Red Meat and Rubbish Science

I'm a little late to pass any comment on this, in fact I was going to avoid it because Zoe Harcombe and Gary Taubes have done such an excellent job, but I can't overcome the urge any longer....

So you have likely heard all the fuss in the mainstsream media regarding the greater likelihood of death from consuming red-meat (or meat in general). All of this stems from a recent journal article which I am more than happy to link to and I  genuinely hope you will go away and read because ultimately it proves some of the points I will be making.

The Media
Firstly people in the media aren't scientists, if they were they'd be in lab coats doing experiments somewhere, not writing or sitting behind a desk/in front of a news camera. I read recently the perfect quotation for media interpretation of science. I think you'll get the point.

SCIENTIST: "When taken out of context my results mean nothing!"

MEDIA: "Scientist reports 'results mean nothing' !"

Scientific Process
So within science there are different kinds of study; there are observational studies where we watch things for however long we deem appropriate and then we use this to come up with a hypothesis and to what they were doing that caused these things. And their are clinical trials or intervention studies, where we test said hypothesis. The first is an observation. It's an observation. It doesn't necessarily mean anything, and the point is that no-one can say that it really doesn't mean anything in the same way that no-one can say that it does. It is used to develop a hypothesis plain and simple.

I've blogged about this before and have shown a Tom Naughton video which discusses all of this in detail. An excellent example he gives was the observation that nurses supplementing with Oestrogen were less likely to suffer a cardiac condition (heart disease, etc.). Everyone jumped up and down and said A (supplement) prevents B (cardiac condition). Cause and effect. Right? Wrong? When the clinical studies were done they actually found that Oestrogen supplements were actually more likely to cause a cardiac condition!! So how did they even think that A caused B. Well imagine the kinds of people who take supplement, they look after their body, possibly exercise, possibly eat 'right', and so forth.

Proof or lack thereof...
So coming back to the present discussion.....well the Harvard School of Public Health guys who've come out with this decided not to do the second part. They did the observation bit, and then they skipped straight in to conclusion. What they're presenting to you is a hypothesis. They're suggesting that red-meat is bad for you. But this is NOT scientific evidence. I could claim that when I sing it rains, thus my singing must make it rain, but you wouldn't just believe that observation without some proof, would you?

Track Record
There's a final point I want to raise here. I want to look at Harvard School of Public Health's track record with hypothesis from observational studies, that are then proven correct or disproven after all. Now then, we can let the stereotypes sink back in here, this is Harvard after all....what percentage do you think? Go on have a guess....

Well...cited from Taubes' blog earlier (who has done the research - whereas I am just re-citing it)...Up to 2007, their average was....(drum roll please). 0.000. Yes, they got them ALL wrong. Not wrong most of the time (like me), or wrong just a bit of the time (like some people I know), or never wrong (like most women I know). They were wrong EVERY. SINGLE. TIME.

Now I could run some fancy statistics on all of this, but really; who needs it. Forget who likely meat are to kill you - how likely are they to be wrong over this!?!?

Be Well

JF

Practice Doesn't make Perfect; Perfect Practice makes Perfect

The title of this blog is a quote from Vince Lombardi. And without question it's true. But over the last year or so I've heard more and more about the 10,000 hour principle (that in 10,000 of good practice a person can become 'elite' at their sport). This blog is simply going to discuss this concept as well as recent revelations, and a recent interview with Anders Ericsson (father of the 10,000 hour principle)..reported from The Science of Sport blog.

A multitude of books have come out within this area discussing this 10,000 rule of thumb, and at initial inspection it seems quite appealing. The fact that anyone can do anything if we just put in the time and energy. It kind of makes me feel warm and cosy that somewhere inside I can switch on genes to help me be better, or more, be 'elite'. Last year I read 'Bounce' by Matthew Syed, and 'The Talent Code' by Daniel Coyle, both of which I would recommend to gain a better perspective of this area. 'Bounce' spends considerable time discussing myelin sheaths, best described as an insulating factor over neural pathways that act to reinforce and protect a skill as we practice it. Which is a nice way to protect the idea that 10,000 hours of practice is what's needed.

But looking back at the quote, it's about the quality of the practice, always challenging, always advancing, always perfect. In one of my first year classes I spend considerable time talking about neuromuscular pathways and skill specificity; that to be better at surfing you need to surf, not stand on a wobble board, or a fit ball or bosu. That to become better at swinging a baseball bat or basketball you need to practice the skill, perfectly, with the right weight and size bat or ball. That 'similar' is not the same, and that not the same is 'different'!

In one of my publications last year I talk of specificity with regard to resistance training: here is a brief extract:

"There is no evidence that skill development is aided by the performance of resistance exercises that bear some superficial resemblance to skills performed on the sports field. Skill enhancement is highly specific, with little correlation between the performances of different skills, even when they appear very similar. For example, Drowatzky and Zuccato [1967] showed that the correlations between performances on different (superficially very similar) balance tasks were extremely low and non-significant. They concluded that there is no such thing as a general phenomenon called ‘balance’. Instead, there are many different balancing skills, and because an individual is good at one type of balancing task it does not follow that he or she will be good at a different balancing task.
Not only is the transfer between superficially similar motor tasks quite low, but the performance of tasks in training that are similar (but not identical) to those used in actual performance can lead to negative transfer and a concomitant decrease in performance on the criterion task. For example, Mount [1996] examined the effect of learning a dart throwing skill in two different body positions (sitting on a chair and reclining on a table). Not only was performance poorer after switching position compared to remaining in the same position, but performance after practice in the alternate position was poorer than after no practice."


The article goes on to discuss resistance training movements so please check out the article here. However, I digress....

Ross Tucker and Jonathon Dugas spend considerable time arguing against Ericsson's 10,000 rule, with some key points, and you should definitely check out the blog mentioned above. However, I would suggest that Ericsson is perhaps misguided with his concept and has simplified what is a far more complex area than he presents.

For example the concept that 10,000 hours of training can make anyone elite does not consider the physiological training stimulus, e.g. the prescribed amount of exercise for each individual (it is not the same for everyone!). Tucker and Dugas discuss this and use it against Ericsson, however if you simply adapt the model to state that the 10,000 hours is required for skill acquisition then it becomes more realistic. In support of this is the concept that many people have a ceiling on their physical attributes, be it their height, or trainable variables like strength or endurance. Genetics will dictate how tall we grow as well as how strong we might be, or fit we can get, even with the right training.

A secondary consideration that I think is under reported is that 'elite' has a spectrum of it's own. Tim Henman would surely be considered an elite tennis player, and yet he never won a grand slam tournament. If you've got reservations on calling Tim 'elite' then consider basketball players in the NBA. They would surely be considered elite; essentially competing at the highest level, and yet they're not all Michael Jordan (not even Kobe Bryant). So you see that perhaps once a decade (or more or less frequent depending on sport, etc.) someone comes along with the genetics and the physical gifts, and the motivation (because we haven't talked about psychology at all!!), and puts in the right kind of training, and competes at the right era (how many elite athletes would have won a major tournament if it weren't for 1 or 2 others that dominated; Michael Jordan, Michael Schumacher, Tiger Woods, Pete Sampras, etc.).

On a final note we have to consider learning rate, some people might master a skill set in sooner than 10,000 hours, I'm sure you would agree. Therefore, logically on the other end of the spectrum some people will not master a skill set until having practised for considerably more than the 10,000 hours!

It is an interesting area, and I don't claim to be an expert on this, on the contrary I consider myself an intelligent lay-person on the area and as such, and as always; welcome any thoughts or comments.

Of course, don't waste your 10,000 hours typing a response, maybe you better get back to it.

Be Well

JF

Cholesterol....the truth: Part 1.

Let's do a quick Cholesterol 101 test....



Cholesterol causes heart disease right?

No wait bad cholesterol causes heart disease, and good ones prevent it right?

And bad ones are LDL (low-density lipoproteins), right?

And good ones are HDL (high-density lipoproteins), right?

And food containing cholesterol raises your blood cholesterol, right?

We all know this, right? I mean we know this?

Errr, no, no we don't know this, because it's all wrong. All of it. Take everything you think you know about coronary heart disease (CHD), and cholesterol, and foods containing cholesterol and bin it. Without hesitation let me clarify; you've been lied to all along. Truly. Read on and let me put things in perspective...

Over the next two blog posts (Part 1 & 2) I shall put to rest some of the existing concepts on cholesterol, saturated-fat and coronary heart disease, and then later discuss what actually causes heart disease. Hopefully.

Now I know some of you are already sceptical because this is what you've been told by the Government and Dr's and health professionals and governing bodies and government agencies. And they took us into Iraq after WMD's and they said that JFK was killed by a lone gunman from a book depository. At this point I'll give you a minute to decide whether you are government fed on prime b*llsh*t or whether you are a smart human being who can self-educate and challenge falsehoods.

Still here, good. Sorry, I had to do that to get rid of the ones who weren't sure.....

Cholesterol the villain.

Not good or bad cholesterol, just cholesterol.

Cholesterol comes from fatty food and is bad for you, right? Wrong. Cholesterol is made in the liver, and is ESSENTIAL for your hormones and for healthy living. People with very low cholesterol suffer from a condition familial hypercholesterolaemia, and without being too blunt; they mostly die young. Very young in some cases. There is no good or bad cholesterol, there is cholesterol (as you will go on to read). So first off scrap the idea that cholesterol is bad. It isn't. I know you're leading on to good and bad cholesterol so just stay with me, remember you've left all you thought you knew at the door so stop trying to protect your previous ideas.

Blood cholesterol
So we can have blood cholesterol measured right, and this is a risk factor for CHD, yes? No; cholesterol does not dissolve in blood, so it is transported around the body via a lipoprotein. This also transports fats, and proteins. The biggest of these molecules is actually called a chlomicron; basically this is manufactured in the gut and fills with triglyceride (fat) along with a little cholesterol. the chlomicron then travels straight to fat cells where the fat is deposited and the chlomicron then basically shrivels up and is returned to the liver. below chlomicrons we have VLDL (very low-density lipoproteins), then IDL (intermediate-density lipoproteins  - no, we don't talk about these much (at all!)) then LDL, then HDL. VLDLs are produced in the gut and in the liver, when they lose some triglyceride to fat cells a VLDL becomes an IDL, then when it shrinks down further it becomes an LDL, and then our HDL is the smallest lipoprotein. So....somehow Lipoprotein became interchangeable with the word cholesterol. They are not the same thing.  Don't confuse them again. You do not have blood cholesterol measured.

Now basically what you've probably been led to believe is that HDLs (the supposedly good lipoprotein) travel around the body and when they find a plaque on an artery wall filled with cholesterol they kind of suck it out and then take it back to the liver for processing. Have a think on that for a second, and then laugh hysterically at how preposterous that is. I mean really, we must have some good evidence to back up this silly idea. Oh, we don't have any evidence, oh it's just an idea? Oh, OK then, shall I believe you anyway based on faith of pharmaceutical companies looking to sell me on this idea so that they can sell me 'cholesterol lowering statins'....it's a tough decision. We might come back to this point.

Saturated Fat
So this bit you know, right? Saturated fat is bad, right! That raises LDL's!!?....That was a test - you're meant to leave your pre-conceived ideas 10 minutes in to the past!! Saturated fat is transported via chlomicrons (well remembered) in to fat cells so it doesn't effect LDL levels at all. If you want to read about the glory that is saturated fat then go back to my palaeo blogs, this blog isn't about saturated fat, it's about cholesterol. Even the saturated fat that does get to the liver doesn't effect cholesterol, none of the so-called experts would tell you this because we know it doesn't. So what does raises LDL levels....well LDL's come from VLDL's so what raises VLDL levels....carbohydrates (you might have guessed eh!). See all the previous palaeo/low-carb blogs I've written. But to make this worse, saturated fat actually LOWERS VLDL's!! You're not sold on this....see what the Journal of the American Medical Association (JAMA) think about this (abstract only I'm afraid), or click here for a full systematic review. Or even check this out:

"In the a recent study, presented at the annual scientific meeting of the American Heart Association in Chicago, Duke University researchers randomly assigned 120 overweight volunteers to the Atkins diet or to the American Heart Association's low-fat “Step I” diet. People on the Atkins diet restricted their carbohydrate intake to less than 20 grams a day, with 60 percent of their calories coming from fat. 

After six months, participants on the Atkins diet had lost 31 pounds, had an 11 percent increase in HDL (good cholesterol) and a 49 percent drop in their tryglyceride levels (LDL). Step 1 dieters lost 20 pounds, showed no change in HDL, and their tryglycerides fell 22 percent. In particular, there was a strong link to VLDL type of cholesterol -- the cholesterol type most related to heart disease risk. Atkins dieters had a 49% reduction in VLDL levels, versus 17% for those on the low-fat group."

Apologies that it refers to lipoproteins as cholesterol; you all know better than that now. But still the point is there....

So what we're saying is that VLDL levels drop when you eat fat. So this should lower LDL levels as well then. Ah, no. I've not given you the whole truth yet. You see, it really doesn't matter what our VLDL levels are, our LDL levels are almost unaffected by this! They know this, now you know this. They don't know why though.  What they tell you is this "If you eat saturated fat, then this will reduce the number of LDL receptors - the things that lock on to LDL and pull it out of the bloodstream - thus causing the LDL level to rise". What they don't tell you is there is no connection between saturated fat consumption and the needs of cells around the body to absorb LDL (see article from the Journal of the American Osteopathic Association). 

In case you're getting a bit baffled by all of this, (which you actually should be, as you will see in a second) let me introduce to you a scientific method pioneered and used by two researchers Law and Wald in their consideration of the diet-heart/cholesterol is bad hypothesis; teleoanalysis. Genius'. Oh you don't know what that is? Ok, well here is what they define it as doing....

"provides the answers to studies that would be obtained from studies that have not been done and often, for ethical and financial reasons, could never be done." 

Translated by me as "makes up data to support or prove our unproven or currently unprovable hypothesis!".

Cholesterol levels, stroke and death
Subheadings don't come more blunt than that, and whilst I can hear you screaming that I've said that cholesterol doesn't cause CHD, please read on....

Just to add to the mix I'm going to begin including the condition of a stroke. A stroke is most often caused when a plaque at the base of the neck (carotid artery) breaks off and then travels into the brain. As the arteries get narrower it gets jammed and blocks the blood flow. The reason I mention this is that if a stroke is caused through a similar process to CHD (e.g. the formation of cholesterol filled plaques) then if LDL levels cause CHD, then they should also be associated with an increase in stroke. Right? Err, no.....In 1995, The Lancet published a massive study that considered 450,000 people over 16 years including 13,000 strokes, and concluded "There was no association between blood cholesterol and stroke". Ah.

In fact, a 2004 study in the journal Stroke reported the following from a 15-year study of Japanese persons; "...the risk of death from stroke was reduced by 64% in the high cholesterol consumption group. Animal protein was not significantly associated with stroke after adjustment for animal fat and cholesterol. This suggests that....a high consumption of animal fat and cholesterol was associated with a reduced risk of cerebral infarction (stroke) death".

At this point I could begin citing a plethora of research which has linked low cholesterol levels with death. not death by CHD, or stroke, but simply death. E.g. that higher cholesterol levels are better for you than lower ones. There is a small mountain of research out there. If you need the information I can forward it on, or you can go and read pages 87-100 of Dr. Malcolm Kendrick's "The Great Cholesterol Con", (or you could use google for something better than you currently do). Yes, I have just revealed my source. This is an absolutely amazing book. Irrespective of your thoughts around my blog you should read this book. It should be everyone's birthday and Christmas present (or at least those you care about).

Summary
The point, other than the fact that I am not trying to rip-off the book and give you all the evidence, is that I am trying to deliver a simple message to people who should know better and to people who might discuss this and pass it forward to others.

Kendrick makes a brilliant reference back to a (mad - my addition) scientist; Iribarren and his hypothesis throughout the book, about proving and disproving a hypothesis, and how to make something fit. To summarise the final section I have talked about regarding the relationship between low cholesterol and death - and the kind of adaptation to a hypothesis that Iribarren would make; researchers have summarised that a persons low cholesterol must be a marker of some disease which is ultimately killing people (as opposed to it actually being low cholesterol (because we are still trying to say that we know that low cholesterol is good)...). But how do we know that they have a disease, well because their cholesterol is low, and they're dying.....sigh. You see what you're fighting against.

I know this has only been a brief introduction to this area, but hopefully we have dispelled some of the myths surrounding this area.

As always, comments or thoughts are very welcome, Part 2 will follow very shortly.

Be Well

JF