Garlic & Red Yeast Rice: Manage Your Blood Lipids W/Out Statins - 12+1 Natural Alternatives Reviewed (Part I)

Red yeast rice is the "+1" in this SuppVersity Mini-Series because it is actually a "statin". Similar effects, similar side effects and all that (probably) because of the similar structure of its lipid lowering active ingredient(s).

"Twelve + 1"? I know that sounds odd, but I have my reason to single one of the natural alternatives, two scientists from the Chulalongkorn University in Thailand list in their 2016 review "A Review of the Efficacy, Safety, and Clinical Implications of Naturally Derived Dietary Supplements for Dyslipidemia", right from the start: red yeast rice (RYR).

While garlic, which will also be discussed in today's first installment of what is going to become a mini-series, also has the ability to decrease your HMG-CoA reductase activity, only RYR does that at a similar potency as statins do; which is why its use entails the risk of similar side effects as they have been reported for regular statin drugs Whether RYR is thus your best "natural alternative" is highly questionable.

All about cholesterol & related stories in previous SuppVersity articles:

Cholesterol Boosts Immunity

Eggs Promote Heart Health

All About Eggs (Focus on Yolk)

Silicon-Powered Anti-CVD Foods

Paleo Works W/ High Cholesterol

Coconut Oil to Control Chol.

On the other hand, the fact that the monacolins, the main bioactive compounds in RYR, is not debatable. Only recently, a meta-analysis by Li et al. (2014) reported no serious side effects and concluded based on 13 RCTs that "red yeast rice is an effective and relatively safe approach for dyslipidemia" (Li. 2014). Li et al. do yet also know that "further long-term, rigorously designed randomized controlled trials are still warranted before red yeast rice could be recommended to patients with dyslipidemia, especially as an alternative to statins" (Li. 2014).

Figure 1: Effects of 1,200mg/d red yeast rice (RYR) on blood lipids in statin-intolerant subjects (left | Venro. 2010) and subject-dependent reductions in LDL in the latest meta-analysis of the effects of RYR (right | Li. 2014).

If you are statin intolerant, however, Venro et al's study in 25 statin-intolerant subjects who received 1,200 mg RYR at bedtime, however, would suggest that you in particular could benefit from RYR as it appears to have a rather good tolerability in those subjects who cannot take regular statins.

Don't be a fool! This article is no statin or anti-cholesterol add. Nobody says that taking statins without a good reason would be wise. In fact, even the relatively well-tolerated RYR which works by the same mechanism, produced (albeit tolerable) muscle weakness and muscle pain as adverse effects in most clinical studies; a downside that points to the 'demusculizing' effects of HMG-CoA reductase inhibitors - even if the difference to placebo reached statistical significance only in few (albeit short-term) studies (Liu. 2006 & Li. 2014).

Further evidence that, as so often, individuality is key comes from the differential effects in European, Asian and US subjects (see Figure 1 showing data from Li. 2014). The latter, however, may be explained by both, the genetic configuration of the subjects, and the high ingredient variability of commercially available RYR preparations of which a comparative analysis of 10 commercial red yeast rice products reports a >30-fold range in total monacolin content. The authors of said study also highlight:

"Furthermore, compared with the full spectrum of monacolins expected in a red yeast rice dietary supplement, with monacolin K representing 55% to 60%, 4 of the 10 products were >90% monacolin K, suggesting that they were actually food-grade red yeast rice “spiked” with lovastatin, the prescription statin that is chemically identical to monacolin K" (Mark. 2010).

And Mark et al. are not the only ones reporting an intolerable degree of cutting in the snake oil industry. Similar results have been presented by Gordon et al. who tested 12 products that are regularly sold and consumed in the US and found total monacolin contents ranging from 0.31 to 11.15 mg/capsule. Just like Mark et al. Gordon et al. also found monacolin K (lovastatin | 0.10-10.09 mg/capsule), which could occur naturally, albeit not at very high doses, in many and the kidney-damaging citrinin in four of the twelve tested products (33%).

Garlic is a HMG-CoA inhibitor that doesn't have the problems of statins & RYR ...

...or, we simply don't know about them yet, because the currently available garlic supplements all suffer from the pathetic bioavailability of allicin (which is broken down enzymatically before it reaches your bloodstream | Lawson. 2001), which could - in very high doses that have not been tested in studies yet - possibly have similar negative side effects as the monocalins in RYR.

More recently, however, studies have suggested that allicin may not even be necessary for some of the beneficial effects of garlic. In particular, its general anti-oxidant and anti-inflammatory effects appear to be mediated mainly by S-allyl cysteine. Furthermore, "various chemical constituents in garlic products, including nonsulfur compounds such as saponins, may contribute to the essential biological activities of garlic" (Amagase. 2006) - including their anti-lipidemic effect.

I want to try it - What's the optimal dosing for garlic and RYR? While the evidence for the more powerful RYR is relatively conclusive and says that effective dosage(s) range from 600 and 3600 mg (depending on product quality and how significant your 'cholesterol-problem' is), reliable dosage suggestions are hard to make for garlic. In the previously cited recent review from Thailand (Thaipitakwong & Aramwit. 2016), the suggestion is 2–5 g of fresh garlic, 0.4–1.2 g of dried powder, 2–5 mg of oil and 300–1000 mg - "any other preparations should correspond to 4–12 mg of alliin or 2–5 mg of allicin" (ibid.). As previously pointed out, however, there's probably one study to refute the efficacy of real-food or supplemental garlic at the given dosages for every two studies that support it. Eventually, you will thus have to self-experiment to find out if and at which dosages garlic can exert a significant effect on your blood lipids.

In contrast to their active ingredient, however, the efficacy of garlic and garlic supplements as anti-hyperlipidemic drugs is well-established. One of the most cited meta-analyses (39 RCTs with 2298 participants | Ried. 2013) found that, overall, garlic consumption caused significant changes in serum levels of total cholesterol (–15.25 mg/dl; p < 0.0001), LDL-C (–6.41 mg/dl; p = 0.02), and HDL-C (1.49 mg/dl; p = 0.02), whereas the triglyceride levels appeared to be unaffected (I will address this in a follow-up, but if you eat your garlic with fatty fish, this should address the triglyceride issue). In addition, a more recent meta-analysis revealed that it will also reduce the level of lipoprotein (a) in the blood of hyperlipidemic subjects (Sahebkar. 2016).

Figure 2: Effects of garlic supplements on LDL (left, red) and HDL (right, green) according to a 2013 meta-analysis of  39 RCTs with 2298 participants (Ried. 2013) - the results have generally been confirmed more recently (Ried. 2016). 

Needless to say that, for garlic, just like RYR and any other drug or supplement, conflicting evidence exists. Early studies, for example, didn't report consistent effects on LDL and HDL. Whether that's due to different types (raw, powder, oil, and aged extract), processing and doses of garlic products used, or the subjects' baseline lipid levels and the study duration is something neither Thaipitakwong & Aramwit (2016), in their review, nor I can tell you due to the lack of studies that directly investigate the individual effects of these parameters. studies. The latter is also true for the bioavailability of raw garlic vs. supplements and the various types of 'garlic products' on the market. As the previously cited study from Thailand rightly concludes: the individual bioavailability simply has not been studied, yet (Thaipitakwong & Aramwit. 2016).

It should never be your goal to eradicate cholesterol. What you want is to control your levels within a rationale range that is probably much higher (esp. for total cholesterol) than the US recommendations to reap the benefits this essential hormone precursor and building block of your cells will have on endocrine, immune, muscle and brain function.

To be continued: If you miss the promised 11 'true' alternatives that won't mess with your HMG-CoA enzyme activity, I can reassure you, there will be a follow-up in which you can learn more about phytosterols, sesame, green tea, probiotics, fiber, chitosan, soy, flaxseed, guggul, krill and fish oil.

Until then, I would like to leave you with the conclusion that garlic is both, the less effective, and less side-effect prone natural alternative to statins. In contrast to red yeast rice, which is practically a "natural statin", it is yet able to control only "slightly elevated" (Ried. 2016) cholesterol levels; and not those you will see irrespective of your diet due to an inheritable genetic disposition and/or known or unknown pathologies (oftentimes one or several of the other components of the metabolic syndrome) | Comment!

References:

• Amagase, Harunobu. "Clarifying the real bioactive constituents of garlic." The Journal of nutrition 136.3 (2006): 716S-725S.
• Gordon, et al. "Marked variability of monacolin levels in commercial red yeast rice products." Arch Intern Med 170.19 (2010): 1722-1727.
• Lawson, Larry D., and Z. Jonathan Wang. "Low allicin release from garlic supplements: a major problem due to the sensitivities of alliinase activity." Journal of agricultural and food chemistry 49.5 (2001): 2592-2599.
• Li, Yinhua, et al. "A meta-analysis of red yeast rice: an effective and relatively safe alternative approach for dyslipidemia." PloS one 9.6 (2014): e98611.
• Liu, Jianping, et al. "Chinese red yeast rice (Monascus purpureus) for primary hyperlipidemia: a meta-analysis of randomized controlled trials." Chinese medicine 1.1 (2006): 1.
• Mark, David A. "All red yeast rice products are not created equal—or legal." The American journal of cardiology 106.3 (2010): 448.
• Venero, Carmelo V., et al. "Lipid-lowering efficacy of red yeast rice in a population intolerant to statins." The American journal of cardiology 105.5 (2010): 664-666.
• Sahebkar, Amirhossein, et al. "Effect of garlic on plasma lipoprotein (a) concentrations: A systematic review and meta-analysis of randomized controlled clinical trials." Nutrition 32.1 (2016): 33-40.
• Ried, Karin, Catherine Toben, and Peter Fakler. "Effect of garlic on serum lipids: an updated meta-analysis." Nutrition reviews 71.5 (2013): 282-299.
• Ried, Karin. "Garlic lowers blood pressure in hypertensive individuals, regulates serum cholesterol, and stimulates immunity: an updated meta-analysis and review." The Journal of nutrition 146.2 (2016): 389S-396S.

Three Servings of Grapefruit /Day Have No Effect on Weight Loss, But Increase Triglycerides and Make a Potentially Deadly Cocktail With A Whole Host of Prescription Meds!

Image 1: Grapefruit does not help with weight loss and, as it turns out, is not even healthy. On the contrary, in conjunction with your favorite statin it is even potentially deadly.

Do you remember the "grapefruit diet" (WebMD)? No? Well, then you are probably male and have always been satisfied with your weight. Otherwise, you would probably have heard how a "magical ingredient" in the subtropical citrus fruit is going kill all those unaesthetic adypocytes, which have made themselves at home on your hips and buttocks, in no time... What do you say? Bullsh*t? Well, I guess you have been reading to much of my stuff already, after all this purported short-cut to six-pack abs is also known as the Hollywood Diet and that alone will have people fall for it by the dozen... I mean, if Brooke Shields and Kylie Minogue got in shape with it, it must be working, right?

The myth and the truth about grapefruits

I know that you would never be so stupid to start eating nothing but grapefruit (you would not, right?), but despite the fact that the Grapefruit Diet has rightly gotten a bad rep within the (self-)educated members and followers of the wealth of good and not-so-good blogs and websites dealing with nutrition and weight loss, many people still believe that there must be something about this fruit that will help you lose weight. And in view of the fact that I myself know a couple of these (interestingly all female) unfortunate critters, I believe that it is still worth to take a closer look at the results of a recently published study on the effects of 1.5 fresh Rio-Red grapefruit per day on the outcomes of a 6-week dietary intervention (Dow. 2012). The study involved 74 male and female subjects (age: 41y; BMI: 32kg/m²; Bodyfat: 35.7%) who, despite having problems with their weight, had been weight-stable in the past 6 months (or more). After an initial 3-week "wash out period" in the course of which the subjects had to follow a diet that was restricted in bioactive-rich fruits and vegetables (the intention, here, was to get all to a baseline level as far as the purported "magic fat loss ingredient" in citrus fruits is concerned), the subjects were randomized to one of two groups:

1. intervention group (n=42) continued eating the "wash-out diet" and supplemented with their 3x0.5 Rio-Red grapefruit per day 15 minutes prior to their regular three meals
    
2. control group (n=32) continued eating the "wash-out diet"

The dietary intake of the subjects, was evaluated with your usual (unreliable, but in want of alternatives obligatory) repeated 24-hour diet recalls (3x during the washout phase and 3x during the intervention phase). Things like the total caloric intake (1800-1900kcal) or the macronutrient composition did not really differ between diets - in other words: The scientists did a pretty good job to isolate the grapefruit intake and the (obviously) correlating vitamin C intake (cf. figure 1) as the single confounding factors in their study.

Figure 1: Total caloric intake, the number of vegetable servings, the overall macronutrient ratio etc. all were identical between the two groups, except the fruit and (consequently) the vitamin C intake (data based on Dow. 2012)

With a subject pool of 74 men and women and virtually identical diets, we should thusly well be able to see an effect on body weight, body fat, lipid or glucose metablism, if there was one, but as the data in figure 2 indicates, "the magic just did not happen":

Figure 2: Relative changes in anthropometric data in the course of the 6-week study period; no statistically significant inter-group differences, not even statistical significant pre-post changes (data based on Dow. 2012)

Aside from the fact that grapefruit does not make you lose fat, the graph in figure 2 carries another important message, which is: Never use a body impedance device to track your progress. And this goes for all those stupid things, and not only the Omron Body Fat Analyzer HBF-306 which was used in the study. Why? Well, take a look at the body fat and the waist circumference data: How can your gut become smaller, when your body fat percentage increases? The answer is easy, because the grapefruit eaters lost water, they lost ~1% more of their waist circumference. This did yet change the impedance of their bodies so that the stupid for the Omron was tricked to believe that the body fat percentage of the study participants had increased (if you are at a loss how you can track your progress, make sure you read the Intermittent Thoughts on "Stocktaking, Goalsetting, -Tracking & -Resetting").

"But, Dr. Andro, weight loss is not everything" - Correct! And another reason not to eat huge amounts of grapefruits

Another argument of the "grapefruit fanatics" is that, although the weight loss effects of the fruit may be negligible, it still is a healthy superfood that will improve your overall and metabolic health... now, if we take a look at what (unfortunately) is still considered the "gold-standard" as far as the assessment of CVD risk is concerned, i.e. the allmighty lipid profile (imagine a fanfare, here), I guess that only those of you who still believe in the black-and-white version of the lipid hypothesis (HDL = good guy; LDL = bad guy; nothing else counts) will wholeheartedly agree with Dow et al. conclusion that ...

grapefruit consumption does elicit beneficial effects compared with baseline values that are
associated with CVD risk reduction.

If you take a look at the actual data in figure 3 you can hardly argue that the 1.5 grapefruits à day gave the "bad guy" (LDL) a slightly more thorough beating than the "wash out diet" with its quasi non-existent polyphenol content, but...

Figure 3: Changes in lipid profile (unadjusted and adjusted with ANCOVA for BMI, age, sex, and washout-phase p-values) for the control and grapefruit group (left) and the questionable conclusion the scientists draw based on the observed reduction in LDL and statistically likewise non-significantly greater reductions in blood pressure in the grapefruit group (right) (based on Dow. 2012)

...with a p-value (indicating the probability that this is mere coincidence; p < 0.05 is considered "statistically significant) of p = 0.871 for the inter-group difference this difference did not only fail to reach statistical significance, it must also be seen in the context of an increase in triglyceride levels (instead of a decrease in the control group), of which a 2009 study by Kannel et al. states that

[...n]onfasting triglycerides maintained an independent graded relationship with CVD in fully adjusted analyses, with elevated 4 h postprandial triglyceride imposing a 4.5-fold increment relative to lower levels [...and that] triglyceride-associated CVD risk occurs even in patients with low low-density lipoprotein cholesterol (Kannel. 2009)

Just to make sure nobody is missing the point here, neither the inter-group differences in LDL reduction nor the different outcomes as far as the trigs are concerned, reached statistical significance, but against the background of the results of the meta-analysis of Kannel and Vasan from 2009 and recent findings on the contribution of elevated triglyceride levels to the etiology of cardiovascular and metabolic diseases, I personally feel that beyond not helping with weight / fat loss, eating grapefruit could potentially even contribute to, or aggravate existing metabolic disturbances.

If you are on any medication grapefruit is a no-go, anyway!

Image 2: If you are healthy eating grapefruits from time to time won't hurt. If you are taking medication, however, it can potentially be fatal - although I's say that the meds, not the fruit are to blame for this

Yet even if you don't care about the pro-diabetic effects of triglycerides and discard the non-existent effect of grapefruits on weight loss / body composition, there is another, probably more important, because potentially fatal side-effects of eating grapefruit (or drinking its juice / taking respective supplements), which relates to the inhibitory effects it exerts on a hitherto not fully elucidated number of liver enzymes in the cytochrome cascade (CYP), which is heavily involved in drug and hormone metabolism. So, even if you don't take a statin, of which Dreier et al. have shown that it can induce profound rhabdamyolysis (=total break down of muscle protein, which can lead to kidney failure and death), when the grapfruit flavenoids and polyphenols block its metabolism in the liver (Dreier. 2004), or any other of the countless drugs the effects of which are profoundly modulated by the ingestion of grapfruit or grapefruit juice (Hanley. 2011), you better stick to no more than a single grape-fruit once in a while... I mean, it has no beneficial health / weight loss effect, anyway.

Eat Whole Eggs All Day and Throw Your Statins Away? 375x Increased Dietary Cholesterol Intake From Eggs Reduces Visceral Fat & Promotes Healthy Cholesterol Metabolism

Image 1: You better make sure you don't miss out on these delicious heart- and brain-healthy cholesterol bombs.

Most of you will probably be familiar with the good old saying "An apple a day, keeps the doctor away!", right? And if you are an otherwise healthy individual the micronutrients from the apple will probably really help you maintain this status. But what if the doctor was already there to put you on the healthy low fat diet, the negative health consequences of which I have addressed in yesterday's blogpost? In that case, whole eggs probably provide a more promising escape route from that low-fat, high-carb trap - at least this is what the the results of a soon to be published study from the Huazhong Agricultural University in Wuhan, China would suggest (Yang. 2012).

Surprising(?) -9% belly-fat reduction on whole egg diet

In their 60 to 90 day experiment, the Chinese researchers put a group of 8-week old Sprague-Dawley rats (n=18 for each group) on dietary regimen which differed in either cholesterol content (control vs. experimental groups) or the source of dietary cholesterol, i.e. 17.5% lard + synthetic cholesterol, 31.25% freeze dried egg yolk or 55.56% whole egg powder.

Figure 1: Composition of the control and the three experimental diets (adapted from Yang. 2012)

If you take a closer look at the exact composition of the diets in figure 1 the you will probably notice that macronutrient-wise the three standard-chow + lard/yolk/whole egg "high cholesterol" diets are miles-apart from what the average "low carber" would consider a healthy high fat diet. Still, the idea of choosing whole eggs as a major constituent (>55%) of one's diet should ring a bell for everyone who is familiar with the practical realization of the so-called "induction phase" of the purportedly (from the perspective of the same people who recommend the purportedly "heart-healthy low-fat diet") artery-clogging Atkins diet.

Figure 2: Body weight gain, food intake, food efficiency (food intake / weight gain) and relative visceral fat weight (per body weight) in Sprague Dawley rats after 60 and 90 days on experimental diets; data expressed relative to control group on standard rodent chow (data calculated based on Yang. 2012)

Interestingly, the data in figure 2 shows that even this version of "Atkins gone wrong", with a 40% carbohydrate content in the whole egg group (cf. figure 1) lead to significant reductions in weight gain and food efficiency (weight gain per gram of chow) and, more importantly, produced statistically significant reductions in the visceral fat / total body weight ratio at the end of the 90day study period (at 60 days there were no statistical significant inter-group differences).

55.56% whole egg diet kickstarts healthy cholesterol metabolism

In view of the fact that it has never been the notion that eggs would make you fat, but rather their purported negative effect on cholesterol levels due to which eggs, in general, and yolks, in particular, have gotten a bad rep over the last years, I guess that the visceral fat argument, alone, won't suffice to convince the egg-white consumer that they are missing out on the best part of the egg. After all, it was and unfortunately still is their purported negative effect on cholesterol that is literally at the heart of the egg(yolk)-scare.

Figure 3: Triglyceride, total, low density (LDL) and high desnity (HDL) cholesterol in Sprague Dawley rats after 60 and 90 days on experimental diets; data expressed relative to control group on standard rodent chow (data calculated based on Yang. 2012)

If you do yet take a look at the actual effects the natural cholesterol from the egg-containing diets had on the blood lipids of the rodents (cf figure 3), you will notice that those were statistically non-existent. In other words, only the lard + synthetic cholesterol diet had a statistically significant negative impact on the plasma lipids of the rats.

Figure 4: mRNA expression of hydroxymethylglutaryl CoA reductase (HMG-CoA R), LDL receptor (LDL-r), cholesterol 7a -hydroxylase (CYP71A), acyl-CoA:cholesterol acyltransferase (ACAT) lecithin cholesterol acyltransferase (LCAT) expressed relative to control (data adapted from Yang. 2012)

The 375x higher dietary cholesterol intake in the egg-groups, on the other hand, did not only shut down the endogenous cholesterol synthesis, as evidenced by the reduction in hydroxymethylglutaryl CoA reductase expression (HMG-CoA R, cf. figure 4) and increase its metabolization into bile acid via cholesterol 7a -hydroxylase (CYP71A), it also increased the LDL receptor expression in the liver (lack of LDL-r expression in the brain is associated with increased plaque formation in Alzheimer's, cf. Katsouri. 2011), lowered the formation and storage of cholesterol esterified cholesterol in the tissue by reducing acyl-CoA:cholesterol acyltransferase (ACAT) and increased the maturation of HDL and peripheral tissue cholesterol efflux via increased lecithin cholesterol acyltransferase (LCAT) expression.

In case you doubt that this rodent data has any significance for human beings, I just want to remind you that a 2008 study by Mayurasakorn et al., which found that "[i]n the majority of healthy adults" the addition of one egg per day to a "normal fat diet" lead to increases in HDL-c and decreases of the total cholesterol to HDL ratio (Mayurasakorn. 2008). Their conclusion that "egg consumption might benefit blood cholesterol" was however similarly ignored as the absence of scientific data to support the "eggs = increased risk of heart disease"-myth.

It is thusly not surprising that the Chinese scientists conclude that contrary to the "conventional approach to weight reduction", of which the scientists state that it is "a high-carbohydrate, low-fat, energy-deficient diet" that "has not proven to be very effective for many obese and over-weight individuals [I am not making that up, it is the exact wording from the study ;-]", an "egg diet", which "theoretically [...] would be more likely to cause obesity", could not only help those individuals finally shed unhealthy visceral fat, it could also lead to significant improvements in their lipid metabolism. If it were not for the statement that

[...] the mechanisms by which an egg diet lowers plasma cholesterol need to be further characterized and the special functional factors in egg need to be identified

one could be led to believe that Yang et al. had finally grasped the notion that just eating the right (whole) foods could solve the problem... the term "functional factors" does yet tell me that they are probably just trying to developing an "egg in a pill" that will soon be patented and sold as an adjunct to the standard statin therapy,

SAD - Human Study Shows: Three Days on "High Fat" Standard American Diet Produce Heart Healthier LDL Particle Profile Than NCEP-Approved Low Fat Diet

Image 1: SAD or just mad? It does in fact look like you better stick to Royal TS, French fries & co instead of following a low fat diet according to the guidelines of the National Cholesterol Education Program if you care about your heart health.

In view of the fact that millions of lives depend on it (literally, not just figuratively!) it is actually quite surprising, some would probably say "scandalous" that the experimental evidence (and I am talking about controlled experiments on real, healthy human beings, not about epidemiological and thusly statistical) for the purported beneficial effects of a non-calorically restricted "healthy low fat diet" in the absence of additional exercise interventions is... scarce, to say the least. I was thusly positively surprised, when I hit on a study from a group of researchers from the Institute of Nutraceuticals and Functional Foods at the Laval University and the Lipid Research Center at the CHUL Research Center in Québec, Canada, the title of which suggested that it could provide exactly that - experimental evidence in support of the purportedly healthy low fat diet (Guay. 2012).

Scientists and their interpretation of a "high fat" diet...

I guess, those of you for whom this is not the first visit to the SuppVersity will be aware that I have made a habit of looking at the data first, to make up my mind, before I even take a closer look at the scientists interpretation of the latter (this is what is usually called the "conclusion"). And, geez! The "high-fat diet", the Valérie Guay and her colleagues advertise in the title of their paper turned out to be another case of the standard American diet, the relative fat content of which (32% of total calories) is not exactly, what's on my mind, when I think of a "high fat" diet.

Figure 1: Relative macronutrient composition of the baseline and the isocaloric test (high and low fat) diets (left); total fiber, cholesterol and phytosterol content, as well as polyunsaturated to saturated fatty acid (PUFA/SFA) ratio and total fat in % of total calories (right; data calculated based on Guay. 2012)

The fact that this paper still made into the news, although the researchers' interpretation of a "high fat" diet was designed to "reflected as closely as possible current North American men averages", does yet already tell you that the results were not that the "healthy low fat diet bet the crap out of the standard American one".

SAD! Standard American Diet beats the nasty small LDL particles out of a healthy low fat diet

In fact, a closer look at the somewhat cryptically presented study results revealed that, at least as far as the measured outcome variables of this particular study are concerned, the exact opposite was the case: It was not the purportedly healthy low-fat diet which was designed according to the recommendations of the National Cholesterol Education Program Adult Treatment Panel III (cf. JAMA. 2001) which induced favorable changes in the lipid profile of the twelve initially healthy normal-weight male volunteers (~27.1y; BMI 25.2kg/m²) who took part in this 3-day randomized, double-blind, crossover study, but the calorie-, fiber- and vegetable- and animal-protein-wise identical "high fat" diet, which had been designed in the image of the infamous "standard American diet" (SAD).

Figure 2: Lipid profile (left) and its relative changes (compared to baseline, right) in response to the 3-day dietary intervention (data calculated based on Guay. 2012)

If you look at the data in figure 2 through Pfizer-ish-blue glasses you will probably say: "Wait a minute! The cholesterol level did decrease in the low fat group! So this must be the better diet." And yes, this may actually be the case, if you define better according to the same fundamentally "cholesterol is bad for you"-paradigm which has been flushing billions of dollars (and of course Euros ;-) into the coffers of Pfizer & Co over the last decades. If you have yet been following the by no means "latest" scientific research on the correlation of cholesterol and heart disease, you will be aware that neither total cholesterol, nor total LDL levels, but rather the amount of highly oxidizable small LDL particles is a relatively reliable marker of the risk of heart disease (Lamarche. 1997)- and, fortunately, Guay et al. are aware of that, as well, and measured the characteristics of LDL particles by the means of electrophoresis.

Figure 3: Relative distribution of LDL particle sizes (left), cholesterol content (mmol/L) of LDL fractions (middle), and mean LDL particle size and LDL peak particle diameter (LDL-PPD; right); * indicates p < 0.05; ** indicates p < 0.001 (data adapted from Guay. 2012)

The results of the LDL-particle analysis shown in figure 3, show quite neatly, that the unquestionably unhealthy standard American diet (Attention: Do not misinterpret these study results as a carte blanche to stick to eating your regular crappy diet!) did not only result in more favorable triglyceride (1.48 vs 1.01mmol/L, p = 0.0003) and HDL levels (1.29 vs 1.41 mg/L, p = 0.05; cf. figure 2), than its allegedly "healthy" low fat counterpart, it was ...

[...] also associated with a significant increase in LDL particle size (255.0 vs 255.9Å; p = 0.01) and a significant decrease in the proportion of small LDL particle (<255.0 Å) (50.7% vs 44.6%, p = 0.01).

And although Guay et al. are quick to point out that "because the present study was only conducted in men, the results cannot be generalized to the whole population", I would say that these results should at least.make you reconsider if following a "healthy low fat diet" in accordance with the dietary guidelines of the National Cholesterol Education Program will help you lower your risk of heart disease... unless, of course, you have already popped so much Lipitor & co that the chronic lack of cholesterol is already hampering your cognitive abilities -.what? Ah, yes... of course, the favorable results occur only if you take you daily dose of statins with your low fat meals... right, how could I forget that ;-)

Creatine Prevents Statin Induced Myopathy

In the Observations section of the November issue of Annals of Internal Medicine Shewman & Craig (Shewman. 2010) report beneficial effects of creatine supplementation in patients on statin drugs:

Myopathy scores were significantly higher after the statin-only treatment phase than at baseline but did not differ from baseline after the other treatment phases. Creatine loading plus maintenance creatine therapy prevented myopathy symptoms in 8 of 10 patients receiving statins. After these 8 patients stopped maintenance creatine therapy and developed myopathy symptoms while receiving statins alone, reloading creatine decreased symptoms to baseline levels. Also, increasing the creatine dosage from maintenance to loading diminished myopathy symptoms to baseline levels in 1 patient who developed symptoms 6 days after a statin was added to maintenance creatine therapy. No significant differences in vital signs or laboratory test results were observed.

So, in case you really think you need to continue taking statins, it may be worth investing a few cents into some plain creatine monohydrate to keep side effects at bay.