Can excess protein get stored as body fat? Pt. 3

body-fat

Introduction

Today I (briefly) bring you yet another study looking at the effects of higher protein intakes on body composition. And by higher intakes, I mean consuming protein at levels >3g/kg of bodyweight (1.3g/lb for those not metrically inclined). By most nutrition recommendations this FAR surpasses the requirements of virtually all individuals, be they sedentary (0.8g/kg) or highly trained (~1.7g/kg on average).

If you haven’t yet read my previous articles on the topic, you can read them here and here.

Today’s article is a follow up study to Antonio et al.’s 2014 paper [1] that looked at the effect of high protein intakes (~4.4g/kg), in conjunction with the subject’s normal resistance training routine (RT), on changes in body composition (i.e. fat mass [FM] and fat free mass [FFM]). What they found was that there were virtually no changes in either FM or FFM when consuming a high protein diet (4.4g/kg) for up to 8 weeks, again supporting the contention that excess protein is not converted to fat and stored as such in the human body. However, what Antonio and colleagues failed to do was prescribe an appropriate RT protocol that was standardized and assigned to each participant that ensured progressive overload; in other words constantly increasing the weight lifted and volume performed over the course of the 8-week study-period.

Enter today’s study: Antonio et al. 2014; A high protein diet (3.4g/kg) combined with a heavy resistance training program improves body composition in healthy trained men and women – a follow up investigation [2].

Pros

First the pros of this most recent paper:

  1. It addresses the dearth of research on high protein diets (>3g/kg or 1.36g/lb) in conjunction with a standardized, periodized resistance training program
  1. It uses already resistance-trained subjects (males and females), which eliminates any unusual gains that are typically seen in those who have never or rarely exercised before
  1. Randomization of subjects (ensures both groups are identical [in theory] from the start)
  1. BodPod for body composition (Siri equation; appropriate for study pop.)
  1. Again, training protocol (5 days/week for 8weeks)

– Adequate volume, intensity and frequency of movements (each body part                1-2x per week)

– Periodized (progressively increased weight lifted and volume performed)

Cons

Like all research there are methodological drawbacks:

  1. Tenuous control of dietary intakes (MyFitnessPal) that brings into question actual amounts of overall protein and calories consumed
  1. 34% dropout rate (very high)
  1. Average years spent training (5 years in HP group vs. 2.5 years in NP)
  2. No control for hydration status during BodPod measurements; however, hydration status less influential for BodPod measurements than DEXA

Results

In brief:

  1. Both groups gained 1.5kg FFM (on average; some wide variations between individuals).
  1. HP lost more BF (1.6 vs. 0.3kg) despite eating more kcals overall (~400kcals) than NP and being slightly leaner at the beginning of the study

– could potentially be explained by increases in NEAT and TEF in HP

group as protein is more thermogenic

– could be due to lack of accurate dietary recall/recordings

– better compliance of HP with RT protocol than NP group

  1. Both groups gained strength with progressive overload
  1. Blood work was normal for both groups, no adverse effects (for more on the safety of high protein diets see an article I’ve written here)

Conclusions

Protein intakes well above (i.e. 2-4x) RDA (0.8g/kg), in conjunction with periodized RT program that provides systematic progressive overload, can produce significant improvements in body composition (i.e. increase FFM, decrease FM and increase strength/performance). Moreover, and to the point of this article series, extra protein does not get stored as body fat. This is just another study refuting the idea that extra protein over the supposed RDA is converted to fat. While the pathways to convert amino acids to fatty acids DO EXIST, they are virtually irrelevant even in the face of excessively high protein intakes (like the ones seen in this study), especially when combined with a well-designed RT program meant to increase strength and muscle mass. Finally, it could be argued that protein intakes as high as, or even greater than, 3g/kg will not confer any additional benefits over ~2g/kg, as this was the intake seen in the NP group that saw near identical increases in FFM and strength. Thus, high protein diets ~2g/kg or higher can be a safe and valuable part of a structured RT program meant to increase muscle size and strength.

References

  1. Antonio J, Peacock CA, Ellerbroek A, Fromhoff B, Silver T: The effects of consuming a high protein diet (4.4 g/kg/d) on body composition in resistance-trained individuals. J Int Soc Sports Nutr 2014, 11:19.
  2. Antonio J, Ellerbroek A, Silver T, Orris S, Scheiner M, Gonzalez A, Peacock C: A high protein diet (3.4g/kg/d) combined with a heavy resistance training program improves body composition in healthy trained men and women – a follow-up investigation. Journal of the International Society of Sports Nutrition 2015, 12:39.

 

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Why weight loss diets work and fail: understanding the energy balance equation

Image

Introduction

Today I want to talk about weight loss: more specifically, how someone loses weight. Given the recent congressional hearings regarding Dr. Oz and his outrageous weight loss claims – not to mention the myriad other diets and diet books out there claiming miracle-like results – I find that a lesson in the basics of weight loss is in order. And while I hate to be the bearer of bad news, it’s not the carbohydrates, or the high-fructose corn syrup, or animal products, or post-agricultural foods that are making you or anyone else overweight and/or obese. It’s simply too many calories. Similarly, it’s not the elimination of these foods, per se, that promotes weight loss. Rather, it’s a reduction in calories overall (be it through arbitrary dietary avoidances or what have you) that is the final arbiter of how many pounds you lose. End of story.

The premise for this, dare I say it, controversial claim stems from a firm understanding of the energy balance equation and how it operates. Unfortunately, numerous diet gurus have tried to persuade the public (for obvious financial reasons) that calories don’t matter and that the energy balance equation is a farce. Well, I am here to tell you that calories absolutely do matter and that any effective weight loss diet must obey the energy balance equation. Any efforts to circumvent or disregard the energy balance equation will wind up being useless and any hopes at losing those excess pounds will be lost. However, the energy balance equation, otherwise known as ‘calories in and calories out’ it a little more complex than what most believe. Leaving the psychological aspects for another day, today we will take a look at the energy balance equation to see how it operates and where most misunderstandings arise. Moreover, we will apply this knowledge towards seeing why most diets (take your pick), do in fact work (to some limited degree) yet tend to fail over the long-term.

By the end, I hope it becomes clear that whatever weight loss diet you choose to undertake (given that it suits your goals, needs and preferences), the reason that it works is not because of some arbitrary dietary avoidance(s) (or inclusions) but rather through good old caloric restriction.

So without further ado, let’s begin!

To read this article in its entirety, visit the guys at Dynamic Duo Training. Also, please subscribe to their newsletter for frequent updates on training and nutrition, as well as fantastic other guest articles from numerous other highly knowledgeable professionals in the exercise and nutrition fields.  

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Can excess protein get stored as bodyfat? Pt. 2

ScaleIntroduction & background

Today’s post will be short and sweet.

Previously I covered the topic of excess protein being converted to fatty acids and contributing to fat gain (found here, here and here; this was a rather popular one). In those articles, I concluded by saying that while the metabolic pathways to convert amino acids to fatty acids do indeed exist in humans, the fact of the matter is that the frequency and relevance of such pathways are basically nil. Simply put, protein being converted to and stored as fat doesn’t happen to any appreciable extent in people consuming moderately more protein, even during a caloric surplus. Only until theoretical extremes (both in terms of calories and protein intakes) are reached, for weeks on end (>8 weeks), will you (potentially) see any significant effect of excess protein intakes on fat gain. Yea, a lot of ‘ifs’ and ‘maybes’ in that sentence.

In support of this notion, I looked at a well-controlled study (and I mean well-controlled!) [1] which saw no further increases in fat mass in subjects consuming 140% of their caloric needs alongside higher protein diets (15% or 25%) for 8 weeks compared to individuals consuming similar caloric intakes (i.e. 140% over caloric needs) with lower percentages of calories from protein (5%). Despite being a tightly-controlled metabolic ward study wherein participant’s activity and food intakes (amongst a whole other array of factors) could be monitored, what this study failed to do was look at the effects of a hypercaloric, high-protein diet(s) on bodyweight/composition in conjunction with a structured resistance training program in highly trained individuals; which brings me to today’s study.

Antonio et al. 2014

In this investigation, Antonio et al. [2] took a group of well-trained individuals (almost a decade’s worth of weight-training under their belts; no newbie gains here!) and randomized them to either their normal diet, lower in protein (control; average intake ~1.9g/kg/d or ~150g/d) or their normal diet, higher in protein (HP; 4.4g/kg/d or ~307g/d; achieved via protein supplementation) for 8 weeks. Both groups also maintained their usual training routines/volumes which were not significantly different from each other throughout the study period.

Body composition was measured via BodPod (much better than BIA but not as accurate as DEXA) and food/protein intakes were measured via food diaries (either hard copy or by using the MyFitnessPal© app). Training was also recorded (sets, reps, weight used) throughout the study period. So what did the investigators find?

Results & conclusions

They found that, despite increasing their caloric intakes by ~800kcals/d compared to the control group which actually decreased their caloric intake over the study period, and consuming protein intakes that were 5 times higher than the current RDA (0.8g/kg) and >2 times higher than the control group’s intake (~1.8g/kg), there was no significant difference in body composition between baseline and post-intervention time points, nor were the two groups significantly different in any other respect (Table 2 below; taken from Antonio et al. [2]).

Antonio et al. Table 2In reality, the high-protein group actually increased their lean body mass while slightly decreasing their fat mass (control groups increased both), although to non-significant degrees. In line with the Bray et al. [1] study that I talked about previously (pick your link), it does not appear that high/excessive intakes of protein result in significant fat gain compared to lower, more realistic intakes (in this case, realistic for active, weight-trained individuals, i.e. ~2.0g/kg/d). I should note, however, that the Bray et al. study and the current study do differ in methodology (metabolic ward vs free-living, respectively) and study populations (middle-aged, healthy but sedentary individuals vs. highly-trained individuals, respectively). Nonetheless, the theme remains the same; excess protein under most conditions, even those where protein consumption is increased beyond the theoretical performance benefits while in the face of a mild caloric surplus, does not lead to excess body fat storage/gain. So, while we do possess the metabolic pathways to convert protein to fatty acids, again, this just doesn’t happen in real life situations.

Until next time!

References

  1. Bray GA, Smith SR, de Jonge L, Xie H, Rood J, Martin CK, Most M, Brock C, Mancuso S, Redman LM: Effect of dietary protein content on weight gain, energy expenditure, and body composition during overeating: a randomized controlled trial. JAMA 2012, 307:47-55.
  2. Antonio J, Peacock C, Ellerbroek A, Fromhoff B, Silver T: The effects of consuming a high protein diet (4.4g/kg/d) on body composition in resistance-trained individuals. JISSN 2014, 11.

 

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Protein: is it really as bad as they say it is?

red-meat-danger-300x300Introduction & background

Early last March a provocative study published by Levine et al. [1] in the prestigious Cell Metabolism has really shaken up the nutritional science world ever since one of the authors of the study suggested that eating a diet higher in protein is potentially more harmful than smoking cigarettes. Talk about rustling some jimmies!

Now, before we go any farther, let’s keep one thing in mind: this was not a randomized controlled trial wherein participants were randomly assigned to either high or low protein groups and followed for a period of time at which point various health outcomes could be tallied and assessed. No, instead this study was part epidemiological and part rodent research, each of which has their own serious limitations when extrapolating to health policy and human physiology. That being said, Levine et al. reported that in people aged 50-years and over, moderate and high protein intakes were associated with increased type 2 diabetes mortality, but not cardiovascular disease (CVD), cancer, or all-cause mortality. However, when the study population was split into persons aged 50-65 and those 66 and over, high and moderate protein intakes were associated with increased mortality from cancer and all-causes in the 50-65 age group, but not the latter. In addition, when animal protein was accounted for, the harmful associations between protein intake and mortality risks disappeared, suggesting that animal proteins, and not plant-based proteins, are potentially harmful at higher intakes during middle-age. With respect to those over 65, it appears that higher protein intake had a protective effect and was not associated with increased disease mortality risk, save type 2 diabetes. But wait, there’s more!

In subsequent analysis the investigators looked at insulin-like growth factor-1 (IGF-1) and its association with protein intake and mortality risks. In recent years insulin and IGF-1 have been suggested to contribute to the pathogenesis of cancer, due to their similar intracellular signaling pathways and downstream effects on various targets that favor cell survival rather than death [2]. Therefore, cells which should probably die are instead salvaged and are at an increased likelihood of becoming cancerous through various metabolic “reprogramming” mechanisms. This has prompted a recent interest in examining the potential therapeutic effects of low-carbohydrate and/or ketogenic diets in treating cancer due to their ability to drastically reduce serum levels of glucose and insulin [3] – two factors that are predictive of future cancer risk and cancer-related mortality [4-6]. The current study, however, chose to focus only on protein and IGF-1. So, what did the researchers find?

They found that IGF-1 levels were positively associated with protein intakes and that for every 10ng/mL increase in IGF-1 for those ages 50-65, mortality risk of cancer increased by about 9%. No association was observed in those over 65. But that’s not all!

*To read the full article, you must subscribe to Alan Aragon’s monthly Research Review. It is only $10 per month and it is chock-full of the latest research + commentary regarding nutrition, fitness, and supplementation. If you aren’t already a subscriber, I can’t speak highly enough of Alan and urge you to please subscribe!*

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The Great Cholesterol Consensus, Pt. 3

PUFAs

“Polyunsaturated fats can help reduce the cholesterol levels in your blood and lower your risk of heart disease.” – American Heart Association

Introduction

Today we will be wrapping up, at least for now, my series on cholesterol, saturated fat, and coronary heart disease (CHD). In part 2 of The Great Cholesterol Consensus we discussed some of the commonly cited observational research that is used to support the lipid hypothesis and how those studies do no such thing. We left off with me saying how we would discuss the relevant randomized controlled data looking at PUFAs and CHD, and that’s exactly what we are going to do now.

It just so has it that today’s discussion proves to be quite timely because just this morning the prestigious Annals of Internal Medicine published a new systematic review and meta-analysis of 45 observational and 27 randomized controlled trials (RCTs) looking at the association between dietary fatty acids and CHD. The article revealed that our current nutritional guidelines, which, in part, promote replacing saturated fats with PUFAs, are… well… unfounded. To those who have read my previous two articles on saturated fat, cholesterol and heart disease, these findings should come as no surprise. For the vast majority of others, I’m sure this is quite a big shock. While I do not intend on discussing the recent Annals review – as I’ve basically covered the vast majority of what it says about the observational research regarding SFAs, PUFAs and CHD – I do point it out as the findings, more or less, sum up my cholesterol, saturated fat and CHD series. Either way, I promised you all that we would dissect the relevant RCT data, and that’s what we’re going to do – not to mention that I’ve had this article typed up for some time now!

So let’s get to it!

RCTs replacing saturated fats with polyunsaturated fats

Obviously, the strongest evidence either for or against the diet-heart theory is reserved for RCTs which can better deduce cause and effect. Given that the American Heart Association recommends reducing saturated fatty acid (SFA) intake (to as little as 5% of total calories) and replacing them with more unsaturated fats, we should easily be able to see a strong effect of SFA replacement with unsaturates on CHD and overall death.

In 2010 a group of researchers wondering the exact same question conducted a systematic review and meta-analysis of all relevant RCTs that examined the effects of replacing SFAs (control) with polyunsaturated fatty acids (PUFA; diet) on CHD events and deaths [1]. There is, to my knowledge, only one RCT that evaluated the effects of monounsaturated fatty acids (MUFA) on CHD end-points – something I will come back to later on.

Of the almost 350 identified publications and abstracts, eight were ultimately selected and analyzed. Those that did not make the cut were either; review papers, observational studies, studies lasting < 1 year, studies that had multiple interventions, or studies that used only non-CHD end points (e.g. overall mortality). I have provided a tabulated representation of the eight selected trials and their results:

RCT tableBriefly looking over the table one would sensibly come to the conclusion that replacing SFAs with PUFAs does reduce ones chances of CHD events and/or death. Indeed, the meta-analysis of the authors found a reduced risk for CHD when SFAs are replaced with PUFAs. To quote from their concluding remarks;

This current meta-analysis of RCTs of clinical CHD events […] provides strong concordant evidence that consumption of PUFA, in place of SFA, lowers CHD risk… [O]ur findings demonstrate reductions in CHD events, and no evidence for increased risk, in long-term trials utilizing PUFA consumption at very high levels.”

Thus, it would seem that SFAs most likely increase one’s risk of CHD and that replacing them with PUFAs reduces one’s risk. However, when you actually analyze the papers individually, the “strong concordant evidence” quickly falls apart.

Trials on trial

Starting with the earliest, the Los Angeles Veteran’s Administration Study [2], conducted from 1959 to 1961, compared a PUFA-rich diet (38% linoleic acid) to a control diet higher in SFAs (only 10% linoleic acid) in 846 semi-institutionalized veterans. At the end of the study the researchers observed a noticeable reduction in both total serum cholesterol levels and heart disease deaths in the PUFA-rich group. Aha! Lowering cholesterol levels does prevent death from heart disease! Unfortunately, the PUFA group also saw a marked increase in cancer deaths which effectively offset any differences in overall mortality. Moreover, when one looks at the autopsy data of selected participants from both groups who succumbed to CHD during they study [10], one notices that there were virtually no differences with regards to the degree of atherosclerosis. As a matter of fact, despite having lower total serum cholesterol concentrations, those in the PUFA-rich group actually had slightly more atherosclerotic buildup, albeit to a non-significant degree.

Furthermore, with regards to randomization, one notices that the control group – simply due to chance – had significantly more heavy smokers (>1 pack/day) than the PUFA-rich group (70 vs. 45, respectively) [11] [12]. Smoking is a complete and utter juggernaut when it comes to ruining cardiovascular health. Compared to non-smokers, smokers have been shown to have endothelial dysfunction leading to thrombosis as well as a heightened susceptibility to undergo vascular spasm which can cause a heart attack [13]. It’s no wonder the control group had a higher incidence of CHD events!

Moving down the list, in our second study the Medical Research Council of London, England [3] randomized 393 male patients, between 50-60 years old and who had survived their first heart attack, to either a PUFA-rich diet supplemented with soybean oil, or to their normal diet, high in SFAs. Despite greater reductions in serum cholesterol levels (12% in the diet group compared to less than 6% in the control), the PUFAs offered little benefit towards preventing future heart disease events or death. To quote the author’s concluding remarks;

Indeed, the results of this trial alone lend little support […] to the suggestion that a diet of the kind used should be recommended in the treatment of patients who have suffered a [heart attack].”

The Oslo Diet-Heart Study [4] – the next investigation supportive of replacing PUFAs for SFAs in prevention of CHD – randomized 412 men between 30-64 years old with previous heart attack to one of two groups. The diet group, as in the last study, was PUFA-rich and low in SFA. The control group was told to consume their normal diet, high in animal products and SFAs. By the end of study the diet group had significantly lowered their blood cholesterol levels and suffered from significantly less CHD, CVD, and all-cause mortality. On the surface this seems like an obvious win for PUFAs and heart disease treatment. Unfortunately, some major methodological limitations make this claim very weak.

Firstly, dietary intake between the two groups was horribly reported (only 4% in diet group and none in control group). Secondly, the diet group was receiving multiple dietary interventions at once! A fact that could only be found out by digging through the 92-page original publication in Acta Medica Scandinavica [14]. The other often cited publication, that doesn’t include dietary information, is available in the Bulletin of NY Academic Medicine [15] and Circulation [4]. Indeed, in addition to replacing their SFAs with PUFAs, subjects were also told to increase their fruit, nut, and vegetable consumption and to completely eliminate margarines rich in trans fats. Soybean oil and omega-3-rich sardine/cod liver oils were also supplied, free of charge. In aggregate, those in the diet group were already at an advantage of increasing their antioxidant, as well as, omega-3 status – all of which could potentially have beneficial impacts on cardiovascular health. Lastly, the diet group was shown to lose weight over the course of the study, another very important confounding factor when considering cardiovascular health and disease risk. All in all, this study is hardly evidence that replacing PUFAs for SFAs is beneficial for one’s heart – saying so would be cherry-picking from a host of multiple dietary interventions and confounding factors.

Moving on to the Finnish Mental Hospital study [5, 6] we see yet another reason to conclude that PUFAs, when substituted for SFAs, reduce one’s risk of CHD. In this study, the primary dietary alteration was replacing SFAs with PUFA-rich soybean oil. The results were published in two separate papers: one for the men and one for the women. Unfortunately, the Finnish Mental Hospital study was a NON-randomized affair. It should not have even been in the meta-analysis in the first place. Rather, the study was a cluster-randomized trial, meaning that, of the two hospital locations (abbreviated N and K), one was randomly assigned to the diet group while the other was assigned to the control – i.e. there was absolutely no randomization of the actual patients whatsoever. Furthermore, they used a crossover study design (usually a methodological strength) wherein, after 6 years, the hospitals simply reversed the diets. However, in this case, there was no washout period between diets. Lastly, some patients were discharged intermittently throughout the study wherein they could eat whatever they wanted to at home and thus affecting the dietary treatment. All in all, this study is nothing more than a bad joke.

Next, the Minnesota Coronary Study (MCS) [7] was a double-blind RCT and self-described “outgrowth” of the National Diet-Heart Feasibility Study – the predecessor of a highly anticipated NHBLI-sponsored national trial using over 100,000 men. The feasibility project, however, was a rather huge disappointment when the results showed absolutely no benefit of replacing PUFAs for SFAs on heart disease in over 2,000 subjects. The subsequent NHBLI study was then abandoned due to “reasons of cost” [16]. Nevertheless, MCS randomized over 9,000 men and women free of CHD to either a diet high in PUFAs, low in SFAs or one high in SFAs and low in PUFAs. Despite greater reductions in cholesterol levels in the high PUFA group, there were no statistical differences in CHD events, death or total mortality between the groups. In actuality the treatment group had slightly more cases of CHD and overall deaths in both men and women, albeit to a non-statistically significant degree.

In the Diet and Myocardial Reinfarction Trial (DART) [8] over 2,000 men who had a recent heart attack were randomized to one of three advice-groups or a non-advice control (Group 4): Group 1 was advised to reduce fat intake and achieve a high PUFA to SFA ratio; Group 2 was a high fatty fish advice group; and Group 3 was a high cereal fiber advice group. In the end there were no significant differences in mortality between the fat intake and cereal fiber advice groups. Total mortality in the fatty fish advice group, however, was significantly reduced, attributed entirely to a decrease in ischemic heart disease deaths. With regards to the failure of the high PUFA group, the authors state that, “If serum cholesterol had decreased more in our trial, mortality might have been reduced.” Perhaps they forgot that those in fish advice group managed to reduce their mortality despite increasing their cholesterol levels by over 2% during the first two years of follow-up before falling back to initial levels. Either way, there was no overall decrease in cholesterol levels in the fish advice group yet a significant reduction in heart disease deaths.

Rounding out our RCTs, just like the Oslo Diet-Heart Study, the St. Thomas Atherosclerotic Regression Study (STARS) [9] is rife with multiple interventions in the diet group – e.g. reducing their intake of junk food, avoiding trans-fat-rich margarines, and increasing their intake of fruits and vegetables. All in all, this is just another weak example in support of replacing PUFAs for SFAs.

But what about Sydney?

Remember when the authors of the meta-analysis stated that their, “findings demonstrate reductions in CHD events, and [that there was] no evidence for increased risk, in long-term trials utilizing PUFA consumption at very high levels.Well that’s because they left out (albeit, not purposefully) one of the most telling RCTs, to-date, on the effects of PUFA consumption and CHD.

The study not mentioned in the meta-analysis is that of the Sydney Diet-Heart Study (SDHS), conducted between 1966 and 1973 [17]. This study was excluded based solely on its non-CHD end-point (i.e. overall mortality). However, had this meta-analysis been published in 2013 or later, the re-evaluation of the SDHS – which does include CHD and CVD end-points – would most certainly have made the cut [18].

The SDHS randomized 458 men aged 30-59 years with a recent coronary event to either replace their saturated fat intake with safflower oil – a PUFA devoid of any omega-3 – or to continue their normal diet rich in SFAs. This study is unique in that it provides a dietary source of PUFAs that is not confounded by the potential cardiovascular benefits of omega-3s. Only two other studies exist that utilized a similar protocol – the first of which was the Minnesota Coronary Study which resulted in slightly more deaths in the PUFA group (despite not being significant), followed by an RCT in England that used corn oil in patients with previous heart attack [19]. The latter was not analyzed in the 2010 meta-analysis based on the fact that all of the patients were also receiving “conventional treatments” for heart disease. Nonetheless, what did the researchers find in their re-evaluation of SDHS?

Despite reducing their cholesterol levels by 13% – compared to only 5% in the control group – and comparatively doubling their PUFA:SFA ratio, those receiving the cholesterol-lowering safflower oil enjoyed statistically significant increased rates of death from CVD (17% vs. 11%) and CHD (16.3% vs. 10.1%) compared to control (all-cause mortality was only borderline significant with death rates of 17% vs. 11.8% in treatment and control groups, respectively). So much for no evidence demonstrating an increased risk with regards to long-term PUFA intake and CHD.

Lastly, remember the other two studies that used omega-3-devoid oils? Well, along with the SDHS re-evaluation, the authors also conducted a meta-analysis on the three studies that used PUFAs lacking omega-3s and saw a marked increase in both CHD and CVD deaths compared to controls. The increases in deaths, however, were only approaching significance (p=0.06 and p=0.07 for CHD and CVD, respectively). Either way, replacing SFA with PUFAs lacking omega-3s seem to be nothing but detrimental to heart health.

MUFAs: under-researched and over-hyped 

Lastly, let us touch upon monounsaturated fatty acids (MUFAs) and their effects on heart health. Unfortunately, the research here is considerably lacking. In the aforementioned English study that used corn oil as their PUFA source, the researchers also had an olive oil (MUFA) arm. Olive oil is commonly touted as a “heart healthy,” cardio-protective oil based on its high MUFA content. This, however, is largely based on studies replacing SFAs with MUFAs and measuring blood cholesterol levels – or worse yet, studies involving the “Mediterranean diet” which institutes a whole host of dietary changes in addition to olive oil – rather than actual incidents of CHD events/deaths. Nevertheless, the English corn oil/olive oil study is the only RCT conducted on olive oil/MUFAs and their effects on CHD mortality. What’s more is that the results do not support all of the hype surrounding the poster-child of MUFAs.

Indeed, by the end of the study the researchers tallied 12 major cardiac events in the corn oil group, nine in the olive oil group, and only six in the SFA-rich control group. In terms of cardiac deaths, the corn oil group had five, the olive oil group had three, and the control group had but one. Therefore, despite all the wonderful claims about olive oil being “heart healthy,” the only relevant findings bear out a strikingly different conclusion. This, however, isn’t to condemn olive oil, per se, as drawing conclusions from one study would be wrong. Rather, the moral of the story is that olive oil’s “heart-healthy” claims are largely based on extrapolation from blood cholesterol measurements rather than actual data on incidents of heart disease events/deaths.

Comments and conclusions

Well, there you have it, almost five decades’ worth of diet-heart RCTs and not one single study provides a shred of convincing evidence that you or anyone else (either with or free of heart disease) should replace their SFA intake with unsaturated fats (e.g. MUFAs and omega-6-rich PUFAs). Instead, one could argue that replacing their SFA intake with unsaturates might actually increase their risk of heart disease and death. If the lipid hypothesis were as strong a hypothesis as we are made to believe, such that people should drastically alter their diets and take potentially life-threatening drugs (e.g. statins), then the evidence should be overwhelming. Sadly (for lack of a better word), it is not – a finding that is echoed in today’s Annals publication. Rather, cherry-picked and misquoted studies make up the backbone of our current nutrition and medical recommendations for the prevention of heart disease. What is even worse is that copious amounts of tax-payer money have been wasted in the process. If you truly want to do your heart a favor, a) don’t smoke; b) eat a well-balanced diet that includes plenty of fruits and vegetables and high-quality proteins like fish, chicken and yes, steak; and c) exercise regularly and maintain a healthy body weight/composition (something to talk about in subsequent articles!). Trying to replace your SFAs with PUFAs in order to prevent and/or treat heart disease has been shown to be nothing more than a complete and utter farce, not to mention a potentially life-threatening undertaking.

References

1.         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 Med 2010, 7:e1000252.

2.         Dayton S, Pearce ML, Goldman H, Harnish A, Plotkin D, Shickman M, Winfield M, Zager A, Dixon W: Controlled trial of a diet high in unsaturated fat for prevention of atherosclerotic complications. Lancet 1968, 2:1060-1062.

3.         Controlled trial of soya-bean oil in myocardial infarction. Lancet 1968, 2:693-699.

4.         Leren P: The Oslo diet-heart study. Eleven-year report. Circulation 1970, 42:935-942.

5.         Turpeinen O, Karvonen MJ, Pekkarinen M, Miettinen M, Elosuo R, Paavilainen E: Dietary prevention of coronary heart disease: the Finnish Mental Hospital Study. Int J Epidemiol 1979, 8:99-118.

6.         Miettinen M, Turpeinen O, Karvonen MJ, Pekkarinen M, Paavilainen E, Elosuo R: Dietary prevention of coronary heart disease in women: the Finnish mental hospital study. Int J Epidemiol 1983, 12:17-25.

7.         Frantz ID, Jr., Dawson EA, Ashman PL, Gatewood LC, Bartsch GE, Kuba K, Brewer ER: Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota Coronary Survey. Arteriosclerosis 1989, 9:129-135.

8.         Burr ML, Fehily AM, Gilbert JF, Rogers S, Holliday RM, Sweetnam PM, Elwood PC, Deadman NM: Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet 1989, 2:757-761.

9.         Watts GF, Lewis B, Brunt JN, Lewis ES, Coltart DJ, Smith LD, Mann JI, Swan AV: Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine, in the St Thomas’ Atherosclerosis Regression Study (STARS). Lancet 1992, 339:563-569.

10.       Dayton S, Hashimoto S, Pearce ML: Influence of a diet high in unsaturated fat upon composition of arterial tissue and atheromata in man. Circulation 1965, 32:911-924.

11.       Dayton S, Pearce ML, Hashimoto S, Dixon WJ, Tomiyasu U: A controlled clinical trial of a diet high in unsaturated fat in preventing complications of atherosclerosis. Circulation 1969, 40 (Suppl 2):1-63.

12.       Los Angeles Veterans Administration diet study. Nutr Rev 1969, 27:311-316.

13.       Nitenberg A, Antony I, Foult JM: Acetylcholine-induced coronary vasoconstriction in young, heavy smokers with normal coronary arteriographic findings. Am J Med 1993, 95:71-77.

14.       Leren P: The effect of plasma cholesterol lowering diet in male survivors of myocardial infarction. A controlled clinical trial. Acta Med Scand Suppl 1966, 466:1-92.

15.       Leren P: The effect of plasma-cholesterol-lowering diet in male survivors of myocardial infarction. A controlled clinical trial. Bull N Y Acad Med 1968, 44:1012-1020.

16.       The National Diet-Heart Study Final Report. Circulation 1968, 37:I1-428.

17.       Woodhill JM, Palmer AJ, Leelarthaepin B, McGilchrist C, Blacket RB: Low fat, low cholesterol diet in secondary prevention of coronary heart disease. Adv Exp Med Biol 1978, 109:317-330.

18.       Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM, Hibbeln JR: 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. BMJ 2013, 346:e8707.

19.       Rose GA, Thomson WB, Williams RT: Corn Oil in Treatment of Ischaemic Heart Disease. Br Med J 1965, 1:1531-1533.

Posted in Reviews | 2 Comments

The Great Cholesterol Consensus: a long overdue Pt. 2

American Heart MonthIntroduction

In lieu of “American Heart Month” and the American Heart Association’s (AHA) campaign to “Go Red” – in support of women preventing heart disease and living longer, healthier lives – I thought it would be apropos to (finally) post part two of The Great Cholesterol Consensus. For those who have not read part one, it can be found here.

Indeed, when referring to heart disease and potential modifiable risk factors – like blood cholesterol levels – a question presents itself, and it is this: what is it that we are really talking about? In the very real sense you and I (and anyone for that matter) are talking about preventing disease in order to prolong life. Therefore, if an entity, like the AHA, is to make recommendations concerning blood levels of cholesterol (which they most assuredly do), then those recommendations should be based on a clear body of evidence that shows that reducing one’s cholesterol a) reduces their risk of dying from heart disease, while b) increasing their chances of living a longer and healthier life (red clothing optional). Thus, the importance of not only heart disease mortality (i.e. death) comes into play, but that of overall mortality as well. Put simply, it makes no sense to reduce one’s risk of dying from heart disease just to arbitrarily increase their risk of dying from some other life-threatening disease instead!

Today’s follow-up will delve into such questions by taking a look at some of the commonly cited observational research that is used to support the lipid hypothesis and the notion that everyone should mindlessly work to lower their blood cholesterol levels in order to live a longer and healthier existence. This is usually done through either nutritional means, such as replacing saturated fats with unsaturated fats, and/or the administration of prescription drugs (i.e. cholesterol-lowering medication like statins). What you will soon find out, however, is that the current nutrition and health orthodoxy might actually be increasing your risk of dying at a younger age by promoting such recommendations that ignore contradictory evidence. So without further ado, let’s begin!

Falling cholesterol levels in Framingham

We’ll start with one of the longest running, and perhaps one of the most popular, diet-heart studies in the United States – the Framingham Heart Study (FHS). Conceived in 1948 FHS started out as a public health effort which sought to identify common factors/characteristics that contribute to cardiovascular disease (CVD). It was postulated that as the years pass by, participants in the study will inevitably succumb to disease and theories with regards to various factors and heart disease would be able to be tested. From this framework, FHS has had almost 2,500 publications in a multitude of prestigious scientific journals. So, just how beneficial has cholesterol-lowering been shown to be in one the most famous diet-heart studies ever conducted?

In a 1990 joint statement by the AHA and the National Heart, Lung, and Blood Institute (NHLBI), it was reported that:

The […] results from the Framingham Study indicate that a 1% reduction in an individual’s total serum cholesterol level translates into an approximate 2% reduction in CHD risk” [1]. This, however, couldn’t be farther from the truth.

The study you were told about – the results you weren’t

From 1951 to 1955, almost 2,000 men and 2,500 women between 31 to 65 years old and free of CVD had their blood levels of cholesterol measured. In a 30-year follow-up paper reporting on the rate of all new cases of both overall and CVD deaths researchers found that, in those under 50 years old, higher cholesterol was indeed associated with increased overall and CVD mortality [2]. However, only a fraction (<10%) of all CVD deaths occur in those under 50 years old [3]. Therefore any association between cholesterol and heart disease death is relevant to only a trivial proportion of cases. In those older than 50, when the vast majority (>90%) of people die of CVD, there was absolutely no association between cholesterol levels and CVD mortality.

Framingham isn’t the only study to show discordant findings between cholesterol levels and mortality in older individuals. There is a multitude of research showing either an inverse [4-7] or a ‘U-shaped’ association (i.e. highest risk at both low and high levels of cholesterol) [8-13] between cholesterol levels and risk of CVD incidence and/or death for those older than 60. Moreover, there is evidence that shows that increased cholesterol levels are associated with increased longevity in the elderly [6, 14-17]. Simply put, for older individuals, moderate to high cholesterol levels may not be such a bad thing and may even be predictive of an increased life-span! Nevertheless, this still doesn’t answer the question of whether or not lowering blood cholesterol by 1% leads to a 2% reduction in heart disease risk as suggested by the 1990 AHA/NHLBI joint statement.

For those in the Framingham cohort over 50 years old and whose cholesterol decreased over the first 14 years of the study actually saw an increase in both all-cause and CVD mortality. I’ll repeat that: those who saw their cholesterol levels drop saw a simultaneous increase in total and CVD death. Indeed, for every 1mg/dL/year drop in cholesterol during the first 14 years of the study there was a 14% and 11% increase in both CVD and all-cause mortality, respectively – not quite the 2% reduction in heart disease risk we are led to believe.

The Japanese non-argument

With almost religious fervor, supporters of the diet-heart theory bring up the Japanese as if they were proof that cholesterol and saturated fat cause heart disease. This, as it is commonly argued, is because the Japanese tend to eat much less total and saturated fat than Americans do, thus allowing them to keep their blood cholesterol levels low as well as their rates or death from heart disease. So, do lower intakes of saturated fat and lower levels of blood cholesterol offer some protective effect against heart disease and death in the Japanese?

The Ni-Hon-San Study

In 1975 Dr. Michael Marmot and colleagues showed that the Japanese, after immigrating to the United States (specifically Hawaii and California), increased their risk of coronary death similar to that of Americans. Even more interesting, however, was that there appeared to be a gradient in the occurrence of coronary heart disease (CHD) between the geographical locations – Japan (Nippon) having the lowest rates, Hawaii (Honolulu) intermediate, and California (San Francisco) with the highest. Given that the Japanese tend to eat less total and saturated fat and have lower cholesterol levels than Americans do, increased total and saturated fat consumption was offered as a potential explanation as to why Japanese emigrants increased their risk of dying from heart disease. However, at similar serum cholesterol levels, compared to the native-born Japanese, there was still a greater risk of CHD mortality among Japanese emigrants living in Hawaii and California [18] – i.e. blood levels of cholesterol could not fully explain the trends in CHD mortality.

To help better explain their earlier findings, Marmot and Syme conducted another study in 1976 and showed that the greatest factor predicting heart disease risk in the Japanese was actually cultural upbringing and not blood cholesterol levels. Indeed, Japanese emigrants who retained more of a traditional upbringing (defined as, among other characteristics; years spent in Japan/Japanese speaking school; religion while growing up; and wife’s cultural background) actually experienced prevalence of CHD similar to those in Japan. Moreover, and quite unexpectedly, those who maintained their Japanese culture the most AND ate a more Westernized (i.e. high-fat) diet actually had lower rates of CHD than those who maintained their culture while eating a traditional lower-fat, Japanese diet [19]. In the end, some of the original studies looking at the Japanese and heart disease did little to help further the lipid hypothesis.

More contradictory evidence provided by the Japanese

In the Honolulu Heart Program (HHP) study, which followed Japanese emigrants living in Hawaii over a 20-year period, researchers found that those, aged 71-93, who maintained low serum cholesterol levels actually increased their risk of death [20]. Moreover, the lowest mortality risks were seen in those who maintained intermediate levels of cholesterol and/or increased (from low to high) their cholesterol levels. Furthermore, in a separate 16-year follow-up of the HHP cohort [21], the authors observed a significant risk of cancer and all-cause mortality in those, aged 45-68 years whose cholesterol fell from intermediate (180-239mg/dL) to low (<180mg/dL) levels. These findings, again, are all in stark contrast to the perpetuated mantra that, “lower total cholesterol is better.”

Evidence from Japan itself offers similar contradictory evidence to the prevailing medical orthodoxy that lowering you cholesterol will lead to a longer and healthier life. Between 1975 and 1984, researchers began looking at the relationship between cholesterol and mortality in over 12,200 men and women between the ages of 40-69 years old from Osaka, Japan [22]. After almost 9-years follow-up they found that a 34mg/dL drop in cholesterol led to a 21% increased risk of all-cause mortality. Moreover, low cholesterol levels were also accompanied by a 26% increased risk of cancer death! Again, lower has not proved to be better, in any sense of the word.

In the Japanese Lipid Intervention Trial, which studied over 47,000 patients treated with simvastatin (commonly known as Zocor™), researchers saw that those with cholesterol levels between 200-219mg/dL had lower rates of coronary events than those above or below this range [23]. Furthermore, those with total cholesterol between 200-259 mg/dL and LDL cholesterol between 120-159mg/dL (20-59mg/dL above the NCEP recommended levels) had the lowest all-cause mortality rates. The highest death rate was actually seen in those whose total cholesterol was below 160mg/dL – a number I’m sure most doctors would salivate at the sight of.

Lastly, in the Jichi Medical School Cohort Study [24], conducted in Japan from 1992 to 1995, cholesterol levels were measured in almost 12,300 men and women between 40 to 69 years. Subjects were then followed for a period of 11.9 years and mortality data was assessed. In men, total mortality risk showed a ‘U-shaped’ association. A ‘U-shaped’ association is one where higher mortality can be seen in individuals with both high and low levels of cholesterol compared to those in the middle. Indeed, the highest mortality risk was seen in those in the lowest category of cholesterol levels (<160mg/dL) followed by those with the highest levels (>240mg/dL). Women, however, showed an inverse relationship between cholesterol levels and mortality. With regards to cancer deaths in men, cancer mortality showed an inverse association with cholesterol levels, while women showed the distinct ‘U-shaped’ association. In the end, however, the theme remains the same: lower cholesterol does not necessarily mean a longer, healthier life.

The Multiple Risk Factor Intervention Trial (MR. FIT)

Another commonly touted study in support of the diet-heart theory is the famous Multiple Risk Factor Intervention Trial (MRFIT) – well, sort of. Rather than citing the actual MRFIT Trial (which was a total bust), diet-heart theorists boast the findings of the 350,000 primary screenees who did not make the cut for the actual randomized controlled trial [25]. These men were excluded based on a number of clinical features that run the gamut; history of heart attack, diabetes requiring medication, high systolic and diastolic blood pressure, serum cholesterol over 350mg/dL, history of chest pain, 150% over desired body weight, and various drug treatments for lipids and blood glucose, just to name a few. Simply put, these men were already very unhealthy and predisposed to disease. However, instead of just ignoring these subjects, they were followed for a period of six years and the results on cholesterol and CHD mortality were published in the prestigious Journal of the American Medical Association. In this observational study, Stamler et al. saw a “continuous, graded (dose-related), and strong” relationship between cholesterol levels and CHD mortality in men aged 35 to 57. Unfortunately, what this study failed to do was also report on overall mortality.

A few years after the 1986 publication, another group of researchers took the MRFIT data and divided the study participants into 10 categories according to serum total cholesterol level and looked at both CHD mortality as well as overall mortality [26]. While CHD mortality risk did show a steady gradual increase with each successive category, overall mortality showed (if graphed) the distinct ‘U-shaped’ relationship. Indeed, those in the lowest category of total cholesterol (<140mg/dL) had higher death rates (308.6 deaths per 10,000) than all but those in the highest category (>300mg/dL with 352.8 deaths per 10,000).

Another note of importance is that if we are going to talk about the MRFIT screenees who did not undergo the clinical trial it would make sense to also talk about the almost 13,000 subjects who were included in the official study and who were randomized to either 1) anti-hypertensive medication plus encouragement of smoking cessation and dietary counseling aimed at reducing fat and cholesterol, or 2) no intervention at all (i.e. usual care) [27]. After about 7-years follow-up, despite slightly greater reductions in blood pressure and cholesterol levels in the treatment group, there was little difference in CVD or all-cause mortality between the two groups. The only noteworthy reduction in mortality was seen in those who stopped smoking, regardless of treatment.

The MONICA Project – The WHO Project?

At the time of the MRFIT Trial the 350,000+ screenees constituted of one of the largest cohorts with standardized cholesterol measurements and long-term mortality follow-up data. To this day I’m sure some people still think it is. However, to their dismay, the largest study ever conducted on the relationship between diet and cardiovascular mortality is not the MRFIT Trial but rather the MONItoring trends in CArdiovascular diseases (MONICA) Project conducted by the World Health Organization (WHO) in the 1980’s [28]. Involving 32 centers in 21 different countries, MONICA consisted of a total of ten million men and women between the ages of 35 to 64 and followed them for a period of 10 years. Quite simply, this is the mother of all diet-heart studies… that you haven’t heard of.

And why haven’t you heard of MONICA? To quote a 1999 British Medical Journal letter-to-the-editor, “MONICA did not deliver on task it set out to accomplish” [29] – e.g. assessing the impact (of which there was none) of traditional risk factors (like high blood cholesterol levels) on CVD mortality. Indeed, cholesterol explained very little (<25%) of the variance in cardiovascular and heart disease death rates. Moreover, despite mean high blood cholesterol levels and dietary animal/saturated fat intakes lower than those in Western Europe, CVD mortality was highest in the former communist countries of Central and Eastern Europe. The intake of antioxidant-rich fruits and vegetables was also lower in Central/Eastern Europe along with increased alcohol consumption and psycho-social stress undoubtedly caused by fragile economic and political climates. To quote the concluding remarks of another study that analyzed 40 of the European MONICA populations (15 communist, 25 democratic) and similarly found no association between high levels of blood cholesterol and CVD mortality [30];

In communist [i.e. Eastern/Central] Europe there was high consumption of spirits, low consumption of fruits and extremely low intake of citrus fruit. Instead of exaggerated anti-cholesterol propaganda emphasis should be given to the prevention of antioxidant deficiencies by the increase of fruit and vegetable consumption and to the decrease in salt, spirit and cigarette consumption.”

Well if that’s not the understatement of the century! In a subsequent 2004 observational study [31], 19 countries were divided into 4 distinct groups based on cultural patterns (Central/Eastern Europe; Western Europe/US; Mediterranean Countries; and Asia) and then diet and CHD mortality was assessed. It was shown that CHD mortality was highest in Central/Eastern Europe despite dietary cholesterol and saturated fat intakes on par with the other groups (except for Japan – no shocker there). Instead, the model that explained the majority (86% in men, 90% in women) of the variation in heart disease death was one which included a diet rich in fruits, vegetables, and their accompanying cardio-protective antioxidants.

Denying science, inventing paradoxes

But MONICA doesn’t stop there! Intra-country comparisons within the MONICA project are also in stark contrast to the diet-heart theory [32]. In Italy, residents from the city of Friuli decreased their mean levels of serum cholesterol by about 0.5mmol/L while those in Brianza increased their cholesterol levels to a similar degree. Despite the divergent trends, both groups saw an almost identical decline in CHD mortality over the 10-year study period!

In Switzerland, residents of the Vaud/Fribourg region saw a slight decrease in their mean serum cholesterol levels while those from Ticino saw the greatest rise in mean serum cholesterol in the entire study. CHD mortality, however, ignored the lipid hypothesis and decreased to a similar degree in both populations.

In Sweden, mean blood cholesterol levels remained stable in Northern Sweden while dropping by about 0.5mmol/L in Gothenburg. CHD death rates, however, declined to a greater extent in Northern Sweden despite the lack of decreasing mean blood cholesterol levels.

Finally, in France, the residents of Strasbourg saw the fourth largest increase in mean serum cholesterol concentrations in the entire study while those of Lille saw the greatest reduction in mean serum cholesterol levels in the entire study. According to the prevailing nutritional dogma, Strasbourg should have increased their rate of CHD death while Lille reduced theirs. While Lille did reduce their rate of CHD death over the study period (by about 1-2%), Strasbourg actually reduced their CHD mortality to a greater degree (~5%).

In the end, the largest study ever conducted on the relationship between cholesterol levels and heart disease is nothing more than a giant flop. Instead of supporting the lipid hypothesis it is rife with contradictions to the prevailing nutrition and health dogma. In the words of Galileo Galilei; “By denying scientific principles, one may maintain any paradox.” Indeed, if I were a lipid-theorist, I may be inclined to assign the title of ‘paradox’ to the above scenarios (‘French Paradox’ anyone?). However, once the contradictory evidence is put into perspective, it becomes evident that any ‘paradoxes’ that may exist are nothing more than scientists trying to ignore conflicting evidence and hold on to their preconceived notions about diet and CVD.    

Comments and conclusions on cholesterol

As you can see, upon closer examination, the very studies that are commonly cited as proof that people should lower their blood levels of cholesterol actually show that low and/or falling levels of cholesterol increase one’s risk of overall death and/or death from cancer! Moreover, even if cholesterol reduction were an effective strategy to curb the risk of heart disease it makes no sense to do so only to concomitantly increase the risk of dying from some other life-threatening disease instead! The available evidence suggests such an unfair trade-off, making cholesterol lowering a less-than-appealing undertaking.

One must also realize and keep in mind that the above studies are observational in design. They are NOT meant to establish cause and effect. Even in the studies that do show increased risk of heart disease with increased levels of cholesterol – and conversely, increased risk of cancer with low levels of cholesterol – it still does not mean that high (or low) levels of cholesterol cause disease. Causation can only be established via a randomized controlled trial (RCT) which eliminates the multitude of confounding factors that are rife within observational research. This will be our undertaking in the next installment of this series – i.e. addressing whether or not the RCT data supports or refutes that which is seen in and promoted by the observational research. However, before we do that, we must still examine where the epidemiological research stands with regards to total fat, fat type, and heart disease. Should people be adhering to a lower-fat diet? Does saturated fat lead to the clogging of arteries through the elevation of blood cholesterol levels? Let’s take a look.

Saturated fat and heart disease

Cutting right to the chase, a 2009 meta-analysis of 26 prospective studies examining the association between total fat, fat type, and heart disease showed that total fat intake was not significantly associated with CHD mortality or events [33]. Moreover, saturated fat was also not significantly associated with CHD mortality or events. What may come to surprise many of you is that polyunsaturated fatty-acids (PUFAs) – the allegedly heart-healthy fats that are recommended to reduce the risk of heart disease – were shown to be “strongly [and] significantly” associated with increased CHD mortality. This, however, was only relevant with regards to omega-6 PUFAs – e.g. those PUFAs found in sources such as sunflower, safflower, corn, cottonseed, and soybean oils. Indeed, omega-6 PUFAs were shown to also be significantly associated with increased CHD mortality while omega-3 PUFAs (like those found in fish and flaxseed) were significantly associated with decreased CHD mortality. So far it’s not looking too good for the diet-heart proponents.

Slightly more recently, in similar a 2010 meta-analysis, researchers analyzed 21 prospective studies looking at the association between saturated fat intake and CHD, CVD, and stroke risk [34]. In the end, no association was found between dietary saturated fat intake and disease risk. Therefore, the totality observational research overwhelmingly does not support the notion that saturated fat causes heart disease. However, to quote the concluding remarks of the authors of the aforementioned 2010 meta-analysis,

“[N]utritional epidemiologic studies provide only one category of evidence for evaluating the relation of saturated fat intake to risk for CHD, stroke, and CVD. An overall assessment requires [the] consideration of results [from] clinical trials as well” – which is exactly where we will pick up next time.

Until then!

References

1.         LaRosa JC, Hunninghake D, Bush D, Criqui MH, Getz GS, Gotto AM, Jr., Grundy SM, Rakita L, Robertson RM, Weisfeldt ML, et al.: The cholesterol facts. A summary of the evidence relating dietary fats, serum cholesterol, and coronary heart disease. A joint statement by the American Heart Association and the National Heart, Lung, and Blood Institute. The Task Force on Cholesterol Issues, American Heart Association. Circulation 1990, 81:1721-1733.

2.         Anderson KM, Castelli WP, Levy D: Cholesterol and mortality. 30 years of follow-up from the Framingham study. JAMA 1987, 257:2176-2180.

3.         Yazdanyar A, Newman AB: The burden of cardiovascular disease in the elderly: morbidity, mortality, and costs. Clin Geriatr Med 2009, 25:563-577, vii.

4.         Krumholz HM, Seeman TE, Merrill SS, Mendes de Leon CF, Vaccarino V, Silverman DI, Tsukahara R, Ostfeld AM, Berkman LF: Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. JAMA 1994, 272:1335-1340.

5.         Tsuji H: Low serum cholesterol level and increased ischemic stroke mortality. Arch Intern Med 2011, 171:1121-1123.

6.         Raiha I, Marniemi J, Puukka P, Toikka T, Ehnholm C, Sourander L: Effect of serum lipids, lipoproteins, and apolipoproteins on vascular and nonvascular mortality in the elderly. Arterioscler Thromb Vasc Biol 1997, 17:1224-1232.

7.         Risk of fatal coronary heart disease in familial hypercholesterolaemia. Scientific Steering Committee on behalf of the Simon Broome Register Group. BMJ 1991, 303:893-896.

8.         Petersen LK, Christensen K, Kragstrup J: Lipid-lowering treatment to the end? A review of observational studies and RCTs on cholesterol and mortality in 80+-year olds. Age Ageing 2010, 39:674-680.

9.         Shestov DB, Deev AD, Klimov AN, Davis CE, Tyroler HA: Increased risk of coronary heart disease death in men with low total and low-density lipoprotein cholesterol in the Russian Lipid Research Clinics Prevalence Follow-up Study. Circulation 1993, 88:846-853.

10.       Weijenberg MP, Feskens EJ, Bowles CH, Kromhout D: Serum total cholesterol and systolic blood pressure as risk factors for mortality from ischemic heart disease among elderly men and women. J Clin Epidemiol 1994, 47:197-205.

11.       Weijenberg MP, Feskens EJ, Kromhout D: Total and high density lipoprotein cholesterol as risk factors for coronary heart disease in elderly men during 5 years of follow-up. The Zutphen Elderly Study. Am J Epidemiol 1996, 143:151-158.

12.       Simons LA, Simons J, Friedlander Y, McCallum J: Cholesterol and other lipids predict coronary heart disease and ischaemic stroke in the elderly, but only in those below 70 years. Atherosclerosis 2001, 159:201-208.

13.       Okamura T, Tanaka H, Miyamatsu N, Hayakawa T, Kadowaki T, Kita Y, Nakamura Y, Okayama A, Ueshima H: The relationship between serum total cholesterol and all-cause or cause-specific mortality in a 17.3-year study of a Japanese cohort. Atherosclerosis 2007, 190:216-223.

14.       Brescianini S, Maggi S, Farchi G, Mariotti S, Di Carlo A, Baldereschi M, Inzitari D: Low total cholesterol and increased risk of dying: are low levels clinical warning signs in the elderly? Results from the Italian Longitudinal Study on Aging. J Am Geriatr Soc 2003, 51:991-996.

15.       Weverling-Rijnsburger AW, Blauw GJ, Lagaay AM, Knook DL, Meinders AE, Westendorp RG: Total cholesterol and risk of mortality in the oldest old. Lancet 1997, 350:1119-1123.

16.       Tuikkala P, Hartikainen S, Korhonen MJ, Lavikainen P, Kettunen R, Sulkava R, Enlund H: Serum total cholesterol levels and all-cause mortality in a home-dwelling elderly population: a six-year follow-up. Scand J Prim Health Care 2010, 28:121-127.

17.       Weiss A, Beloosesky Y, Schmilovitz-Weiss H, Grossman E, Boaz M: Serum total cholesterol: a mortality predictor in elderly hospitalized patients. Clin Nutr 2013, 32:533-537.

18.       Marmot MG, Syme SL, Kagan A, Kato H, Cohen JB, Belsky J: Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California: prevalence of coronary and hypertensive heart disease and associated risk factors. Am J Epidemiol 1975, 102:514-525.

19.       Marmot MG, Syme SL: Acculturation and coronary heart disease in Japanese-Americans. Am J Epidemiol 1976, 104:225-247.

20.       Schatz IJ, Masaki K, Yano K, Chen R, Rodriguez BL, Curb JD: Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study. Lancet 2001, 358:351-355.

21.       Iribarren C, Reed DM, Chen R, Yano K, Dwyer JH: Low serum cholesterol and mortality. Which is the cause and which is the effect? Circulation 1995, 92:2396-2403.

22.       Iso H, Naito Y, Kitamura A, Sato S, Kiyama M, Takayama Y, Iida M, Shimamoto T, Sankai T, Komachi Y: Serum total cholesterol and mortality in a Japanese population. J Clin Epidemiol 1994, 47:961-969.

23.       Nakaya N, Kita T, Mabuchi H, Matsuzaki M, Matsuzawa Y, Oikawa S, Saito Y, Sasaki J, Shimamoto K, Itakura H: Large-scale cohort study on the relationship between serum lipid concentrations and risk of cerebrovascular disease under low-dose simvastatin in Japanese patients with hypercholesterolemia: sub-analysis of the Japan Lipid Intervention Trial (J-LIT). Circ J 2005, 69:1016-1021.

24.       Nago N, Ishikawa S, Goto T, Kayaba K: Low cholesterol is associated with mortality from stroke, heart disease, and cancer: the Jichi Medical School Cohort Study. J Epidemiol 2011, 21:67-74.

25.       Stamler J, Wentworth D, Neaton JD: Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? Findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA 1986, 256:2823-2828.

26.       Iso H, Jacobs DR, Jr., Wentworth D, Neaton JD, Cohen JD: Serum cholesterol levels and six-year mortality from stroke in 350,977 men screened for the multiple risk factor intervention trial. N Engl J Med 1989, 320:904-910.

27.       Multiple risk factor intervention trial. Risk factor changes and mortality results. Multiple Risk Factor Intervention Trial Research Group. JAMA 1982, 248:1465-1477.

28.       Ecological analysis of the association between mortality and major risk factors of cardiovascular disease. The World Health Organization MONICA Project. Int J Epidemiol 1994, 23:505-516.

29.       Laurance J: MONICA did not deliver on task it set out to accomplish. BMJ 1999, 318:732.

30.       Ginter E: Cardiovascular risk factors in the former communist countries. Analysis of 40 European MONICA populations. Eur J Epidemiol 1995, 11:199-205.

31.       Connor SL, Ojeda LS, Sexton G, Weidner G, Connor WE: Diets lower in folic acid and carotenoids are associated with the coronary disease epidemic in Central and Eastern Europe. J Am Diet Assoc 2004, 104:1793-1799.

32.       MONICA Monograph and Multimedia Sourcebook. Geneva: World Health Organization; 2003.

33.       Skeaff CM, Miller J: Dietary fat and coronary heart disease: summary of evidence from prospective cohort and randomised controlled trials. Ann Nutr Metab 2009, 55:173-201.

34.       Siri-Tarino PW, Sun Q, Hu FB, Krauss RM: Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr 2010, 91:535-546.

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The Great Cholesterol Consensus, Pt. 1

consensus“Historically, the claim of consensus has been the first refuge of scoundrels; it is a way to avoid debate by claiming that the matter is already settled. Whenever you hear the consensus of scientists agrees on something or other, reach for your wallet, because you’re being had.” – Michael Crichton

Introduction

Today’s undoubtedly controversial article will be but one of many articles dismantling the myth surrounding cholesterol, saturated fat and cardiovascular health. Indeed, it’s not uncommon, even from so-called medical and health professionals, to hear something along the lines of;

“Cholesterol and saturated fat are bad because they increase blood cholesterol levels; therefore we must try to limit both in our diets such that we lower our blood cholesterol levels and prevent heart disease.”

Bad fats AHAStraight from the American Heart Association website

Indeed, the anti-saturated fat, anti-cholesterol fear-mongering propaganda campaign – or as it’s commonly known in medical and research circles as the ‘lipid hypothesis’ or ‘diet-heart theory’ – is the scientific consensus that saturated fat and cholesterol promote cardiovascular disease (CVD) through elevated levels of blood lipids. What’s worse is that this flawed dogma has dominated medical and nutritional orthodoxy for decades, affecting the lives of millions of people worldwide. Despite not having one shred of convincing evidence showing either of these nutrients as causative of CVD, major health organizations around the globe still promote diets lower in saturated fat and cholesterol to help reduce purportedly deadly levels of blood cholesterol. This has undoubtedly caused many people to take potentially harmful prescription medication and completely transform their diets into an unpalatable one that has no cardiovascular benefit whatsoever. In reality, some of the recommended changes (like consuming so-called ‘heart-healthy’ polyunsaturated fats) have actually been shown to increase ones risk of CVD, as well as, all-cause mortality and even some cancers!

Today we will be looking through a historical lens whilst unraveling the myth at hand. In doing so we will examine some of the fundamental research that pushed the idea that saturated fats and cholesterol promote CVD. In subsequent articles we will delve further into the research that both (apparently) supports the diet-heart theory, as well as, outright contradicts its. By the end of this series (however long it is), I hope you will see what complete and utter nonsense it is to fear arbitrary blood levels of cholesterol, and more importantly, some of your favorite fatty foods that have never been proven to cause CVD. In addition, I hope to shed some light on the actual causes of CVD as well as outline some recommendations that will assuredly do more for preventing CVD than our currently flawed dietary ways.

So without further ado, let us examine the foundation for which the greatest scam in the history of medicine was built upon!

From Russia with lipids [1]

Our story begins over 100 years ago in the, then, Russian Empire. Here in 1908, Alexander Ignatovski of the Russian Imperial Military Medical Academy first demonstrated that diet-induced atherosclerosis could be produced in rabbits fed full-fat milk, meat and egg yolks. The following year, Starokadomsky and Ssobolew verified Ignatovski’s results using a similar feeding protocol. While Ignatovsky and others thought that it might be animal proteins that clogged the arteries of the rabbits, it wasn’t until 1913 when NW Wesselkin and, subsequently, Anitschkow et al. demonstrated that it was indeed cholesterol, and not protein, that was the primary driver behind the aortic lesions and cardiovascular buildup in the rabbits.

It was from these among many, many other animal studies that pushed the idea that dietary fat and cholesterol cause CVD – an idea that apparently never let go. Of importance, however, is that these studies are hardly evidence of cholesterol’s artery clogging capabilities in humans. For one, rabbits are herbivorous animals and are not well-adapted to metabolize large amounts of animal protein, fat or cholesterol (and believe me, these animals were eating an insane amount of each). It’s no wonder that, when force-fed a completely alien diet comprised of animal sources, the rabbits developed atherosclerosis, cirrhotic livers, and kidney disease. Indeed, subsequent trials to induce experimental atherosclerosis were effective in other herbivorous animals – such as chickens and guinea pigs – but failed completely in carnivorous animals –like cats and dogs – that are well-adapted to consume animal protein, fat and cholesterol. It is only until the dog’s thyroids are experimentally removed and/or suppressed with drugs that scientists see any effects from diet on serum cholesterol and CVD.

It is also worth noting that cholesterol feeding in rabbits and other experimental animals has a profound effect on serum cholesterol levels and producing CVD. Unlike early animal experiments, however, more recent human feeding trials have consistently shown cholesterol elevations to be trivial with respect to dietary cholesterol intake [2]. While these early animal studies offered a potential model for human CVD, they were far from supportive of cholesterol’s causative role in human disease progression, despite what many proponents of the diet-heart theory initially believed.

The diet-heart theory

Before we continue, it would behoove me to expand on what the ‘diet-heart theory’ or ‘lipid hypothesis’ is (I’ll be using them interchangeably throughout the article). After all, it is this very hypothesis that health professionals base their (blatantly unfounded and politically biased) medical and nutritional guidance off of.

As alluded to earlier, the diet-heart hypothesis proposes that cardiovascular disease – that is, the buildup of cholesterol in the arterial walls – is due simply to high levels of cholesterol in the blood. Moreover, the relationship between cholesterol and cardiovascular disease has been (falsely) deemed linear, meaning that the higher one’s blood cholesterol levels the more sclerotic one will become. Don’t believe me?

The American Heart Association states online that;

“When too much LDL (bad) cholesterol circulates in the blood, it can slowly build up in the inner walls of the arteries [;]”

While the Centers for Disease Control and Prevention states that;

“Low-density lipoproteins (LDL) cholesterol make up the majority of the body’s cholesterol. LDL is known as “bad” cholesterol because having high levels can lead to a buildup in the arteries and result in heart disease [;]”

And lastly, the National Heart, Lung and Blood Institute states that;

“When there is too much cholesterol…in your blood, it builds up in the walls of your arteries.”

It is from this insanely simplistic and faulty reasoning that these same organizations promote the unnecessary lowering of cholesterol – usually with the mindless prescription of toxic statins as well as flawed nutritional guidance – because, if high cholesterol is bad, than lower is obviously better. Unfortunately, this outdated and politically driven claim has no roots in sound science whatsoever.

Early autopsy studies

If we are to take the lipid hypothesis at face value, one should expect to see greater plaque buildup in the arteries of people whose serum cholesterol is higher than those whose is lower. One of the first autopsy studies to examine this relationship was conducted in 1936 by pathologist Kurt Landé and biochemist Warren Sperry of the Department of Forensic Medicine at NYU [3]. Landé and Sperry meticulously analyzed the fatty buildup in the aortas of subject’s who had just violently died and compared that to the patient’s post-mortem measurements of serum cholesterol. As you can see below, they found absolutely no relationship between serum cholesterol and fatty deposition in the arteries. This flies right in the face of the lipid hypothesis!

Lande Sperry 1936For years, however, this research was discounted by early diet-heart proponents based on the claim that serum cholesterol measurements taken post-mortem weren’t reliable.

The next autopsy study wasn’t conducted until 1956 in London, Canada [4]. Here, Paterson and co. took blood samples – starting in 1953 – of 800 hospitalized war veterans periodically over the course of each patient’s lifespan. Upon death, the patient was autopsied and the degree of atherosclerosis was evaluated in the aorta and compared to ante mortem blood concentrations of cholesterol. Like Landé and Sperry, Paterson et al. found no relationship between blood levels of cholesterol and the degree of fatty deposition in the arteries of the 136 patients for which they had autopsy and blood measurements for. Again, however, these results were largely ignored by diet-heart theorists.

It wasn’t until the early 1960’s that another autopsy study, conducted by KS Mathur in Agra, India, lent some much needed credence to the aforementioned Landé and Sperry paper [5]. Here, over 500 subjects were autopsied and their blood levels of cholesterol were compared to the degree of atherosclerotic buildup. This time, however, samples were taken both before and after death in a subgroup of 20 patients to see whether or not ante and post mortem blood lipid samples remained similar. The researchers noted two important findings; 1) serum cholesterol levels remain relatively unchanged after death as long as the sample is taken within 16 hours post-mortem, and; 2) there was no relationship between serum cholesterol and atherosclerotic buildup in the 200 patients whose serum cholesterol levels were taken within 16 hours post mortem. This was important as these findings verified Landé and Sperry’s highly criticized study 30 years earlier.

If higher cholesterol truly is – as we are brainwashed to believe – indicative of worsening atherosclerosis, there should be a strikingly and convincingly obvious relationship between blood lipid levels and arterial fatty deposition. The strongest correlation, however, between serum cholesterol and atherosclerosis that any of the autopsy studies could provide was a paltry r value of 0.36 [6-10]. To put this into perspective, an r value is a statistical method used to determine the strength of the relationship between two values – like that of serum cholesterol and arterial fat deposition. A perfect association would be 1. Much to the chagrin of lipid hypothesists, a weak r value of 0.36 is, at best, nothing more than wishful thinking. The more probable possibility – and something that we will talk about more in the next installment – is that any association seen between cholesterol and atherosclerosis is secondary in nature.

Enter Ancel Keys’ Six Countries “Study”

As reality would have it, the current cholesterol theory of heart disease was founded upon highly irrelevant animal feeding experiments as well as some of the worst “research” ever conducted. And yes, I’m talking about the “research” of one, Ancel Keys from The University of Minnesota. Keys is probably one of the most well-known and often cited researchers when it comes to our current understanding of diet and cardiovascular health. And while his diet-heart “research” is complete and utter bat crap, I feel some obligation to at least mention that he made great advancements in what we known about human physiology during his famous Minnesota Starvation Study during the Second World War [11]. While his earlier career and prestige are not in dispute, I do take umbrage with the carelessness that scientists and researchers, to this day, still cite his rubbish of coronary heart disease “studies” – the first of which was his hugely biased Six Countries “Study” [12].

Quite simply, this “study” examined six hand-picked countries and their intake of fat and compared that to the number of deaths from coronary heart disease. Keys noticed a perfectly positive curvilinear association between fat intake, as a percentage of calories, and coronary deaths (shown below, EDIT: must click on graph to see it, for some reason the image doesn’t show properly within the text).

Keys Six Countries GraphWhile Keys was initially somewhat conservative in his concluding remarks, stating that, “dietary fat somehow is associated with cardiac disease mortality at least in middle age,” ZA Leitner, in a subsequent publication in Medical World, interpreted Keys’ findings slightly more emphatically [13]:

“There appears to be a strong if not convincing correlation between the amount of fat in the diet and the death rate from degenerative heart disease.”

Perhaps this gave Keys a sense of confidence over his prior remarks, because in a follow-up publication using the same data, one could read from Keys that [14];

“[T]here is a remarkable relationship between the death rate from degenerative heart disease and the proportion of fat calories in the […] diet.”

Leitner’s and Keys’ enthusiasm, however, was not unanimous. Researchers skeptical of Keys’ “study” pointed out that relevant data was available for 22 countries at the time and that Keys did nothing more than cherry-pick his data set to include the countries which supported his preconceived hypothesis of diet and heart disease. Indeed, when data from all 22 countries are incorporated into the analysis, the perfect relationship between fat and heart disease disappears [15]. Anyone who even considers themselves a student of science should be appalled at Keys’ blatant disregard for the scientific method. Indeed, at a subsequent World Health Organization convention held in Geneva, Switzerland in 1954, Keys’ “study” was met with considerable criticism leaving him completely embarrassed and humiliated. Long-time research assistant from The University of Minnesota, Henry Blackburn, recounts the occasion [16];

Ancel fell into a trap, he made a mistake; he cited a piece of evidence and they were able to destroy it. Instead of citing ‘well, this theory’s based on a body of evidence that we’ve seen here and here from the clinic, from the laboratory, and from comparing populations’, he didn’t make his case. He cited a piece–destroyed.”

It was from this public humiliation that Keys’ more widely known Seven Countries Study was born (hell, if six countries weren’t good enough surely seven will do the trick!).

The infamous Seven Countries Study

Unfortunately, Keys’ subsequent “study” in the late 1950’s was nothing more than a fancier extension of his first piece of epidemiological garbage. As before, another hand-selected set of seven countries were analyzed and, again, another positive association was seen between countries with the highest intakes of saturated fat/cholesterol and rates of coronary, as well as, all-cause mortality [17]. However, when the “study” is analyzed more closely, one starts to notice that comparisons within countries – as opposed to between countries – start to dismantle Keys’ initial claims about diet and heart disease. It is funny how science doesn’t give a damn about one’s preconceived dietary biases.

Within-country contradictions

Take for instance the reported similar intakes of saturated fat in the Finnish populations of Turku and North Kerelia. Despite comparable intakes diets, heart disease was three times higher in North Kerelia than in Turku.

In Greece, despite the residents of Crete and Corfu having near identical levels of serum cholesterol (202mg/dl and 198mg/dl, respectively), heart disease was five times higher in Crete than in Corfu.

Lastly, Crevalcore and Montegiorgio – two cities in Italy – had identical levels of serum cholesterol despite Crevalcore having almost two and half times greater heart disease mortality rates!

Nevertheless, despite these discordant findings, Keys’ went on to conclude that lower cholesterol and saturated fat intakes reduce the risk for heart disease. Perhaps he also overlooked that, while the Japanese (a population we will cover more in subsequent articles) had the lowest levels of cholesterol in the entire study it was actually the residents of Crete, Greece who, despite having considerably higher cholesterol levels, exhibited the lowest overall rates of heart disease and all-cause mortality! Only in American can biased research get you a cover spot on Time magazine and have your false conclusions become dietary dogma for the next 60+ years!

Keys TimeThe Anti-Coronary Club

Riding in the wake of the early animal feeding experiments and the poorly conducted paper-excise that was Ancel Keys’ Six Countries Study was one of the first U.S. trials to be published on diet and heart disease – The Anti-Coronary Club Program (ACC) [18]. This study took place around the same time that Keys’ was conducting his follow-up Seven Countries Study and was meant to test whether or not lowering one’s cholesterol via dietary means would be associated with a decreased incidence of heart disease. Before we continue, though, I just want to point out the humor with which diet-heart theorists conduct themselves in the scientific literature.

In a 1980 publication of The American Journal of Clinical Nutrition some of the original members of the ACC study tried to justify their reasoning for their experimental dietary intervention – albeit 14 years late and a dollar short [19]. Indeed, the original paper makes no mention of the previous research suggesting potential dietary strategies for the prevention of heart disease – quite simply because there was none! Nevertheless the authors, over a decade later, state that:

“At that time, sufficient epidemiological evidence […] implicating serum cholesterol in the development of coronary heart disease (CHD) was already available to warrant a public health approach to the prevention of CHD by means of dietary intervention.”

However, in 1957 when the ACC study was just taking flight, a review paper in Circulation, examining the literature to-date, concluded the following [20]:

“Thus, the evidence at present does not convey any specific implications for drastic dietary changes, specifically in the quantity or type of fat in the diet of the general population, on the premise that such changes will definitely lessen the incidence of coronary or cerebral artery disease.”

It’s funny how people only see what they want to see when trying to push their dietary agenda.

Still, in the ACC study, researchers assigned one group of men with no prior history of heart disease to replace their saturated fat intake from whole milk, eggs, butter and beef with polyunsaturated fats from vegetable oil, margarine, and fish (the ‘Prudent Diet’ group). The control group, on the other hand, went on consuming their normal diet, rich in eggs, whole milk, butter and beef. After four years, the Prudent Dieters successfully managed to lower their cholesterol levels from about 260mg/dl to an average of 225mg/dl while the control group shamefully maintained their cholesterol around 250-255mg/dl. Throughout the paper the authors heralded the prudent diet’s ability to drive down cholesterol levels as well as reduce non-fatal heart disease events. However, one must read the paper carefully, because amidst all the praise and commendation, ones sees clearly that eight subjects in the experimental group – that’s right, those consuming ample amounts of “heart-healthy”  PUFAs (which lower LDL and raise HDL) and hammering down their cholesterol levels by an average of 30mg/dl – died of coronary heart disease (CHD). The control group on the other hand, tallied not one death from CHD. So while the control group had a slightly higher incidence of heart disease events, the prudent diet actually caused more deaths from heart disease than control diet rich in “artery clogging” saturated fat and cholesterol. Perhaps it was the vegetable oil talking when the authors touted a huge success of the dietary intervention.

Concluding remarks

The facts presented above aren’t just a recount of a few isolated cases. No, the blatant disregard for contradictory research and the misquoting or playing down findings is rife within the diet-heart literature over the past 60+ years. To quote Professor George Mann of Vanderbilt University, the diet-heart hypothesis it is quite possibly, “[t]he greatest scam in the history of medicine.” As we continue analyzing the literature it will become more and more obvious how those who are fully invested in the lipid hypothesis only hear what they want to hear, see what they want to see, and disclose what they want to disclose.    

Next time we will talk about cholesterol and its role in the human body as well as take a look at more of the often cited epidemiological evidence and see why the very studies used to support the lipid hypothesis do no such thing and, in most cases, outright contradict it!

References

1.         Kritchevsky D: Dietary protein, cholesterol and atherosclerosis: a review of the early history. J Nutr 1995, 125:589S-593S.

2.         McNamara DJ: The impact of egg limitations on coronary heart disease risk: do the numbers add up? J Am Coll Nutr 2000, 19:540S-548S.

3.         Landé K, Sperry, W.: Arch Pathol 1936, 22:301-312.

4.         Armstrong EC, Cornish BR, Paterson JC: The serum lipids in human atherosclerosis; an interim report. Circulation 1956, 13:224-234.

5.         Mathur KS, Patney NL, Kumar V, Sharma RD: Serum cholesterol and atherosclerosis in man. Circulation 1961, 23:847-852.

6.         Feinleib M, Kannel WB, Tedeschi CG, Landau TK, Garrison RJ: The relation of antemortem characteristics to cardiovascular findings at necropsy–The Framingham Study. Atherosclerosis 1979, 34:145-157.

7.         Solberg LA, Strong JP, Holme I, Helgeland A, Hjermann I, Leren P, Mogensen SB: Stenoses in the coronary arteries. Relation to atherosclerotic lesions, coronary heart disease, and risk factors. The Oslo Study. Lab Invest 1985, 53:648-655.

8.         Mendez J, Tejada C: Relationship between serum lipids and aortic atherosclerotic lesions in sudden accidental deaths in Guatemala City. Am J Clin Nutr 1967, 20:1113-1117.

9.         Rhoads GG, Blackwelder WC, Stemmermann GN, Hayashi T, Kagan A: Coronary risk factors and autopsy findings in Japanese-American men. Lab Invest 1978, 38:304-311.

10.       Okumiya N, Tanaka K, Ueda K, Omae T: Coronary atherosclerosis and antecedent risk factors: pathologic and epidemiologic study in Hisayama, Japan. Am J Cardiol 1985, 56:62-66.

11.       Keys A, Brozek, J., Henschel, A., Mickelson, O., Taylor, H.L.: The Biology of Human Starvation I-II. Minneapolis, MN.: University of Minnesota Press; 1950.

12.       Keys A: Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp N Y 1953, 20:118-139.

13.       Leitner ZA: Diet and coronary disease. Med World 1954, 81:249-254.

14.       Keys A, Anderson, JT. : Symposium on Atherosclerosis, National Academy of Sciences, National Research Council. 1955, 338.

15.       Yerushalmy J, Hilleboe HE: Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med 1957, 57:2343-2354.

16.       Health revolutionary: The life and work of Ancel Keys. School of Public Health, University of Minnesota: University of Minnesota; 2002.

17.       Keys A: Coronary heart disease in seven countries. Circulation 1970, 41:1-211.

18.       Christakis G, Rinzler SH, Archer M, Kraus A: Effect of the Anti-Coronary Club program on coronary heart disease. Risk-factor status. JAMA 1966, 198:597-604.

19.       Singman HS, Berman SN, Cowell C, Maslansky E, Archer M: The Anti-Coronary Club: 1957 to 1972. Am J Clin Nutr 1980, 33:1183-1191.

20.       Page IH, Stare FJ, Corcoran AC, Pollack H, Wilkinson CF, Jr.: Atherosclerosis and the fat content of the diet. Circulation 1957, 16:163-178.

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