Is salt really so bad for you? - Fenster

Is salt really so bad for you?

Decades of science show NO conclusive evidence that cutting back on dietary sodium reduces cardiovascular morbidity

By Michael S. Fenster                     
                        

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(Credit: This piece originally appeared on Pacific Standard.

 

No salt, low salt, salt free, heart-healthy salt substitution–any added salt will hurt your constitution. It reads like some bizarre, Seussian tale. Excepting that we’ve heard it not from the good Dr. Geisel but from the medical community and public health advocates everywhere. We watch as celebrity chefs take the salt elimination cooking challenge to prepare an “improved healthy” cuisine. Self-anointed “experts” cadge, coax, and cajole us to decrease our salt, or, more specifically, sodium intake. If that doesn’t work then the specter of heart attacks and strokes is unleashed upon us, along with a dash of fire and brimstone for good measure. It is, after all, clearly in our best personal and the greater public interest.
The hypothesis is sound and the supporting data is impeccable, right?

The theory goes as follows: Salt acts to make us retain fluid. When we retain more fluid it increases our blood pressure (albeit temporarily). Increased blood pressure is hypertension. Hypertension is a risk factor for cardiovascular disease like heart attacks and stroke. Heart attacks and strokes are bad. Therefore, hypertension is bad. Thus, sodium must be bad; A causes B which causes C, therefore A causes C. Get rid of A and you get rid of C—simple basic arithmetic, no? Reduce sodium intake and you will reduce blood pressure and thus reduce the incidence of stroke and heart attack. Reducing sodium intake is good—simple, effective, and undeniably the prevailing conventional wisdom these days.

Except… one thing is missing.

The conclusive data—or any data-that definitively shows that cutting back on dietary sodium reduces mortality or significantly reduces cardiovascular morbidity. For over half a century, starting in the 1960s, there has been a vehement and salty exchange just out of public earshot involving respected scientists on both sides of this line. But with the advent of an aggressive public policy to reduce dietary sodium intake for presumed public health benefit and studies emerging suggesting negative consequences of a low-sodium diet, the clamor of dissension is heating up.
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JAMA on salt HERE.
Read the complete article here.

Here is an article from The Kennebec Journal on the division regarding the salt controversy. Here are a couple of quotes:

"Four months after an Institute of Medicine report said reducing salt to the lowest recommended level doesn't improve health and may harm it, the U.S. Centers for Disease Control and Prevention said they disagree. In an article published Monday in the American Journal of Hypertension, the CDC and New York City health officials said getting Americans to eat less salt remains a key objective with the potential to save thousands of lives."

and

"Lowering sodium to the extent required to lower blood pressure has a variety of other effects," including some that boost heart attacks, strokes and death, he said. "It's just not that simple. The message from the evidence is we don't know."

Here is another article from Food Politics by Marion Nestle.
Another article on salt here.

More data in the Salt Wars - Aug 14, 2014; http://www.medpagetoday.com/Cardiology/Hypertension/47203

An article by Marion Nestle - http://www.foodpolitics.com/2014/08/its-salt-arguments-again-new-research-arguments-over-public-health-recommendations-and-issues-of-conflicts-of-interest/
 

Liver saving saturated fats

Liver saving saturated fats

August 2, 2012 by principleintopractice

As my last post started to explore, different types of dietary fats have different effects on the progression of alcoholic liver disease. This post will further explore the protective effects of saturated fats in the liver.

For many, the phrase “heart healthy whole grains” rolls off the tongue just as easily as “artery clogging saturated fats”. Yet where is the evidence for these claims? In the past few decades saturated fats have been demonized, without significant evidence to suggest that natural saturated fats cause disease (outside of a few well touted epidemiological studies). Indeed, most of the hypothesis-driven science behind the demonization of saturated fats is flawed by the conflation of saturated fats with artificial trans fats (a la partially hydrogenated soybean oil).

In the face of a lack of any significant scientific evidence that clearly shows that unadulterated-saturated fats play a significant role in heart disease (and without a reasonable mechanism suggesting why they might), I think the fear-mongering “artery clogging” accusations against saturated fats should be dropped. On the contrary, there is significant evidence that saturated fats are actually a health promoting dietary agent- all be it in another (though incredibly important) organ.

Again (from my last post), here is a quick primer on lipids (skip it if you’re already a pro). For the purpose of this post, there are two important ways to classify fatty acids. The first is length. Here I will discuss both medium chain fatty acids (MCFA), which are 6-12 carbons long, and long chain fatty acids (LCFA), which are greater than 12 carbons in length (usually 14-22; most have 18). Secondly, fatty acids can have varying amounts of saturation (how many hydrogens are bound to the carbons). A fatty acid that has the maximal number of hydrogens is a saturated fatty acid (SAFA), while one lacking two of this full complement, has a single double bond and is called monounsaturated (MUFA) while one lacking more (four, six, eight etc.) has more double bonds (two, three, four, etc.) and is called a polyunsaturated fatty acid (PUFA).

Next time you eat a good fatty (preferably grass-fed) steak, or relish something cooked in coconut or palm oil, I hope you will feel good about the benefits you are giving your liver, rather than some ill-placed guilt about what others say you are doing to your arteries. From now on, I hope you think of saturated fats as “liver saving (and also intestine preserving) lipids”. Here’s why:
In 1985, a multi-national study showed that increased SAFA consumption was inversely correlated with the development of liver cirrhosis, while PUFA consumption was positively correlated with cirrhosis [1]. You might think it is a bit rich that I blasted the epidemiological SAFA-heart disease connection and then embrace the SAFA-liver love connection, but the proof is in the pudding- or in this case the experiments that first recreated this phenomena in the lab, and then offered evidence for a mechanism (or in this case many mechanisms) for the benefits of SAFA.

The first significant piece of support for SAFA consumption came in 1989, when it was shown in a rat model that animals that were fed an alcohol-containing diet with 25% of the calories from tallow (beef fat, which by their analysis is 78.9% SAFA, 20% MUFA, and 1% PUFA) developed none of the features of alcoholic liver disease, while those fed an alcohol-containing diet with 25% of the calories from corn oil (which by their analysis is 19.6% SAFA, 23.6% MUFA, and 56.9% PUFA) developed severe fatty liver disease [2].

More recent studies have somewhat complicated the picture by feeding a saturated fatty-acid diet that combines beef tallow with MCT (medium chain triglycerides- the triglyceride version of MCFAs). This creates a diet that is more highly saturated than a diet reliant on pure-tallow, but it complicates the picture as MCFA are significantly different from LCFA in how they are absorbed and metabolized. MCFA also lead to different cellular responses (such as altered gene transcription and protein translation). Nonetheless, these diets are useful for those further exploring the role of dietary SAFA in health and disease.

These more recent studies continue to show the protective effects of SAFA, as well as offer evidence for the mechanisms by which SAFA are protective.

Before we explore the mechanisms, here is a bit more evidence that SAFAs are ‘liver saving’.
A 2004 paper by Ronis et al confirmed that increased SAFA content in the diet decreased the pathology of fatty liver disease in rats, including decreased steatosis (fat accumulation), decreased inflammation, and decreased necrosis. Increasing dietary SAFA also protected against increased serum ALT (alanine transaminase), an enzymatic marker of liver damage that is seen with alcohol consumption [3]. These findings were confirmed in a 2012 paper studying alcohol-fed mice. Furthermore, these researchers showed that SAFA consumption protected against an alcohol-induced increase in liver triglycerides [4]. Impressively, dietary SAFA (this time as MCT or palm-oil) can even reverse inflammatory and fibrotic changes in rat livers in the face of continued alcohol consumption [5].

But how does this all happen?
Before I can explain how SAFA protect against alcoholic liver disease, it is important to understand the pathogenesis of ALD. Alas, as I briefly discussed in my last post, there are a number of mechanisms by which disease occurs, and the relative importance of each mechanism varies based on factors such as the style of consumption (binge or chronic) and confounding dietary and environmental factors (and in animals models, the mechanism of dosing). SAFA is protective against a number of mechanisms of disease progression- I’ll expound on those that are currently known.
In my opinion, the most interesting (and perhaps most important) aspect of this story starts outside the liver, in the intestines.

In a perfect (healthy) world, the cells of the intestine are held together by a number of proteins that together make sure that what’s inside the intestines stays in the lumen of the intestine, with nutrients and minerals making their way into the blood by passing through the cells instead of around them. Unfortunately, this is not a perfect world, and many factors have been shown to cause a dysfunction of the proteins gluing the cells together, leading to the infamous “leaky gut”. (I feel it is only fair to admit that when I first heard about “leaky gut” my response was “hah- yeah right”. Needless to say, mountains of peer-reviewed evidence have made me believe this is a very real phenomenon).
Intestinal permeability can be assessed in a number of ways. One way is to administer a pair of molecular probes (there are a number of types, but usually a monosaccharide and a disaccharide), one which is normally absorbed across the intestinal lining and one that is not. In a healthy gut, you would only see the urinary excretion of the absorbable probe, while in a leaky gut you would see both [6]. Alternatively, you can look in the blood for compounds such as lipopolysaccharide (LPS-a product of the bacteria that live in the intestine) in the blood. (Personally, I would love to see some test for intestinal permeation become a diagnostic test available to clinicians.)

Increased levels of LPS have been found in patients with different stages of alcoholic disease, and are also seen in animal models of alcoholic liver disease. Increased levels of this compound have been associated with an increased inflammatory reaction that leads to disease progression. Experimental models that combine alcohol consumption and PUFA show a marked increase in plasma LPS, while diets high in SAFA do not.

But why? (Warning- things get increasingly “sciencey” at this point. For those less interested in the nitty-gritty, please skip forward to my conclusions)

Cells from the small intestine of mice maintained on a diet high in SAFA, in comparison to those maintained on a diet high in PUFA, have significantly higher levels of mRNA coding for a number of the proteins that are important for intestinal integrity such as Tight Junction Protein ZO-1, Intestine Claudin 1, and Intestine Occludin. Furthermore, alcohol consumption further decreases the mRNA levels of most of these genes in animals fed a high-PUFA containing diet, while alcohol has no effect on levels in SAFA-fed animals. Changes in mRNA level do not necessarily mean changes in protein levels, however the same study showed an increase in intestinal permeability in mice fed PUFA and ethanol in comparison to control when measured by an ex-vivo fluorescent assay. This shows that PUFA alone can disturb the expression of proteins that maintain gut integrity, and that alcohol further diminishes integrity. In combination with a SAFA diet, however, alcohol does not affect intestinal permeability [4].

Improved gut integrity is no doubt a key aspect of the protective effects of SAFA. Increased gut integrity leads to decreased inflammatory compounds in the blood, which in turn means there will be decreased inflammatory interactions in the liver. Indeed, in comparison to animals fed alcohol and PUFA, animals fed alcohol with a SAFA diet had significantly lower levels of the inflammatory cytokine TNF-a and the marker of macrophage infiltration MCP-1 [4]. Decreased inflammation, both systemically and in the liver, is undoubtedly a key element of the protective effects of dietary SAFA.
This post is already becoming dangerously long, so without going into too much detail, it is worth mentioning that there are other mechanisms by which SAFA appear to protect against alcoholic liver disease. Increased SAFA appear to increase liver membrane resistance to oxidative stress, and also reduces fatty acid synthesis while increasing fatty acid oxidation [3]. Also, a diet high in SAFA is associated with reduced lipid peroxidation, which in turn decreases a number of elements of inflammatory cascades [5]. Finally- and this is something I will expand on in a future post- MCFAs (which are also SAFA) have a number of unique protective elements.

I realize that this post has gotten rather lengthy and has brought up a number of complex mechanisms likely well beyond the level of interest of most of my readers…

If all else fails- please consider this:
The “evidence” that saturated fats are detrimental to cardiac health is largely based on epidemiological and experimental studies that combined saturated fats with truly-problematic artificial trans-fats. Despite the permeation of the phrase “artery clogging saturated fats”, I have yet to see the evidence nor be convinced of a proposed mechanism by which saturated fats could lead to decreased coronary health.

ON THE CONTRARY…
There is significant evidence, founded in epidemiological observations, confirmed in the lab, and explored in great detail that shows that saturated fats are protective for the liver. While I have focused here on the protective effects when SAFA are combined with alcohol, they offer protection to the liver under other circumstances, such as when combined with the particularly liver-toxic pain-killer Acetaminophen [7].

Next time you eat a steak, chow down on coconut oil, or perhaps most importantly turn up your nose at all things associated with “vegetable oils” (cottonseed? soybean? Those are “vegetables”?), know that your liver appreciates your efforts!

1. Nanji, A.A. and S.W. French, Dietary factors and alcoholic cirrhosis. Alcohol Clin Exp Res, 1986. 10(3): p. 271-3.
2. Nanji, A.A., C.L. Mendenhall, and S.W. French, Beef fat prevents alcoholic liver disease in the rat. Alcohol Clin Exp Res, 1989. 13(1): p. 15-9.
3. Ronis, M.J., S. Korourian, M. Zipperman, R. Hakkak, and T.M. Badger, Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition. J Nutr, 2004. 134(4): p. 904-12.
4. Kirpich, I.A., W. Feng, Y. Wang, Y. Liu, D.F. Barker, S.S. Barve, and C.J. McClain, The type of dietary fat modulates intestinal tight junction integrity, gut permeability, and hepatic toll-like receptor expression in a mouse model of alcoholic liver disease. Alcohol Clin Exp Res, 2012. 36(5): p. 835-46.
5. Nanji, A.A., K. Jokelainen, G.L. Tipoe, A. Rahemtulla, and A.J. Dannenberg, Dietary saturated fatty acids reverse inflammatory and fibrotic changes in rat liver despite continued ethanol administration. J Pharmacol Exp Ther, 2001. 299(2): p. 638-44.
6. DeMeo, M.T., E.A. Mutlu, A. Keshavarzian, and M.C. Tobin, Intestinal permeation and gastrointestinal disease. J Clin Gastroenterol, 2002. 34(4): p. 385-96.
7. Hwang, J., Y.H. Chang, J.H. Park, S.Y. Kim, H. Chung, E. Shim, and H.J. Hwang, Dietary saturated and monounsaturated fats protect against acute acetaminophen hepatotoxicity by altering fatty acid composition of liver microsomal membrane in rats. Lipids Health Dis, 2011. 10: p. 184.
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Read the complete article here.

Magnesium

Reduce High Cholesterol with Nutritional Magnesium   

Written By:  William Davis, MD       

February is Heart Health Month and heart health expert and cardiologist Dr. William Davis, M.D., talks about the importance of lowering high cholesterol naturally and reducing your chances of coronary heart disease with the use of magnesium and other nutritional strategies.

Tired of the media onslaught promoting statin drugs? What happened to the conversation about nutritional strategies that reduce cholesterol? Since February is Heart Health Month, now is a great time to highlight the importance of magnesium for the reduction of high cholesterol.

There are a number of ways to significantly reduce cholesterol using diet and nutritional supplements. Reductions in bad cholesterol, or LDL cholesterol, of 25, 30, 50, even 100 mg/dl are possible—if you have the right information.

At the top of the list of natural strategies to reduce LDL and supplement and/or sometimes replace your need for prescription medication (in consultation with your doctor) is magnesium.
Magnesium can act like a natural statin drug and lower bad cholesterol (LDL), reduce triglycerides and increase good cholesterol (HDL) (1).

In order for the body to make cholesterol, it requires a specific enzyme called HMG-CoA reductase. Magnesium regulates this enzyme so as to maintain only a proper amount of cholesterol in the body. When the body is magnesium deficient, cholesterol continues to be produced in excess, which can cause a cholesterol buildup and may lead to coronary heart disease.

The HMG-CoA reductase enzyme is the exact same enzyme that is targeted and inhibited by statin drugs. The inhibiting process is similar to magnesium's function, except that magnesium is the natural way that the body has evolved to use to control and limit cholesterol when it reaches a certain level; statin drugs are used to destroy the entire mechanism.

The term metabolic syndrome describes a set of conditions that many believe may be another name for the consequences of long-term magnesium deficiency. The list includes high cholesterol, hypertension and elevated triglycerides that lead to and promote coronary heart disease, stroke and type-2 diabetes. In a 2006 study (2) published in the American Heart Association's journal Circulation, entitled: Magnesium Intake and Incidence of Metabolic Syndrome Among Young Adults researchers concluded: “Our findings suggest that young adults with higher magnesium intake have lower risk of development of metabolic syndrome.”

In an age when statins dominate conventional heart disease prevention, an important role remains for nutritional approaches. Because statin drugs are principally LDL-reducing agents and do not address other causes of heart disease, nutritional strategies add a real advantage. Nutritional approaches can be used to minimize and sometimes eliminate the use of statin drugs altogether. Perhaps it would be better to regard statin therapy as a solution only when natural, nutritional means have been exhausted.

The adherence to a healthy diet is not enough in the majority of cases. The American Heart Association’s diet, for instance, yields a 7% drop in cholesterol. That’s too small to make any real difference (3) and, by itself, virtually guarantees a future of heart disease. The formerly popular ultra low-fat diets (≤10% of calories from fat) yield variable drops in cholesterol, but HDL or the good cholesterol is also substantially reduced and harmful triglycerides increased (4). The net effect can be increased risk of heart disease and diabetes.

The restriction of processed carbohydrates is an effective way to lose weight and thereby reduce cholesterol, particularly for people starting with lower HDL and higher triglycerides. Reducing intake of flour products (pasta, breads, bagels, pastries, cookies, cakes, pretzels, and other processed foods) may, in fact, yield larger drops in cholesterol than now outdated low-fat diets (5).
While dietary restriction of total fat intake has only limited power to reduce cholesterol, avoidance of saturated fat (e.g., in butter, greasy meats, cured meats, fried foods) and hydrogenated fat (“trans fats” in margarine, shortening, and many processed foods) remains a well-proven means of reducing LDL cholesterol modestly. Replacing saturated fat sources with healthy monounsaturated oils (olive, canola, flaxseed) provides even greater benefits for cholesterol reduction, as well as reduced triglycerides and VLDL (6, CM Williams, et al., 1999).

Weight loss (if you’re overweight) has broad effects on risk reduction: reduction of cholesterol levels (total and LDL), increased HDL, reduced triglycerides, and correction of small LDL, VLDL, and abnormal postprandial (after-eating) fat clearance (7).

Magnesium can help. Magnesium helps the body digest, absorb, and utilize proteins, fats, and carbohydrates and helps prevent obesity genes from expressing themselves.

As a practical solution, supplementation at a level of 2.3 milligrams of magnesium per pound of body weight per day (this comes to about 345 milligrams per day for a 150 lb individual) can really help. When supplementing with magnesium, start on a gradient of a low dose and gradually build up. If you get diarrhea you can lower the dose back down until you are at a comfortable level. While magnesium supplementation is generally quite safe, people on certain antibiotics should not take magnesium. If you have kidney disease (renal failure) or any kidney disorders, you should not take any magnesium supplements without consulting a physician.

In all practicality, because of magnesium’s crucial role in health, its widespread deficiency in Americans, and the growing depletion of magnesium in water and foods, supplemental magnesium is necessary for nearly everyone to ensure healthy levels. Not all forms of magnesium are equally absorbed by the body. One of the most absorbable forms of nutritional magnesium is magnesium citrate in powder form. Start out slow and build up to and find your body's tolerance level.

For most people, no single supplement or diet change will reduce LDL to your target. A combination of several strategies usually yields the large drops that we need to achieve dramatic LDL reduction, but nutritional magnesium and the above diet adjustments will help.

Heart health expert and cardiologist, William Davis, M.D., is the author  of "Track Your Plaque: The only heart disease prevention program that  shows how the new CT heart scans can be used to detect, track, and  control coronary plaque" (www.trackyourplaque.com). Dr. Davis is a  member of the Nutritional Magnesium Association and invites you to get  more information that will help you avoid the magnesium deficiency. Go  to www.nutritionalmagnesium.org.

The ideas, procedures and suggestions contained in this article are not intended as a substitute for consulting with your physician. All matters regarding your physical health require medical supervision. Neither the author nor the publisher shall be liable or responsible for any loss, injury or damage allegedly arising from any information or suggestion in this article. The opinions expressed in this article represent the personal views of the author and not the publisher.
References

1. Rosanoff A, Seelig MS, “Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals.” J Am Coll Nutr 2004;23(5):501S-505S.
2. Ka He, MD, ScD; Kiang Liu, PhD; Martha L. Daviglus, MD, PhD et al. Magnesium Intake and Incidence of Metabolic Syndrome Among Young Adults. Circulation 2006;113:1675-1682.
3. Pearson TA, Blair SN, Daniels SR, Eckel RH, Fair JM, Fortmann SP, et al. AHA guidelines for primary prevention of cardiovascular disease and stroke: 2002 update. Consensus panel guide to comprehensive risk reduction for adult patients without coronary or other atherosclerotic vascular diseases. Circulation 2002;106:388–91.
4. Krauss RM, Dreon DM. Low-density lipoprotein subclasses and response to a low-fat diet in healthy men. Am J. Clin Nutr 1995: 62:478S–87S.
5. Krauss RM, Blanche PJ, Rawlings RS, Fernstrom HS, Williams PT. Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Am J Clin Nutr 2006 May;83(5):1025–31.
6. Gulesserian T, Widhalm K. Effect of a rapeseed oil substituting diet on serum lipids and lipoproteins in children and adolescents with familial hypercholesterolemia. J Am Coll Nutr 2002 Apr;21(2):103–8.
7. Miller WM, Nori-Janosz KE, Lillystone M, Yanez J, McCullough PA. Obesity and Lipids. Curr Cardiol Rep 2005 Nov;7(6):465–70.

Published online, Feb. 2010, WholeFoods Magazine
http://www.wholefoodsmagazineonline.com/

European Heart Journal on "Low Fat/Low Cholesterol"

I came across this article from the European Heart Journal with evidence from clinical trials about the so called heart healthy diet. It can be found on line at http://www.omen.com/corr.html. I reduced the text size of the 'Reference' section not because that information is less important rather to save some space. In fact the #1 principal to defend against junk science (as found in "The Junk Science Self-Defense Manual" by Anthony Colpo) is to 'Check the research yourself!'.

Here's a quote from that publication.

"I’ve lost count of the number of times I’ve checked studies that were cited in support of a specific stance, and found they either did not support that stance or even contradicted it!

A striking example of this phenomenon can be found in a joint statement by the American Heart Association and the NIH's National Heart, Lung, and Blood Institute entitled The Cholesterol Facts, where one finds the following claim: "The results of the Framingham study indicate that a 1% reduction…of cholesterol [corresponds to a] 2% reduction in CHD risk"[1].

Incredibly, one of the papers cited in support of the above statement was a thirty-year follow-up report from Framingham that flatly contradicts any claim that cholesterol reduction is beneficial. This report found that those whose cholesterol levels decreased during the study experienced an increase in both total and cardiovascular mortality! To quote the Framingham researchers themselves: "There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years…". So don’t be satisfied with the fact that someone has posted a bunch of scientific-looking citations at the end of their article. Check those citations for yourself! Doing so will often paint a very different picture to the one the original author wants you to see!"

Well enough intro - on to the article that prompted this post.
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The low fat/low cholesterol diet is ineffectiveReprinted with permission from: European Heart Journal (1997) 18, 18-22
L.A. Corr, Guy's and St. Thomas' Hospitals, London, U.K. M.F. Oliver, National Heart and Lung Institute, London, U.K.
Correspondence: Dr. Laura A. Corr, MB, BS, MRCP, PhD, FESC,Consultant Cardiologist, Guys and St. Thomas' Hospitals, St. Thomas Street, London SE1 9RTAsk almost member of the general public about a diet which would reduce their chance of heart disease and the reply is the same: "a low fat diet". On closer questioning, this means a diet with a reduction in cholesterol and saturated 'animal' fats, i.e. less meat, butter, milk and cheese. Most national and international recommendations for the prevention of heart disease, whether for primary prevention of or for patients who have developed the clinical manifestations of coronary heart disease, have made dietary restriction of total and saturated fats and of cholesterol the primary advice and often the sine qua non in relation to all other forms of management. To this extent they are to be congratulated that the message seems to be so universally accepted. Unfortunately, the available trials provide little support for such recommendations and it may be that far more valuable messages for the dietary and non-dietary prevention of coronary heart disease are getting lost in the immoderate support of the low fat diet.

The origin of the 'low fat' diet

The international bodies which developed the current recommendations based them on the best available evidence[1-3]. Numerous epidemiological surveys confirmed beyond doubt the seminal observation of Keys in the Seven Countries Study of a positive correlation between intake of dietary fat and the prevalence of coronary heart disease[4] although recently a cohort study of more than 43,000 men followed for 6 years has shown that this is not independent of fiber intake[5] or risk factors. The prevalence of coronary heart disease has been shown to be correlated with the level of serum total and low density lipoprotein cholesterol (LDL) as well as inversely with high density lipoprotein. As a consequence of these studies, it was assumed that the reverse would hold true: reduction in dietary total and especially saturated fat would lead to a fall in serum cholesterol and a reduction in the incidence of coronary heart disease. The evidence from clinical trials does not support this hypothesis.

The evidence from clinical trials

It can be argued that it is virtually impossible to design and conduct an adequate dietary trial. The alteration of any one component of a diet will lead to alterations in others and often to further changes in lifestyle so it is extremely difficult to determine which, if any, of these produce an effect. Dietary trials cannot generally be blinded and changes in the diet of the 'control' population are frequently seen: they may be so marked as to render the study irrevocably flawed. It is also recognized that adherence to dietary advice over many years by large population samples, as for most people in real life, is poor and that the stricter the diet, the worse the compliance. Nonetheless, the evidence for a reduction in saturated fat from dietary trials for both primary and secondary prevention merits closer scrutiny.

Trials of low fat diets in primary prevention

There have been six randomized, controlled trials with the long-term follow-up designed to modify the development of coronary heart disease in healthy subjects [6-11]. Remarkably, no primary prevention trial of sufficient size or sensitivity to examine the effect of a low total and saturated fat diet alone has ever been conducted. All six primary prevention trials involved alteration of one or more other risk factors such as cigarette smoking, blood pressure and exercise.

Of the three smallest trials(approximately 300-600 subjects per group), two suggested a significant reduction in coronary events. In the Oslo Study[7], men at high risk were given dietary advice aimed at reducing saturated fat intake and modestly increasing polyunsaturated fat intake, and counseled to stop smoking. General advice was given to increase fish, whale meat, vegetable and fruit intake. Over 5 years the mean difference in serum cholesterol between the two groups was relatively large for a dietary trial - 13% and tobacco consumption was lower in the intervention group. There were fewer coronary events in the control group (P<0.028)Trials of low fat diets in secondary prevention
There have been two trials of the effect of a low saturated fat diet alone in patients with coronary heart disease. The MRC study[13] followed 252 men randomized to a very low fat diet or no change in diet over three years: the low fat diet was poorly tolerated but achieved a 10% reduction in cholesterol. There was no difference in the rate of reinfarction or death and the researchers concluded that the low fat has no place in the treatment of myocardial infarction. An Australian trial of 458 men substituted polyunsaturated margarine for butter and found a slightly lower 5 year survival in the intervention group (3.3% deaths per year) than in the control group (2.4% deaths per year) although multivariate analysis showed that none of the dietary factors was significantly related to survival[14]. Following the negative results of these trials, no further studies of a low saturated fat diet alone have been conducted.

Should we be recommending diet at all?

The overwhelming importance of coronary heart disease in terms of morbidity, mortality and economic cost in the Western world made dietary advice, which was perceived to be cheap and safe, very attractive to Governments and their Health Departments. Vast sums of money have been invested in nutritional programs, dietary advice and nurse counseling to promote low saturated fat, low cholesterol diet--yet the trials to date for both primary and secondary prevention suggest that these diets do not work. However, this does not mean that all dietary interventions are futile. Other trials of secondary prevention have to a greater or lesser extent tried to alter the quality of the dietary fat intake and other components in patients with coronary heart disease, rather than restrict the quantity of saturated and total fat, and the results are more encouraging.

Trials of diets not dependent on fat reduction

Vegetable oil supplements were used in four of these trials[15-18]. In the LA Veterans Administration study, increasing ingestion of corn, safflower, soyabean and cottonseed oils significantly reduced total cardiovascular events after eight years[15]. The study by Rose et al, found no evidence of clinical benefit in patients given a low fat diet and supplements of olive or corn oil[16]. Similarly, the MRC group added soyabean oil as a supplement to the diet and found no difference in the incidence of death or myocardial infarction compared to men taking their normal diet[17], but a similar study from Oslo did show a significant reduction in pooled coronary heart disease relapses after 5 years and fewer fatal myocardial reinfarctions by 11 years[18]. However, none of these produced a significant difference in total mortality.

Saturated fat reduction, vegetable oil supplements and lifestyle changes in keeping with the current recommendations of the American Heart Association were advised for both the intervention and control groups in a study of Indian patients randomized within 48 h of a suspected myocardial infarction, but in addition the intervention group received a diet high in dietary fiber, omega-3 fatty acids (from fish and nuts), antioxidant vitamins and minerals[19]. The intervention group achieved remarkable wide-ranging and sustained changes in their nutrient intake associated with a modest reduction in serum cholesterol and weight loss. Cardiovascular events were reduced in the intervention group after only 6 weeks and after 1 year there was a significant reduction in myocardial infarction, a 42% reduction in cardiac deaths and a 45% reduction in total mortality compared to the control group on the standard 'low fat' diet. The study does not seem to have been continued beyond on year.

The first successful dietary study to show reduction in overall mortality in patients with coronary heart disease was the DART study reported in 1989[20]. The three-way design of this 'open' trial compared a low saturated fat diet plus increased polyunsaturated fats, similar to the trials above, with a diet including at least two portions of fatty fish or fish oil supplements per week, and a high cereal fibre diet. No benefit in death or reinfarctions was seen in the low fat or the high fibre groups. In the group given fish advise there was a significant reduction in coronary heart disease deaths and overall mortality was reduced by about 29% after 2 years, although there was a non-significant increase in myocardial infarction rates. The reduction in saturated fats in the fish advice group was less than in the low fat diet group and there was no significant change in their serum cholesterol.

Finally, the more recent Lyon trial[21] used a Mediterranean-type of diet with a modest reduction in total and saturated fat, a decrease in polyunsaturated fat and an increase in omega-3 fatty acids from vegetables and fish. As in the DART study there was little change in cholesterol or body weight, but the trial was stopped early following a 70% reduction in myocardial infarction, coronary mortality and total mortality after 2 years.

The most effective diet for secondary prevention is therefore not reduction of saturated fats and cholesterol but appears to be an increase in polyunsaturates of both omega-6 and omega-3 fatty acids. Unfortunately, the design and conduct of these trials are insufficient to permit conclusions about which polyunsaturates and other elements of these diets are the most beneficial. The long term effects of these trials[20,21] and the compliance with the dietary regimes remain to be seen. But the mechanism of any benefit of the omega diets would appear not to be associated with reduction in the total or LDL cholesterol levels and may be more related to reduction of a thrombotic tendency.

The case for recommending similar changes in diet in primary prevention is less clear cut. Although the benefit of olive oil receives strong epidemiological support from several Mediterranean countries, particularly Crete, and short-term studies of diets rich in oleic acid (the principle monounsaturate in our diet) have demonstrated a reduced LDL susceptibility to oxidation, no formal randomized long-term trial of monounsaturates has yet been attempted. There is no consensus from population or cohort follow up surveys about the protective effects of increased fish consumption on coronary mortality. The recently published report from the physicians Health study[22] found no evidence of an inverse association between the intake of fish or fish oils and the risk of myocardial infarction and, while the highest coronary mortality was found among men who ate no fish, the risk did not decrease with increasing fish intake. At present, there does not appear to be any dietary advice which is effective in primary prevention.

Is drug treatment better?

An important aspect of the lipid-lowering dietary trials is that on average they were only able to achieve about a 10% reduction in total cholesterol. The results of recent drug trials have demonstrated that there is a linear relation between the extent of the cholesterol, or LDL, reduction and the decrease in coronary heart disease mortality and morbidity, and a significant effect seen only when these lipids are lowered by more than 25%[23].

Until 1994, the trials with lipid lowering therapy for primary and secondary prevention had been as disappointing and confusing as the trials with diet. They tended to show a reduction in coronary events, including deaths from myocardial infarction, but no reduction in overall mortality. Even though an excess of deaths from cancer and suicide was not shown to have any casual relationship with the treatment, there was no widespread acceptance of lipid lowering therapy.
This changed in 1994 with the publication of the seminal 4S study on secondary prevention of coronary heart disease in 4444 patients with cholesterol levels greater than 5.5 mmol . 1-1 who were randomized to treatment with simvastatin or placebo in addition to 'usual care' including dietary advice[24]. The 4S study showed highly significant (30%) reduction in cardiac events and deaths from myocardial infarction and, for the first time, in overall mortality. The benefits were apparent after 18 months and the difference between the treated and the control groups continued to increase over the five years of follow-up. The more recent CARE study showed a similar outcome with a 28% reduction in reinfarction using pravastatin in 4159 patients following myocardial infarction despite the fact their cholesterol levels before treatment were not high (mean 5.4 mmol . 1-1)[25]. As part of their usual care, patients in this study also received high levels of antiplatelet agents and beta-blockers and 55% had undergone revascularization with angioplasty or bypass surgery. There was no change in coronary heart disease deaths or in all-cause mortality. Over 5 years of follow-up in both these statin trials the treatment was extremely well tolerated with around 90% compliance and no serious effect, indeed there was almost no difference in the side-effect profiles between the statins and the placebo.

With primary prevention the results of treatment with the statins appears equally encouraging. The West of Scotland Coronary Prevention study treated over 6000 healthy men (aged 44-65 years) who had total cholesterol levels greater than 6.5 mmol . 1-1 with either pravastatin or placebo[26]. Again the trial was continued for 5 years, and normal advice was given to both the intervention and the control groups. The risks of death from coronary heart disease and non-fatal myocardial infarction were reduced significantly in the pravastatin group by 31%, and there was a non-significant but favourable trend for all-cause mortality (-22%) with no adverse effect on non-cardiovascular mortality.

The cost effectiveness of treatment with the statins has been assessed at current prices for both primary and secondary care. It varies greatly according to the risk, being obviously more efficient for those at the highest risk, but has been shown to be greater than drug treatment for mild-to-moderate hypertension which is widely endorsed and used in general practice. For those at lower risk, diet should be able to provide a cheaper regimen but at present none has proved sufficiently beneficial.

Conclusions

The commonly-held belief that the best diet for the prevention of coronary heart disease is a low saturated fat, low cholesterol is not supported by the available evidence from clinical trials. In the primary prevention, such diets do not reduce the risk of myocardial infarction or coronary or all cause mortality. Cost-benefit analyses of the extensive primary prevention programmes, which are at present vigorously supported by Governments, Health Departments and health educationalists, are urgently required.

Similarly, diets focused exclusively on reduction of saturated fats and cholesterol are relatively ineffective for secondary prevention and should be abandoned. There may be other effective diets for secondary prevention of coronary heart disease but these are not yet sufficiently well defined or adequately tested. The circumstantial evidence of benefit from oils, particularly olive oil, vegetables, fruit and fish is strong.

For those at high risk, drug therapy, with the statins provides effective primary and secondary prevention and should be considered, with or without a diet, in the same way as drug treatment for mild or moderate hypertension.L.A. Corr, Guy's and St. Thomas' Hospitals, London, U.K.
M.F. Oliver, National Heart and Lung Institute, London, U.K.

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