be: what is the QALY impact of a Mediterranean Diet?

I can’t really answer either of these questions.  The former is objective but has not been quantified to my knowledge.  The latter is subjective, and each person needs to answer it for themselves.

My conclusions

Overall, I think this is a good study, and a better study than the study prompting it, the famous Lyon Heart Study.  That said, I would have much preferred to see only one Mediterranean arm (in retrospect this is obvious, of course, given the lack of difference between them), in favor of a true control or another arm such as Very Low Carb.

It’s impossible to guess what the ARR would have been for the Med Diet if the control was a standard fare diet (complete with 138 gm per day of sugar!), rather than a much improved low fat diet.  If I had to guess, I’d ballpark the ARR at 1-5%, for a NNT of 20 to 100 people, but this is nothing more than speculation.  Remember, I think the Low Fat arm in this study experienced an enormous benefit over their baseline.

In the coming months and years, as NuSI begins funding remarkable clinical trials, we’ll have plenty more to discuss…

Photo by Carlos Santiago on Unsplash

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  • Thanks for this overview. CNN’s Sanjay Gupta has criticized the compliance rates in the control, which he suspects produced the differences in outcomes. Any thoughts on this?

    • Certainly possible, but we’d need more data to evaluate that claim. This is where the full biomarker panel would have been helpful.

  • This study does not evaluate a Mediterranean diet.

    Look at the supplement, S5 table, at 5 years and note the reported composition of diets. The only difference between the arms: more nuts or EVO, and they were given for free, in unlimited supply. Not a bad thing, but title of paper should reflect intake, not “Mediterranean.”


    • Interesting point. What do you think accounts for the difference between the Med Diet and the LFD?

    • Marco Ermini

      I am Italian and we eat lots of red meat… My granddad used to say “you never throw away anything from a pork”.
      I believe lot of those “experts” who “created” the Mediterranean diet myth have the classic prejudices of the misinformed dieticians, such as “less meat more fish” and the likes.
      Mediterranean diet is a myth because there is nothing such as a “Mediterranean diet”, there are just points in common between different populations living near the sea such as fatty fish, etc., but the rest is a massive mix up of overlapping cultures. Think about the sweets made in Sicily, which are mostly done without sugar but with honey and nuts – this is the typical Arabic cousins, which you also find in parts of Spain, and reflect Arabic domination on those regions. Or pasta, which is massively produced only after the 50s – Italian cultural food goes back much, much more and includes lots of typical cheeses, salamis and so on.
      I believe companies like Barilla and the likes have also lots of influence in defining what “Mediterranean diet” is – pasta is not a tradition in the majority of Mediterranean regions, Cous Cous is. Or in North Italy polenta is used instead. Think again about Greece and the sheep’s feast they always make…
      Nearly every village in Italy – and I’ll bet in the whole Mediterranean region as well – has local traditional plates. At best “Mediterranean diet” is a very reductive classification, and at most is just a very unjust prejudice.
      It is the same misconception that many spreads about Indian cousins being “vegetarian”, when you examine closely they eat very differently in the north and south and they eat lots of lamb and chicken.
      When we try to classify traditions we should be looking very closely at the history and not use common places.

      • Excellent points, Marco. Thanks very much for insights.

  • Bill

    But didn’t the authors say that the “low fat” group didn’t actually reduce their fat very much? It may be that this arm is something not too far from the SSD (Standard Spanish Diet), especially since all of us, Spaniards included, have been bombarded with anti-fat dietary advice for years now anyway. And isn’t the SSD likely to be pretty different from the SAD?

    Also, even if we believe the results (not clear to me if we should with such a tiny absolute risk reduction and the many biases and confounders that could be at work), couldn’t it be that the benefit of the “Mediterranean Diet” really came from, say, just increased fish consumption, or decreased sugar, or some other individual factor? It’s not clear to me how one can interpret the results of such a poorly controlled intervention.

    • Possible, it also may reflect how hard it is to change your diet in a free-living environment, even in the face of a diet “prescription,” right?

  • Dave Nelsen

    Peter, glad to see you back. When I first read it I thought your daughter said you were a “nut case”! I read a Dean Ornish critique of this paper and he was carping about the fact that the low fat arm of the experiment wasn’t low fat enough (for him anyway), thus you can’t derive anything from the study, and from his perspective that is probably true. From my perspective his diet is so drab, boring and unappealing that no one (other than a zealot) could follow it for very long. I wish they had left one group eating their standard diet, and like you said have a HFLC arm.

    • Dave, I never went anywhere! I’m here working harder than ever (just not on the blog and instead on NuSI).

    • jw


      Dean Ornish’s comments from the NEJM’s Comments section:

      Flawed Study: Control Group Was Not Eating a Low-fat Diet!

      This study is highly flawed:

      • The control group did not follow a low-fat diet. The authors wrote, “We acknowledge that, even though participants in the control group received advice to reduce fat intake, changes in total fat were small.” This is not surprising since they gave the control group little support in following this diet during the first half of the study.

      In the “low-fat” group, total fat consumption decreased insignificantly from 39% to 37% (Table S7, appendix). This is much higher than the American Heart Association guidelines of a low-fat diet (<30% fat) or ours for reversing heart disease (<10% fat).

      • There was no significant reduction in heart attacks, death from cardiovascular causes, or death from any cause. They only found a significant reduction in death from stroke (Table 3). They only found a reduction in cardiovascular causes when these were pooled with deaths from stroke (Table 3).

      The conclusion should be, “We found a significant reduction in stroke in those consuming a Mediterranean diet when compared to those who were not making any significant changes in their diet.”

      Dean Ornish, M.D.
      Clinical Professor of Medicine, UCSF

    • Peppino

      I’m sorry, but your conclusion is simply wrong. At the age of 61 I had a surgical intervention (angioplasty with 2 stents inserted). I began the Ornish diet immediately after. About 4 years later I had an angiogram (necessitated by the bias between 2 different scanners) which showed that in fact my arteries had improved. I have maintained this improvement since, as confirmed by an angiogram 1 year ago. In October, 2013 I’ll be 75. The last 7 years I have mainly maintained the Ornish diet except that I have augmented it with EVOO. I live in Italy for 6-8 months a year in a region (Abruzzo) where high quality EVOO is readily available. I take lipitor (10mg) because my LDL is in the low 30’s. So I eat a Mediterranean diet, which includes pasta made from real durum wheat, and which in most respects reflects the Ornish diet. I respect Dr. Ornish, even if I think he’s sometimes a little too defensive about small deviations from his diet.

  • I was not as impressed as you with this study. Buried in the supplementary appendix is a table showing what the members of the three arms actually ate, as well as the biomarkers gathered.

    So how much fat did the MeDiet group eat at the start of the study? 39%. And the low-fat group? 39%.

    That’s odd. What about at the end of the study? Mediet: 41%. Low-fat: 37%.

    Now as much as I’m in favor of a high-fat diet personally, I find it really hard to believe that changing your fat intake from 39% to 41% is going to have much of an impact. Or reducing your carb intake from 41.7% to 40.4%, as the MeDiet group did.

    What really stood out was that the three arms were eating almost identical quantities of everything. The only notable difference was that the nut group was getting more of the fats that one gets from eating a lot of nuts. Shocking, that. Even the fatty acids that come from olive oil were nearly identical across the three groups. Clearly the low-fat group wasn’t listening.

    So I’m a little unclear on what this study is actually showing. It certainly wasn’t comparing a low-fat diet to a Mediterrean diet. The best you can say about it was that the MeDiet had three arms, and no control. (The low-fat group increased its olive oil consumption from 15.8% to 16.4%. This was the group counselled to *avoid* olive oil, mind.)

    So as partial as I am to studies that show the inferiority of a low-fat diet, this one didn’t do it.

    (The biomarkers were to show that the subjects ate olive oil or nuts, that’s pretty much it. Compliance was good.)

    • Maybe, as some have commented, a LFD in this culture is convergent with Med Diet? I wonder, though, what accounted for the separation? Was something in the EVOO and/or nuts that made the difference?

    • This was not a a diet that anyone in “this culture” would ever eat. Both arms were advised not to eat too much fat, the diet was designed by fat-phobic dieticians, not from shipping off the Med wing to Tuscany or Athens.

      “In the Control group, advice on vegetables, red meat and processed meats, high-fat dairy products, and sweets concurred with the recommendations of the Mediterranean diet, but use of olive oil for cooking and dressing and consumption of nuts, fatty meats, sausages, and fatty fish were discouraged.”

      Frankly, having gone through the dietary composition, I can’t for the life of me figure out why one wing might have done better than the other. It may well have been dumb luck, as I just don’t think that minor differences in macro- and micronutrients are going to make much difference.

      Olive oil arm: 22.0 % of daily energy from Olive Oil
      Nut arm: 17.6 % of daily energy from Olive Oil
      Control: 16.4 % of daily energy from Olive Oil

      That 5.6% difference must be pretty important…

      It may have been something else, also. The fat numbers they report for their fat subtypes don’t add up to total fat. Maybe the third intervention arm was chugging down the trans fat? That could easily cause a difference as small as what they report.

      I suspect that if they’d just left the Control group alone, they would have seen a much bigger difference in the result, although I can’t help but think that if anything explains the difference in the Control group, it was that they did not get this advice:

      “Negative recommendations are also given to eliminate or limit the consumption of … carbonated and/or sugared beverages, pastries, industrial bakery products (such as cakes, donuts, or cookies), industrial desserts (puddings, custard), French fries or potato chips, and out-of-home pre-cooked cakes and sweets.”

      That’s pretty good advice for anyone! But again, how is avoiding “carbonated and/or sugared beverages” low-fat?

  • David Prentiss

    Thanks for your quick analysis, Dr. Attia. I was eager to hear what you had to say about this study. Keep up the good work. We are all looking forward to the results of NuSI funded research.

  • LarryB

    The fact that this study has gotten such good coverage is a good indicator that the media is ready to talk about alternatives to the standard-issue medical guidance that a low-fat diet is best. That said, they’ll still have a problem with things like grain and sugar elimination.

    As to the low-compliance on the low-fat branch of the study, that speaks for itself. Not only is low-fat a poor choice, it’s so hard to follow that the medical consensus that diets don’t work.

  • Mark


    Totally agree that it would have been nice for them to have included a different group, either “standard” diet or very low carb. In fact, the way they designed it, it almost seems like they had a foregone conclusion that some Med diet would be better, question was only which would be preferrable. From this study, I only conclude that a diet higher in fat resulted in reduced cardiac events (consistent with results of Ludwig and other recent studies), but the study does absolutely nothing to disentangle which kind of fat or if kind even matters. As for me, I’ll happily stick with red meat, cheese, eggs, and whole milk… seems to work for me!

  • Bob

    Personally, I find this study to be complete garbage. For instance, assuming the people followed the recommendations, the high oil group was supposed to eat at least 4 tbsp of oil per day, while the low fat group was supposed to eat less than 2 tbsp per day yet eat much higher amounts of bread, potatoes and other carbohydrates. How can you tell the minimal benefit in the high oil group wasn’t due to the differences in carbohydrate content between the two groups (the high oil group and the low fat group)? There are so many variables they changed you have no idea what’s causing what. Is it the oil that’s helpful? Is it the 7+ glasses of wine per week? The amount of vegetables eaten (2+ servings per day versus 2+ servings per WEEK)? It’s ludicrous. That this is classified as “science” (and that they stopped the study due to the purported benefit) is sickening.

    • Fair point, Bob. But remember the difference between an efficacy study (what it sounds like you’re after) and an effectiveness study.

    • Russ

      Bob, Just want to emphatically concur… this study is “complete garbage.” On the sole basis that the the “control” group asked people to consume >3 servings per day of carbs including bread, pasta, and the study group was told to avoid bakery goods, it would have been equally valid for the study to conclude that bread and pasta cause heart disease (a-la Dr. Davis). But per the other points about the study design, I don’t think it can even claim that either.

      I think it’s a very poor statement about the state of peer review that a paper like this could make it to press making the claim it did. And sorrier still that the popular press didn’t spot this right away. You don’t have to be a diligent sleuth like Denise Minger to spot this fatal flaw.

  • Hi Peter,
    Nice post, and thanks for the statistical insights.

    I think it was a very well done study too, but one thing that stuck out at me was that none of the study participants got healthier. That is, after 5 years people in all 3 groups were taking more prescription medications than they were at baseline. In other words, I don’t think any of the diets were optimal for this high risk subject population.

    Best regards,

    • Very interesting point, Bill. Certainly suggests there is room to improve in all arms.

  • Kelcy

    Hi Peter!
    I love your blog, I think I have read every one of your posts!
    I was googling and ran into a few posts and studies on palmitoleic acid and omega-7s. I would love to hear your thoughts on the subject. Perhaps an idea for a future post?


    • Well, I guess it depends on your question. Palmate is a SFA that is created during de novo lipogenesis.

  • Teddy

    Great analysis. Question/comment…. Marco point one emphasizes how the study included subjects with metabolic syndrome. You comment that healthy individuals did not predominate. This may be true but how much do the subjects in this study represent an unbiased cohort of spain or america? ie Sure all these people had metabolic syndrome but isnt this what we are dealing with here in the US?

    • Great question, Ted. In the US, 37-39% of the population is obese. Of this group, about 66% have MetSyn. Conversely, 31% of the US population is “below or normal weight” according to the latest stats, and about 7-9% of them have MetSyn. So obesity is really just a (very good, but far from perfect) proxy for MetSyn. So, I think this population is good representation for the (sadly not small) segment of the US population most at risk for metabolic diseases.

    • Dan

      According to the latest AHA statistics (2012), quoting NHANES II or III, more than 46% of americans have either frank diabetes or impaired fasting glucose. When you consider that insulin resistance tends to manifest in elevated blood sugar LAST among its many manifestations, that means that well over half of the population likely has metabolic syndrome (insulin resistance syndrome, carbohydrate intolerance, or syndrome of increased waist circumference, elevated glucose, elevated blood pressure, depressed HDL, increased triglycerides). Therefore, primary prevention has now become all about the treatment of metabolic syndrome and its legacy.

      • Very, very important point, Dan (and Teddy). Thanks for raising.

  • Stephen

    Thanks for the interpretation of that study, Peter.
    I think you have your work cut out for you on NUSI, based on my doctor’s reaction to my yearly checkup today.
    I told him I wanted the NMR LipidProfile Test done, and he got angered at my request, and refused to write a script for a lab test.
    I then told him that my mother passed away from MI the day after her doctor told her that her bloodwork was fine.
    He said that God wanted to take her.
    Then I told him about the low carb/high fat diet I was on for the last eight months, and he asked if I could name him as my beneficiary, because I was going to be dead in a very short time.
    I then told him that I thought I was insulin resistant, because I was on a low fat /high carb diet for the last twenty years, but I was still overweight for my height and body frame.
    He said if I was insulin resistant, I’d be diabetic.
    I then said that I probably had metabolic syndrome, and he said that it didn’t exist.
    Then I told him I lost 20 lbs. on the diet, and eliminated my sugar cravings, and he just ignored that.
    I asked him again for the NMR Lipoprofile Test script, and he said he was giving me a Lipid Profile Test to measure LDL-C, and that LDL-P is nonsense, and has no bearing on cardiac health.
    I started to mention your website, and he got extremely angry, and said he wasn’t interested in some nut with a website had to say that contradicted years of scientific work by reputable doctors. He then told me I was suffering from the new DSM classification of “Internet Hypochondria”.
    At this point, he started to use some four letter words that might not be appropriate on this blog, and turned his back on me, and I realized my visit was over.
    Another story from the Naked City (NY)!

    • I normally would not speak so candidly, Stephen, but I’m sure others reading this will agree…you need a new doctor. This person, if for reason other than their arrogance, has no reason to be practicing medicine.

    • Dave Nelsen

      Stephen, I asked Peter something similar some time back. I had a Dr. who I educated about this new Lipid test, but she was bound by certain rules in helping me any further for my LDL-P issue. Peter referred me to the Jimmy Moore website as he has a listing of Low Carb Dr.’s. Here is the link: http://lowcarbdoctors.blogspot.com/

      There are several Dr’s to chose from in NYC. Your current guy seems to be living in the past where Dr’s patronized you and patted you on the head and told you what was best. Well the Internet is here now and that is both a good and bad thing when it comes to health. I think highly of the information on this site, however, it is sometimes hard in a sea of health websites to find what is true or likely to be true vs. total BS. Even among the Low Carb community there are various points of disagreement, but in general they agree more than they diverge. Everyone has some degree of selection bias, I just like to think there is some data behind mine. Good luck finding a new physician.

    • Maryann

      You definitely need a new doctor. There are a couple of lipidologist websites with a search feature; some of the doctors are cardiologists and primary care physicians: lipidboard.org and lipid.org. Jimmy Moore mentioned on a podcast that he gets his labwork through privatemdlabs.com. I just checked, and they have the NMR for $125. Best wishes, maryann

  • Dan

    Very interesting trial. Hard to get such a study funded in this environment (Pharma is completely disinterested in this, for obvious reasons). Fantastic that the results were achieved in an environment in which nearly two thirds were on LLA’s and >80% on AHT’s. I think that the dietary differences were more significant than can be appreciated in that technical appendix, and probably the INTENSITY of dietary counselling (especially regarding trans fats and PUFAs) is what drove the difference. The effect size is about what you would expect for statin in this population and about double what you would expect for aspirin in high-risk primary prevention. That it occurred on top of what looks like optimal medical therapy is quite gratifying.

    Personally, it will not change much my approach to dietary counselling – minimization of acellular carbohydrates, maximization of healthy plant-based fats and oils – in fact, that is what they recommended in this trial, rather than a true mediterranean diet (which is very high in carbs).

  • Brad

    Everyone is always touting olive oil. It would be nice to see a study that compares it to other lipids, both SFA’s and other MUFA heavy fats like lard, avocado, etc. Do they know what in particular is the healthy part of olive oil? Is it the MUFA or polyphenols or other?

    Also, is this statement in the comments section of the NYTimes article true?…
    “this was not an independent peer reviewed study. The funders were the olive oil and nut companies.”

    • Brad, to your first point, there is a very interesting paper coming out, probably in the NEJM, probably before summer, that shows some interesting benefits of EVOO.
      To your second point, not correct. The olive oil and nut companies, which provided food for free, neither funded, nor ran the study.

    • LarryB

      Or course, the challenge with olive oil is the degree to which it’s adulterated. Have a look at “Extra Virginity” by Tom Mueller. It’s made me a LOT more careful about where I buy my oil.

  • I think the Mediterranean diet has a great balance to it and is not too restricted. Great in depth article.

  • Superstar worthy analysis Dr. Attia-well done! I’d love to compare and contrast gut microbiota when altering the diet in future studies. Fingers crossed. Best, SM

  • The doctor-patient relationship in the world of information/internet is certainly an interesting issue. It is obvious that doctors have to be better prepared because their patients nowadays have access to a lot of information. Here is an article you might like to read that on the subject of heart disease prevention, diet and drug therapy: http://www.docsopinion.com/2013/03/02/diet-or-drugs-to-prevent-heart-disease/

  • jim bowron

    Follow up piece in the NYT times had this lead in;
    “A study (the Mediterranean diet study)has infused the field of cardiovascular medicine with optimism, as scientists are calling for similarly rigorous studies of other popular diets.”
    Maybe they should check out your website where they may try ‘even more rigorous studies’.

    • One of my Board members sent this along with a similar comment today!

  • I think there is some substance in this so called rumor of Mediterranean diet being very healthy, there are results which prove that. I guess lot of it has to do with olive oil, which is known to be the most healthy cooking medium and this makes all the difference.

    I think there should be a comparative study between Olive oil and other cooking medium, then more conclusive results can be obtained.

  • Jeff Johnson

    Studies Methodology Questioned

    1….. You could learn the same thing or similar by putting 10 people in a metabolic ward for three months and measuring their arterial health – and extrapolating that arterial health into a reasonable heart/stroke event outcome –

    saving millions – accomplishing the same in three months instead of five years of fatally flawed nonsense (people failed to follow diet)

    Arterial health can change rapidly – plaque and calcium decrease or increase or or stay the same – other markers of arterial health can also make rapid changes – again – extrapolating these findings into a heart risk event makes sense – at least to me – contrary opinions welcome (let me know how stupid I am)

    • Jeff, not stupid at all. In fact, I struggle with this exact question more than any other in my role at NuSI. Are there ways to study and fully elucidate the impact of food on health without hard outcome studies if we can identify good enough biomarkers?

  • One of the problems in asking Spaniards (or Greeks or Italians) to use corn oil or other such poison instead of olive oil is like asking a Canadian to watch cricket instead of hockey. It’s just not going to happen. No wonder compliance was poor in the “control” group.

    Good job bringing forth some of the good points we can take from this study (and for explaining the power correctly).

    • As a Canadian, I can vouch for that. I don’t think I’ve ever watched a cricket match..

  • Evan

    I recently had both a VAP Profile and a NMR done on the same day but the results are off somewhat on TC and Triglycerides. Which is more accurate analysis?

    A little history,

    Was low fat forever, TC 221, HDL 42, Tri 105, LDL 158

    Doc wanted me to take Statin, so instead I went low carb.(perhaps 50 net carbs a day)…..some good news some bad….TC 282, HDL 73, Tri 98, LDL 189 (lost 5 lbs and 2 inches on waist, and got lean)

    Then a year later went very low carb (less than 30 net carbs a day) with a lot of nuts and a fat shake every morning, but TC 359, LDL 259, HDL 67, Tri: 115, LP(a) 6.0

    Got nervous, added ‘safe starches’, perhaps 10-15% of calories, cut out nuts, cut out fat shakes, continued 2-3 tablespoons of coconut oil (in coffee) a day.

    Got VAP Profile and NMR. Results slightly improved but different.

    VAP Profile
    TC 315
    HDL 67
    Tris 103
    LDL 220
    LP(a) 7.0
    LDL1-Pattern A 49.8
    LDL2-Pattern A 67.5
    LDL3-Pattern B 60.5
    LDL4-Pattern B 0.0 (good?)

    NMR Profile
    TC 292
    HDL 69
    Tris 71 (way off from VAP PROFILE)
    LDL-C 209
    Small LDL-P 711 (good or bad?)
    LP-IR Score: 10
    LDL size 21.3 nm

    Why are the results so different? Would you recommend I start a statin? If not, what can I do?

    • Evan, I can’t give medical advice or comment on this.

    • Wade H

      Evan, just curious about your history, given the results you’ve had in various trys

      “A little history,
      ” Was low fat forever, TC 221, HDL 42, Tri 105, LDL 158″

      What was the version of low fat you were on.

      As we saw in this recent study of the Mediterranean Diet, the fat as a percentage of calories was 37% for the low-fat group. The American Heart Associatons version of low-fat is about 30% of calories as fat.
      While the Ornish, Esselstyn low-fat heart healthy types, often portrayed as the sterotypical “low-fat” doctors both limit fat to 10% of calories.

      Where did your years of eating low-fat fall in to that spread of <10% to 37% seen in this study?
      And what was the low-fat level when you got those results ( TC 221, HDL 42, Tri 105, LDL 158)

  • Evan

    Sure. I understand.
    Can you comment on which is a more accurate test, VAP or NMR and why any difference?
    Thanks in advance

    • NMR is better, but VAP doesn’t actually do what NMR does, so it’s not apples-to-apples.

  • KC

    ARGH!!! That darn doctor thing!!! Evan keep us posted if you take this to another site and get some answers or recommendations. (note: fully understand why Peter can’t answer)

    I started my journey Jan 1.. Got both a VAP-NMR. Doc didn’t know what an NMR was, that was a knock down drag out. Last time I was in (thyroid) the blood draw assistant, whispered into my ear, “the Doc is now ordering those NMR things for everyone”, this made me chuckle. Any way my biggest fear is my TG/HDL ratio (right now) 5.2 gets better, but my over all numbers blow up. Since I can’t consult a MANUAL, your information may be helpful if I find myself in same situation. This probably goes for others as well.

    So don’t be put off if Peter can’t answer you, I am sure he (sort of) wants to, and we are all paying attention.


  • Jenn Lentz

    Peter –
    I have been prescribing low carb/real food (high fat) to most of my patients (family doc) and am now checking NMR lipoprofile on all patients that are borderline or that I am considering statins for. However, I don’t have a good resource for numbers to treat – do you have any info on that? Most of these people have been LDL-P >1500, with a few in the 2200 range, and I just can’t find any guidelines of where a statin should be used in people who have not had previous cardiac disease with a high LDL-P.
    Also, I follow several blogs now (dietdoctor, authority nutrition, protein power, etc) and have been searching for any and all info on constipation in the low carb diet – seems to be a common issue and just wanted to see what all the low carb gurus are doing. Any advice as to where to look? (aside from the usual psyllium flakes, miralax, etc – anything better while doing low carb that you know?)

    Jenn Lentz

  • Arthur

    Hi Peter

    Could you comment on the study linked below, which basically found that substituting high omega 6 linoleic acid for saturated fats actually increases risks of cardiovascular disease. “Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis” [http://www.bmj.com/content/346/bmj.e8707?view=long&pmid=23386268]
    In Table 1 of the study, only two oils had low Omega 6 linoleic acid: canola and olive oil. Olive oil is said to be an important constituent of the “Mediterranean Diet”.
    Could you also comment on canola oil, as there seems to be some reservations about the heathiness of this oil by readers on certain health websites.

    • In another post, at another time. Far too complicated to address with a short response, which is all I can muster these days.

  • Richard S.

    Another great post — thanks!

    What about weight change during the study? Specifically, did the control group continue to gain weight while the test groups maintained or loss weight? If so, might that not explain the important observed differences?

    Surveys like the ones in this study are notoriously inaccurate, and biomaker analyses are limited. It seems like weight change would be an important objective measurement of what and how much the subjects ate. More importantly, as you noted these subjects were mostly overweight with metabolic syndrome, and many were on statins. Almost any weight loss (or weight improvement relative to the control group) would be beneficial in reducing the tested events.

    I don’t have access to the study details. Do you? Did they consider weight change at all?


    • I think there was actually a bit of weight gain.

  • steve

    Excellent review: Unless before and after NMR is done to measure LDL-P and correlated with events, I do not place much validity in any diet study. Ornish/Esselstyn low-no fat seems to get some results as do high fat low carb diets. Note I am only speaking with regard to CAD/Heart events. Weight loss seems to be accomplishable by many different kinds of diets, and as you have written most have success as they eliminate/drastically reduce sugar and junk carbohydrates.
    While we don’t know why, I would bet that the many who still incur any event under any diet are not at LDL-P level for their risk profile. Of course, that is just my view.

  • Evan

    My ldl-p of 2320 scares the heck out are me.
    Not sure how much comfort I should derive from a 71 TG and nearly 70 hdl.

    I believe cholesterol is essential and low is bad. Would explain cognitive issues etc for those on statins.

    I also believe a low ldl in itself is not the solution. Check the Get With it Guidelines by the AHA and ASA showing half of those with events had ldl below 100 and 3/4 had ldl below 130. Yet very very few with high hdl had an event, almost regardless of ldl levels.

    Question is if cholesterol is essential but if your body can’t get it, I mean extract what it needs from the bloodstream, and then what? Reduce via statins?

    If genetically disposed to high cholesterol / faulty receptors is stains the only choice?

    However for non genetic reasons like faulty receptors due to diet or thyroid issues, what can be done?

    Can’t find a flow chart on the Web to run diet and supplement changes.

    Some of what I found was:

    Supplement with iodine, along with selenium and copper and Zinc. But all very balanced and measured amounts. I did that for 4 months. Did feel better, much less fatigue etc. Did low low carb induce adrenal fatigue?

    I added some carbs in the former of safe starches like white rice, to the tune of 60 more carbs a day, total then to about 15 percent of calories. I did notice far less muscle fatigue during Cardio and a far easier time going to the bathroom. (low carb does reduce mucin production). Even with these carbs weigh stayed low.

    Before alot of nuts (mostly almonds) and I mean alot, and didn’t notice much change in TC.

    However I am pretty convinced my high ldl is driven by high saturated fat intake. Once I added daily Attia fat shakes my numbers popped 60 points. Removing them it fell by same amount. Since going low carb I eat a ton more meat and cheese which I believe is the cause of my high ldl. But I believe this food and the subsequent lack of sugars grains and most carbs helped my hdl and TG.

    The 64,000$ question is, Is it worth it, high ldl for better everything else.

    I do realize that on the same diet I have a few of my buddies who saw no pop in ldl but saw the benefits on the other lipids. However, I have run across a subset of individuals in the same predicament as me.

    My next self experiment perhaps is the exclusions of all cheese? Hopeful that I can achieve this before I drop dead or my cardiologist scares me into a statin.

    • Russ

      Evan, I want to suggest you investigate another line of thinking… i.e. maybe higher LDL-P is not bad if inflammation is low? See Robb Wolf’s AHS12 talk beginning at 18:40 where he explicitly notes of his own discussions with our own Dr. Attia here on this subject…

      Video – https://www.youtube.com/watch?feature=player_embedded&v=ns2oS1WXDvc
      Slides – http://www.slideshare.net/ancestralhealth/ahs-2012

      I agree we don’t know from scientific studies yet, but we have at least one piece of anecdotal evidence from Dr. Rakesh Patel’s self treatment of a paradoxically *improved* arterial thickness score in the presence of an *increase* in LDL-P…


      If you don’t have it already, one thing you might consider is genetic testing (e.g. via 23andMe) and look at your APOE allele status. The behavior you describe is consistent with something that appears to be common for people with at least one APOE4 allele. What we don’t seem to have definitive evidence on is whether this is good or bad in such cases?

    • Colleen

      Check out these recent videos by Dr. Tom Dayspring (who Peter has referenced on the blog). I don’t know that it answers your question per se about LDL-P but will show you the latest thinking. (I don’t think there is a conclusive answer based upon the state of our knowledge and if there is a lack of inflammation). Depending on your age, perhaps you will need additional and/or more invasive testing. If no plaque, no worries . . .

  • Frank

    (1) How does consuming 4tbs of EVOO per day compare with the amount and type of fat in the typical American daily diet?
    (2) In general it seems that the direct consumption of olive oil while satiating the need for fat does seem to discourage taking in excessive amounts . (Your thoughts please!)

  • KC

    Hi Evan,

    Have you seen this Graph?


    I am in fear, I will see the same results as you, as I have Hypothyroid. I have talked to my Endo about taking Armour T3/T4, but he wasn’t buying it, so I am now currently flooding my system with T4 to improve my TSH.

    • Evan


      Yes. I have followed Paul quite frequently on PHD in my attempt to avoid a statin via diet modification.

      I really wish there was a ‘recipe’ for me. I am willing to stick to something proven and make sacrifices. Heck, I haven’t had pizza or pancakes or more than a nibble of bread since November 2010. I forgot what frozen yogurt, ice cream or chocolate cake tastes like. But heavily buttered veggies, steak, cheese, whole eggs seafood are more than a fantastic trade off.

      Energy levels super and high hdl gives me some comfort. My primary says he agrees with my diet but my ldl is just too high not to take a statin. I have low body fat, and bp of 120/75 and gained 5 pounds since college (25 yrs ago) mostly muscle mass.

      Perhaps Peter provides suggestions to optimize lipids in Part X of his cholesterol series…….. I’m waiting for it.

      Fact was when I went low fat my TC was much lower, and ldl much much lower, and but hdl dangerously low…. Even dropping under 40. This low hld resulted n a TC/hdl ratio just over 5x. Now I’m just under 4x due to high hdl. But is that enough to save me? TG/hdl is at 1x. But does all this make up for ldl-p of 2300 particles?

      I like it at 70ish like now, but as per Peters series ldl-p is all that matters (not my big fluffy particles), so at 2300 particles I am at a loss. 95+ percentile. Just horrible.

      And many many others have the same problem and are seeking solutions. Start googling, you will find them.

      FYI. My doc said statins are safe and any side effects can be reversed since I will be monitored. Drink the cool aid, I mean statins?

  • KC

    Evan you and I have almost exact stories. I have also been on diet since abt. 2010, however my journey on low fat is much like Peters in that if I look at a carb I gain weight. NOTE: I too have not had pizza for 3 year, or anything else bad for that matter, with exception of Thanksgiving.

    Once I discovered metabolic syndrome it all came together for me. In 2012 I discovered I was hypothyroid about mid year which is exactly the same time I discovered met. syn. The one thing that seemed to be a reoccurring theme was Paleo/LCHF/ Atkins community with thyroid issues is your exact outcome and fingers crossed hopefully not mine but probably so. So on Jan1 I scheduled a battery of tests, and got in a fight with my Doc about NMR’s. I was able to win him over (sort of) . He agreed June 30 we do second round of testing. Meantime we are trying to treat the thyroid with minimal response. I gently broached the T3 data but my GP didn’t feel comfortable with his knowledge on T3 so he sent me to Endo. The good thing is, thanks to Peter, Jimmy, Jeff, Eric, etc. I was able to talk to the Endo at a level which I think allowed him to upen up to me. But he too doesn’t want to mess with T3 he stated it acts much like speed on the body and only prescribes as last resort .

    Like you I have good BP, FEEL BETTER than I have for a long time, some things that have plagued me since my 20’s have disappeared. I am at abt. 80 to 85% fat, and haven’t deviated since Jan1. As I said before I am worried my TC is going to blow up on June 30s testing. I have more data to give to my doc after I pull him off the ceiling about T3 to try to make my case.

    At one point Peter stated he was going to do a Thyroid article. Fortunately (unfortunately for me) Peter is busy trying to save the planet. There are some great T3 articles on PubMed, and it looks to me that there needs to be more research on T3 effects on LDL /LDL-p. To me, it appears thatT3 has a massive effect on LDL. Problem may be it is too hard on the system as a whole.


    • Evan

      Although studies in vitro and in hypothyroid animals show that thyroid hormone can, under some circumstances, modulate the actions of low-density lipoprotein (LDL) receptors, the mechanisms responsible for thyroid hormone’s lipid-lowering effects are not completely understood. We tested whether LDL receptor (LDLR) expression was required for cholesterol reduction by treating control and LDLR-knockout mice with two forms of thyroid hormone T(3) and 3,5-diiodo-l-thyronine. High doses of both 3,5-diiodo-l-thyronine and T(3) dramatically reduced circulating total and very low-density lipoprotein/LDL cholesterol (?70%) and were associated with reduced plasma T(4) level. The cholesterol reduction was especially evident in the LDLR-knockout mice. Circulating levels of both apolipoprotein B (apo)B48 and apoB100 were decreased. Surprisingly, this reduction was not associated with increased protein or mRNA expression of the hepatic lipoprotein receptors LDLR-related protein 1 or scavenger receptor-B1. Liver production of apoB was markedly reduced, whereas triglyceride production was increased. Thus, thyroid hormones reduce apoB lipoproteins via a non-LDLR pathway that leads to decreased liver apoB production. This suggests that drugs that operate in a similar manner could be a new therapy for patients with genetic defects in the LDLR.

    • Bill

      For anyone interested in the use of T3 in hypothyroidism, I strongly suggest my own endo’s new book:


      He probably has more experience with combined T4/T3 therapy for hypothyroidism than anyone in the world.

      Be forewarned, however, that after many years of experimenting he has found that neither conventional nor holistic medicine has gotten this subject right, despite very strongly held dogmas on both sides. For example, he has found that while, contrary to conventional dogma, almost all hypothyroids need T3 as well as T4 replacement, the optimal T3 dose is at least an order of magnitude lower than that commonly used by “alternative” practitioners, whether in the form of pig thyroid extract (e.g., Armour thyroid), Cytomel, etc.

      He has also learned much more about how to construct optimal therapy, including seasonal dose variation, the limitations of standard thyroid blood work, and the relationship between hypothyroidism and other health problems. Highly recommended.

      I will say, though, that while I feel better than I ever have under his care, it hasn’t prevented my LDL-C from skyrocketing on low carb. I’m not convinced that’s a problem, but if lowering LDL is judged to be an important goal, not sure this is the way to do it.

    • Evan


      Perhaps Peter can correct what is wrong in what i am about to say, but from what my very limited medical knowledge surmises is that the benefits of statins may actually be driven from their inflamation lowering abilities.
      That lower inflamation and not lower LDL is what helps to avoid CHD or stroke.

      With that in mind, do you think doctors, and perhaps Peter, would say that taking an aspirin a day (or a baby aspirin) is a vary safe way to mitigate potential adverse effects of high ldl. That is, ldl by itself is not a problem as long as inflamation can be avoided.

      Then heck, high ldl, hdl etc would be desired as it good at containing infections etc……

      Have you read Paul PHD book, the Perfect Health Diet, great read (but i wish he picked a different title). At half the cost of a co-pay at my doc office, getting this book is a no brainer.

      Other good links to review (in my attempt to bring comfort to myself i am not about to drop dead at any moment):

      http://www.ncbi.nlm.nih.gov/pubmed/19074985 – Diabetics taking statins had an increase of 2% in total death rates and an increases of 31% in death from cardiovascular diseases.
      http://www.ncbi.nlm.nih.gov/pubmed/18757089 – Virtually no difference in mortality rates and cardiovascular incidents between statin-takers and placebo.
      http://jama.ama-assn.org/content/291/18/2243.abstract – No difference in overall mortality between statin-taking women and non. Heart disease mortality was actually HIGHER for women who began taking the drugs *before* they had heart disease.
      http://www.jnrbm.com/content/10/1/6/abstract – A HUGE observational study following statin use in the general population of Sweden between 1998 and 2002. Statin use tripled. Rates of heart disease were unchanged.
      http://archinte.jamanetwork.com/article.aspx?volume=170&issue=12… – Here’s a meta-analysis study which finds that the risk reduction for all cause mortality when taking statins is an almost insignificant less-than-1% for all groups. Many statins also include an anti-inflammatory, which could easily explain the entire reduction.

      and this article: http://www.drbriffa.com/2010/11/15/recent-review-on-statins-ignores-body-of-evidence-that-suggests-these-drugs-dont-work-through-cholesterol-reduction/

      and this: https://chriskresser.com/the-truth-about-statin-drugs

    • Evan

      Two questions.

      Who is the only person to win 2 (non-shared) Nobel Prizes?
      Do you think this person’s advice can be followed?

      Well, Linus Pauling believed that plaque, CHD, etc was the manifestation of stressed and “cracking” arteries which Lp(a) got stuck onto. Peter, please correct my mis-understanding I won’t be offended.

      Veins don’t have the same stresses, and I guess don’t need the same collagen to repair its membrane walls. As we all know, our lipids (esp LDL) are in the veins too (our blood is taken from there) yet plaque doesn’t form there.

      That being said, cutting to the chase, Pauling advises (well advised – before his death), that hardening of the arteries can be avoided and even “fixed” by:

      Increasing collagen via high doses of vitamin C.
      And, being the chemist that he was, and a specialist (and genius) on bonding between elements etc, that if you can “inactivate” LP(a) by binding it with lysine it won’t “adhere” to arteries.

      Dubbed the Pauling Protocol and composed of natural vitamins and amino acids, no drug company wanted to sponsor studies etc.

      So then what?

      Well, what I found is compelling. And Pauling was a winner. Perhaps that is worth its weight in gold, in and of itself?

      Better than a statin huh?

      Well, I am starting it. Wish me luck.

  • Stephen

    I finally got the results of my blood test, and the basic numbers were better than my last test. The “doctor” I mentioned in my last comment turned out to be a Physician’s Assistant, only they didn’t tell me that.
    When I complained about having a person who isn’t really a doctor giving me advice, the nurse said, ” Well, just because some people can’t afford to get State certified as a doctor, doesn’t mean that they’re not just as qualified.”
    I said, “You’ve got to be kidding!” This guy gave me tons of moronic advice!” She took off.
    Apparently, there’s only one doctor at this walk-in clinic, and they give you a PA unless you ask for the doctor.
    Business as usual in GHI NY health insurance care.
    Anyway, I’ve been on a low carb diet for about nine months, and my HDL went from 41 to 46, My LDL went from 110 to 99, my Triglycerides went from 99 to 73,
    However, there were some tests I’ve never seen before done:
    Oxidized LDL- 45
    OxLDL/HDL – 38
    CRP High Sensitivity 1.33
    All three of these were a little higher than the safe range. Should I be concerned about them?
    The new PA they gave me didn’t say a word about them…

  • AHW

    Here we go again–care to comment on THIS one?


    I eat only “uncured,” nitrate and nitrite free prodcuts like Applegate Farm. Safer? I personally do not believe at ALL that the “fat” is the factor.

    • There is a positive association between women who have had breast augmentation and suicide rate. Do you think getting a breast augmentation increases the likelihood a woman will go on to kill herself?

    • jw

      From the source paper:

      We cannot exclude residual confounding, in particular
      due to incomplete adjustment for active and passive
      smoking. The sub-group analysis for processed meat
      showed heterogeneity according to smoking, with signif-
      icant associations only in former and current smokers
      and no significant associations in never smokers, which
      is compatible with residual confounding by smoking.
      Although EPIC includes ten European countries with a
      wide range of dietary behaviors, we observed relatively
      little heterogeneity in the association between meat con-
      sumption and overall mortality.

      Also, this the paper that they rely on for their statement:
      “Both high saturated fat and cholesterol intake have been found to be related to
      the risk of coronary heart disease.”

      Mozaffarian D, Micha R, Wallace S:
      Effects on coronary heart disease of
      increasing polyunsaturated fat in place of saturated fat: a systematic
      review and meta-analysis of randomized controlled trials.
      PLoS Med2010,7:e1000252.

      Amateur’s reading of this paper’s issues – All of the studies were pre-1993, may be selection bias, does not address cholesterol at all (so where does the original paper get that claim?!), the largest study (n=9,000) is larger than all of the rest combined and is a feeding trial and shows the opposite effect (and I am sure that there are more).

      Another example of the need for NuSI?

  • AHW

    Only if she can’t find a bra that fits! ; )

    Thanks–I’ll continue to enjoy my bacon without wondering if it’s killing me. Now, the bourbon . . . !

    • I wasn’t really trying to be glib. I’m not saying that just because something has a positive associate it is categorically false. It just doesn’t contain causal information. Maybe something (e.g., a chemical) in the implant does drive women to kill themselves at a higher frequency than the general population. Without ever having looked at this problem, I do not find that hypothesis particularly compelling, but it does not guarantee it’s wrong. Similarly, it’s possible that bacon is bad for us, but this study does not prove it, even to the most modest level of evidence available by epidemiology (e.g., Hill’s criteria).
      So, I choose to still consume bacon, because I believe, on average, and in most populations, bacon consumption is merely a marker for bad eating habits. If you want to better understand this topic, I did a post on red meat once. Should have “red meat” somewhere in the title.

  • Russ

    Peter, Love your work and cite it often in conversation with others, so want to note I was a bit blunt in concurring with Bob up above. So I want to address directly to you in case I’m missing something…

    Per that comment, Table 2 indicates that the control group was instructed to eat >3 servings/day of “potatoes, bread, pasta and rice” and the study group was asked to avoid “commercial bakery goods, sweets and pastries.” Not knowing what they actually did, stands to reason that unless the study group got really about making their own bread and pastries, they were differentially reduced in consumption of grains. To make matters worse as regards confusion by lay readers, wherein bread and pasta are understood to be an acceptable part of the Mediterranean Diet, why is this not a fatal flaw? How can the study possibly make the conclusions that it does? Am I the one missing something?

    • Certainly a flaw, though I’m not sure if fatal. This, of course, underscores the challenges of free-living studies. They can’t be perfect, but experimenters should strive to equalize the bias.

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  • Melisa Zachrich

    For months I have read your blog without comment. In the past few years, I have also read dozens of low-carb books, including those by Gary and Atkins. Your example inspires me more than all of these books because it’s tangible and because I’m an endurance runner fighting the uphill battle of “we all need to carb load to perform well”. I’m also 47 and have a very strong history of heart disease and diabetes in my family. Although I don’t understand everything you are saying (you are beyond smart ;-), I do find tremendous hope in your work, passion, example and dedication. THANK YOU a thousand times over for fighting the good fight!

    Melisa Zachrich
    Findlay, Ohio

    • Thanks so much, Melisa. Very happy to hear this is helpful.

  • KC


    Thanks for all the links. Yeah I have read all of those. I too, like you have armed myself with just about all the information I can find on the subject. NOTE; I did click through all the links. I too am looking for a certain amount of confirmation bias to make sure I am not going to keel over. Anyone who thinks people can’t be programmed I urge them to try eating a “healthy” high fat diet, then walk into a supermarket.

    Thank you for the link. Had not seen that book, will be downloading that onto the old Ipud. MORE Information!

    • Evan

      Keep me posted as well.
      BTW did u see my post above (got to scroll up to our prior discussion) on March 15 on the Pauling Protocol?
      I pinged Jaminet on it as well before I start it.
      Have u done a heart/artery calcium scan? I think much comfort or overwhelming fear will result from it. I will ask my doc for one.
      Curious, did u add carbs? I did as per Paul’s recommendation,but just 15 percent in form of white rice (safe starch).
      Helped on…eh hemm…dry stools, and muscle soreness due to cardio.
      No weight gain!

    • Evan

      KC and Peter,

      Good summery here.

      Peter, as a MD what is your take on this? Voodoo science? Safe to try? Makes scientific sense but not validated via controlled studies?


    • Evan

      Oops here is link,


      Sorry bout that.

  • Wade H

    Evan, I’ve been reading your posts, and made a follow-up of your post on March 4. You may have missed it since it was so far up in the thread. Or you may not want to respond, which is OK.

    Wade H March 9, 2013

    Evan, just curious about your history, given the results you’ve had in various trys

    “A little history,
    ” Was low fat forever, TC 221, HDL 42, Tri 105, LDL 158?

    What was the version of low fat you were on at that time?

    As we saw in this recent study of the Mediterranean Diet, the fat as a percentage of calories was 37% for the low-fat group. The American Heart Associatons version of low-fat is about 30% of calories as fat.
    While the Ornish, Esselstyn low-fat heart healthy types, often portrayed as the sterotypical “low-fat” doctors both limit fat to 10% of calories.

    Where did your years of eating low-fat fall into that spread of 10% to 37% ?
    And what was the low-fat level when you got those results ( TC 221, HDL 42, Tri 105, LDL 158)

    • Evan

      Hello Wade,
      Sorry, missed your original post.
      Perhaps the best representation of my low fat diet was Ornish like, 10 -15% max.
      Breakfasts would be cheerios with skim milk or an egg white omelet with dry whole wheat toast and some lettuce or tomato. A treat would be high carb pancakes with syrup.
      Lunch, grilled chicken sandwich on multigrain bread and mustard, or perhaps turkey lettuce and tomato.
      Plenty of salads for lunch with non or low fat dressings.
      Dinner would be pasta with a can of tuna on it (and perhaps plain old tomato sauce and spices). Or, more salad and grilled chicken. Or ground turkey burgers (not the high fat turkey, but 99% lean), same for ground beef, i would buy 90% lean and then drain the fat like crazy.

      And let me tell you, i was always hungry! No matter how many calories i consumed.
      I could and would 3BIG bagels in one sitting.

      Snacks during the day were all fruits (some candy too like good and plenty but no chocolate bars etc). Plenty of apples….many in fact, bananas too, pears, oranges……

      Mayo, butter, oils, nuts, avocado, egg yolks, all avoided……cheese was a rare treat.

    • Evan

      sorry Wade, i tend to be detailed (and long winded) when it comes to diet.
      short answer, 10-15% MAX with the TC 221, HDL 42, Tri 105, LDL 158.
      I am convinced very low fat is bad for optimal HDL.
      I am also certain that saturated fat increases LDL in ~30% of people, but regardless, beneficial on TG and HDL
      But does that really matter?
      My Lp(a) of 7 gives me some comfort.

      What eating style do you follow? Results?

    • Evan

      my low carb diet was 10-15% by fat. perhaps closer to 10%
      egg white omelets, dry whole wheat toast
      cereals with skim milk
      turkey lettuce and tomato with mustard on multi-grain
      pasta with a can of tuna and tomato paste (hey its good!)
      grilled chicken on salad
      no butter
      fat free frozen yogurt
      sugary candies
      diet soda
      bagels with low fat cream cheese
      low fat this and that, etc

      my diet is completely different now
      feel great
      appetite under control
      lost a few pounds
      damn LDL !!!

      Lp(a) a 7 though…can i be proud of that??

    • Evan

      Hello KC and Wade.

      CORONARY CALCIUM SCAN RESULTS……….looking inside my arteries…..got the test!!! some suspense first.

      Reposting here as I wanted to give you both an update (and to hear how I made a cardiologist lose a bet)

      Recap, low fat diet for 20+ years (age 18-42)

      Lipids at age 27 (on low fat diet):
      TC:155, LDL 96, HDL 43 TG 82

      Fast forward to age 42 (still on low fat diet)
      TC:221, LDL 158, HDL 42 TG 105

      numbers crept up, same diet, same exercise, etc

      Doc says take statin. Research lead me to low carb.

      Age 43 (one yr on low carb)
      TC:282, LDL 189, HDL 73 TG 98

      Doc scared of LDL, prescribes statin. I tear up script.

      Age 45 1/2 (~2 more yrs on low carb with last 6 months adding more carbs, perhaps 10-15% and sticking close to PHD with supplements)
      TC:292, LDL 209, HDL 69 TG 71
      (note LDP-p 2323, with small LDL-p 711, LP(a) 7, LP-IR 10)

      Doc sends me to cardiologist as I say I don’t want a statin and I refer to my great HDL and TG numbers and ratio of nearly 1.0, LP(a) of 7, LP-IR of 10, my 7% body fat, and 120/76 BP.

      Cardiolist says, do you want to take a statin?
      I say No, (of course).

      Would you go for a coronary calcium scan?

      If calcium shows up will you take the statin?
      I just say, I’ll take the test.

      Cardiologist called today. Seemed quite upset to give me the good news. ZERO. Nada. Nothing on the scans.

      I said now what?
      Doc says, The right thing to do is take the statin due to high LDL and father who had heart attack at 50 (but smoked 30 yrs and was overweight), the later (family history) being thrown in my face.

      But I got a zero, shouldn’t I just be retested in 3 yrs or so.


      conversation over…..

      question: Did I make the right call?

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  • Dan

    I have proved to myself that it is possible to do a low-carb vegan lifestyle. Interesting serum chemistry results – the best total:HDL ratio I’ve ever achieved, best hsCRP ever, best trigs ever, and weight and BP continue to drop through the floor, nicely. It is possible to minimize cholesterol intake, saturated fat and carbohydrates. If it’s of any value, here is what I eat.

    -bowl of low carb organic low fat yogurt with 7 types of nuts and seeds (hazelnut, almond, brazil, walnut, pecan, sunflower, pumpkin seed)
    -2 avocados
    -15 lupin beans
    -1 tablespoon of macadamia nut butter
    -1 glass of water

    (I stopped drinking coffee or tea entirely.)

    Lunch (5-6 hours later):
    -Israeli salad with fine-chopped tomatoes, cucumbers, green onions, radishes, green pepper.
    drenched in tahini whipped 50:50 with lemon juice and spices.
    -2 tofu sausages on the side, dipped in honey mustard aioli dressing (low carb).
    -1 glass of water

    Dinner (6 hours later):
    -2 low carb fajitas made with seasoned tofu, sauteed broccoli, red onion, mushrooms, orange pepper, high protein greek yogurt (18 g per 175 cc), 4 drops of mexican hot sauce, toasted.
    the seasoning consists of cumin, pepper, salt, smoked paprika, chili powder, garlic powder.
    -1 glass of water

    Snack (at night)
    -nuts or olives or lupin beans or an avocado

    I’ve stopped my statin, don’t worry about salt intake, but make a concerted effort to avoid acellular carbohydrates, as you can see from the above.

  • Jenn Lentz

    Peter – thanks for responding to my inquiries, I’m really trying to figure this out so I can give my patients the best care. I wonder if you can comment on significant discrepancies between our local lab and the Liposcience NMR results – I have had a couple of patients where the results are significant, but most recently a gentleman who had his lipid panel and his lipoprofile tested within 3 days of each other, but the total cholesterol was 247 at our lab and 197 at liposcience, and his LDL was 170 at our lab and 137 at liposcience; I had one other patient who had them drawn at the same time and the LDL was 30 points different – I am feeling very insecure about one test or the other if there is this kind of discrepancy (not the only times I’ve seen it, but in most of the other patients I have had a 3 month difference and thought their labs came down significantly with LC eating). Thanks – Jenn Lentz

    • Not my area of expertise.

    • Dan

      Jenn Lutz, was he fasting in one lab and postprandial in another? More likely, you are comparing direct and calculated LDL – they will be very different, as calculated LDL is based on a number of assumptions, which for the typically American is usually incorrect. For example, a triglyceride count that is either too low or too high will throw off a Friedwald-calculated LDL quite grossly.

  • Evan

    I had both NMR and VAP Profile, same day, with different results.
    TG had delta of 30 pts
    TC had delta of 20+
    I don’t know what to make of it.

    VAP Profile
    TC 315
    HDL 67
    Tris 103
    LDL 220
    LP(a) 7.0
    LDL1-Pattern A 49.8
    LDL2-Pattern A 67.5
    LDL3-Pattern B 60.5
    LDL4-Pattern B 0.0 (good?)

    NMR Profile
    TC 292
    HDL 69
    Tris 71 (way off from VAP PROFILE)
    LDL-C 209
    Small LDL-P 711 (good or bad?)
    LP-IR Score: 10
    LDL size 21.3 nm

  • Jenn Lentz

    Dan – thanks. No, he was fasting for each. I was figuring that the NMR would be more accurate just because it is measured as opposed to calculated, and so I am going with that number. I just was very surprised by the huge discrepancy. Thanks.

  • Joseph

    I recall Lyle Mcdonald mentioning that those pre-disposed to depression would have a difficult time psychologically with a low carb diet. I believe he related this to protein precursors to serotonin and dopamine and insulin but I’m not sure. Any thoughts?

    • Would need to see data to comment, though it seems that would be more an issue with protein restriction than carbohydrate restriction.

  • Dave Nelsen

    Peter, my company partners with the Mayo Clinic for employee health. I got a “personal” reminder today as I take medication for high blood pressure. There were 10 bullet points, and some of them were sensible (lose weight, exercise, reduce alcohol consumption). The ones that stuck out to me were items 3 & 4 (shown below).

    3. Eat a healthy diet

    Eating a diet that is rich in whole grains, fruits, vegetables and low-fat dairy products and skimps on saturated fat and cholesterol can lower your blood pressure by up to 14 mm Hg. This eating plan is known as the Dietary Approaches to Stop Hypertension (DASH) diet.

    It isn’t easy to change your eating habits, but with these tips, you can adopt a healthy diet:
    Keep a food diary. Writing down what you eat, even for just a week, can shed surprising light on your true eating habits. Monitor what you eat, how much, when and why.
    Consider boosting potassium. Potassium can lessen the effects of sodium on blood pressure. The best source of potassium is food, such as fruits and vegetables, rather than supplements. Talk to your doctor about the potassium level that’s best for you.
    Be a smart shopper. Make a shopping list before heading to the supermarket to avoid picking up junk food. Read food labels when you shop and stick to your healthy-eating plan when you’re dining out, too.
    Cut yourself some slack. Although the DASH diet is a lifelong eating guide, it doesn’t mean you have to cut out all of the foods you love. It’s OK to treat yourself occasionally to foods you wouldn’t find on a DASH diet menu, such as a candy bar or mashed potatoes with gravy.

    4. Reduce sodium in your diet

    Even a small reduction in the sodium in your diet can reduce blood pressure by 2 to 8 mm Hg. The recommendations for reducing sodium are:
    Limit sodium to 2,300 milligrams (mg) a day or less.
    A lower sodium level — 1,500 mg a day or less — is appropriate for people 51 years of age or older, and individuals of any age who are African-American or who have high blood pressure, diabetes or chronic kidney disease.

    To decrease sodium in your diet, consider these tips:
    Track how much salt is in your diet. Keep a food diary to estimate how much sodium is in what you eat and drink each day.
    Read food labels. If possible, choose low-sodium alternatives of the foods and beverages you normally buy.
    Eat fewer processed foods. Potato chips, frozen dinners, bacon and processed lunch meats are high in sodium.
    Don’t add salt. Just 1 level teaspoon of salt has 2,300 mg of sodium. Use herbs or spices, rather than salt, to add more flavor to your foods.
    Ease into it. If you don’t feel like you can drastically reduce the sodium in your diet suddenly, cut back gradually. Your palate will adjust over time.

    I think I remember you’ve commented on the DASH diet trials in the past, but I really doubt that eating low fat, whole grain diet would reduce your BP by 14mmHg.

    Similarly, they flog Salt – apparently they haven’t read Gary Taubes article on the Political Science of Salt. I would the Mayo clinic would think for themselves and not just pass along the same old foolishness spouted by the Medical establishment.


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  • Jonny S

    Hi Pete,
    Thanks heaps for your really informative articles. I just have a quick question regarding your thoughts on my own diet that is fairly balanced in terms of macronutrients, but probably with a larger proportion of fats (particularly saturated fats from coconut oil, whole milk, eggs, grass-fed butter). I was wondering whether eating relatively high amounts of saturated fats with moderate-high amounts of carbs (~300g/day) is detrimental to my heart health and arteries. I am a pretty skinny distance runner (64kg, 175cm, 18 y.o) so eat quite a few starchy carbs (sweet potato, white rice, oats) around workouts, even though i’d like to experiment with ketosis when I move out of home. I occasionally eat processed meat as well that my family cooks, begrudgingly as to not receive criticism. If i’m to maintain this balanced diet that include more carbs than is necessary (I’m scared ketosis would decrease my weight too much) am I better off excluding saturated fats and rather emphasise monounsaturated fats? I feel confused as to the real dietary determinants of cardiovascular disease are.
    Thanks again,
    kind regards,

    • Jonny, I can’t really comment on your diet. If you do experiment with NK, though, be sure to do it “right” and give it enough time to allow your body to adapt. In my experience this takes anywhere from 2 weeks to 2 years, with a median of about 3 months.

  • Caitlin

    Hi Peter,

    I really appreciate your blog and your quest to help us all think more critically about nutritional information. NK has been a blessing for me and I am trying to flesh out my understanding of it by reading many of these studies. Perhaps I am even getting to the point where I am biased in picking out the studies that support HFLC, so I’ve tried to diversify my reading, hence the questions I have on this study. (Sidenote: I have also been trying to figure out if there is any good evidence to support the whole 1:1 ratio of omega 3s to omega 6s. I saw this on your upcoming posts and look forward to your thoughts as I’m not having much luck reaching a solid conclusion other than to be sure to include DHA and EPA supplements.) Anyway, I recently came across this NIH study on Alzheimer’s and a diet high in omega-3s vs omega-6s (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3029147/pdf/nihms262591.pdf) and was thinking that diets high in omega-6s are likely also high in glucose, so why did the authors single out red meat and dairy so much? Any thoughts on the validity of this conclusion? They say they created a diet profile for each participant but only discuss the Med diet in much detail and classify the other diet as high in red meat, butter, and high-fat dairy. So… both diets are high in fat, omega 3s are obviously good and protective against AD (though apparently also needs to be low in omega 6s as well) but a diet high in omega 6s (and low in omega 3s) may possibly lead to AD?


    • At some point the “scientific” community needs to stop publishing this type of absolute nonsense. This was not an experiment. There was no intervention. I have neither the time, nor emotional energy to explain how scientifically corrupt this work is, other than to point you in the direction of my previous post on the supposed harm of red meat. Please give it a read. The higher consumption of meat and fat is almost surely a proxy for what is really driving the risk of AD.

  • Caitlin

    It’s shortcomings are more obvious to me now and it frustrates me. I think that studies like this are some of the most harmful to the NK argument, not because they have validity but because they have authority. People trust their doctors (and big institutions like Harvard and NIH) not because they are ignorant but because they understand the limits of their own time, training, and knowledge. Even though diet seems like the root of so many medical problems, it’s going to be challenging to turn the tides on our national health crisis without getting these authorities (for better or worse) on board. For me personally, NK is an obvious choice rooted in sound science. But, for example, when I talked to my doctor about it, she seemed a bit skeptical but gave me the green light based on my youth, healthy weight, and high HDL (I also had low B-12 levels from following a so-called healthy, low fat diet.) I think she’s a very sharp doc and would not discard sound evidence, but I feel a bit silly trying to “teach” someone who is really supposed to be the authority on my health. I couldn’t help thinking what she might have said to another patient though. I hope that you and NuSi can fill this authoritative void. Best wishes, Caitlin

    • Thanks, Caitlin. You’re clearly a quick study on the issues we’re up against. I sometimes wish I knew none of this and lived in ignorant bliss. Kind of like the Matrix…

  • Caitlin

    The knowledge is both a blessing and a burden for sure. If only we could take all that money we spend on treating preventable metabolic diseases and use it on schools and education, what a different world this would be! Keep thinking about all the good your work brings (and can bring on the future) and also how much cooler Neo is than the ignorant dystopians… 🙂

    • That’s true. I guess we need to feel more Neo-like. I just wish I looked like Neo, at least!

  • James

    Thanks so much for your article… I’m looking at this journal article and am new to statistics, so it’s helped immensely. However, could you explain what you mean here?

    “Remember that pesky little statistical thing called power. This study was powered (at 80%) to detect a difference in the primary outcome, which it showed. In fact, the intention-to-treat was greater than 7,500 because the authors expected no more than a 20% relative risk reduction. But they saw a 30% difference, and the study was halted early.”

    • There’s a lot there, so I’m not sure of your question. You can find great examples of statistical power on line. Hopefully that helps. I’ve also defined it in previous posts.

  • nicky

    I’m not a scientist or a doctor. In fact, I’m a stay-at-home mother. Nutrition and food is something of a layperson’s obsession for me, and fresh food shopping and cooking from scratch daily take up an inordinate amount of my time. I have long had the nagging question in my mind about the effects of preservatives and additives in food. I think that, individually, the preservatives in food may not be harmful, per se. But, taken together in the quantities that most people/families consume processed food (precisely for the lack of inordinate time!), I wonder how these chemicals affect hormones and other functions in the body and their knock-on influence on obesity. The example of BPA leaps to mind. How much is too much when it comes to these chemical additives and what degrees of harm do they provoke? How does the body process this stuff? How are the liver, kidneys, brain, pancreas, and immune system affected? A can lined with BPA plastic filled with sodium- and preservative-laden green beans is not the healthy option it appears to be. Multiply this intake by the number of meals in a day, week, month, or year and we may see shocking amounts of “invisible” chemicals. By extension, pesticides and other chemicals in the food system and how they affect the body and obesity should be investigated. GMO food? Fast food could be a complete study on its own. There seems to be less and less food in food. Perhaps the food itself is not the only problem. The coincidence of our “modern” diet and the obesity trend should not be overlooked. We seem to have very little control over what is sold to us in supermarkets and in restaurants and it seems that every component of a meal at home comes from a jar, can, or box –which means lots of additives. What do you think of this? (Forgive me if you covered this topic elsewhere in your blog, I’m new to this one. Just point me in the right direction.)

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  • Dr. Attia,

    I’m interested in the recommendation in many (relatively) northern countries like Canada to take supplemental vitamin D. I wondered how humans in northern climates received vitamin D prior to supplements being available.

    Looking at foods naturally high in vitamin D it’s apparent that fatty meats and fish contain huge amounts. This makes sense as it’s a fat soluble vitamin.

    Is it fair to hypothesize that part of the widespread Hypovitaminosis D is partly due to the current fat paranoia that we seem to have? By my math, even a diet with 30-40% of calories from fat, including fish, is likely to provide plenty of vitamin D, whereas the a diet following the LEARN recommendations would not.

    • I think we’re still working on developing a better understanding of where optimal vit D levels should be and by extension how much, if at all, folks should supplement. May be an inverted U effect–in fact, almost assuredly is–the question is where the curve lies.

  • Justin Kamp

    I agree with your statement, I have read one more blog that also clearly indicate that Mediterranean diet preventing cancer.

  • Andy

    You mention “So, I choose to still consume bacon, because I believe, on average, and in most populations, bacon consumption is merely a marker for bad eating habits.”

    Surely you are not worried about the high fat there, so far we agree. I wondered if you go out of your way to find nitrite- and nitrate-free bacon.

    If not, is it because the amounts are small enough not to worry or is it because you don’t believe that nitrite and nitrate are as evil as advertised (that is, that the studies that “proved” this are weak)?

    • I’m still waiting for one nitrate study to convince me they are harmful in the quantities most people consume them.

  • Michael


    My wife Sarah is following this diet. She says she feels a lot better already, and she has been following it for only 30 days. She loves the Mediterranean diet food and she actually enjoys being on this diet.

    She decided to start following it after reading ebook “Mediterranean diet weight loss results” on Amazon.

    Here is her meal plan:
    On Mondays she eats Greek yogurt with strawberries and oats for breakfast.
    For lunch, she usually has whole grain sandwich with vegetables.
    And when it comes to dinner, she often makes tuna salad; dressed in olive oil (she loves it). It’s really delicious.
    For a dessert she is allowed to take a piece of fruit.

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  • I would like to bring your attention to the endogenous PPAR-alpha agonist- OEA (Oleoylethanolamide) which is implicated in weight loss in obese rats & other experimental animals. (PPAR-Alpha is the target receptor to treat hypercholesterolemia). RiduZone (www.riduzone.com) is the only FDA acknowledged supplement in the market which supplements OEA adequately & results in healthy weight loss.



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