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Chasing the wrong rabbit – why cholesterol levels are just a distraction

CholesterolThere is a 30 billion dollar industry supporting the use of statins for both primary prevention and secondary prevention (after the fact) of heart attacks.  Similarly, hundreds of millions in studies have been spent to “justify the use of statins”.  The JUPITER study is the most recent.  I have already commented on my expectation that Big Pharma will try to position statins as “anti-aging” drugs as soon as enough people are saying the words “anti-aging” to make it OK for conservative medical doctors to look at those words without screaming “fraud and quack”.  To jog your memory, recall my comments on the “Is it Low T” scenario. I still laugh at all the abuse I took in the first 8 years of this century until Big Pharma came out with an acceptable drug for “Low T”.

OK, back to cholesterol and the big 30 billion dollar myth.

Statin drugs lower LDL and this is where, purported anti-aging effects notwithstanding, the major focus of the scientific literature has been.

What an absolute waste!

If you look at the Eskimo population that eats a traditional diet, and the traditional Japanese diet as well, you find loads of people who have high cholesterol.  You will also find more than you’d expect with high blood pressure and, especially in the Eskimos, significant obesity.  But you find almost no heart disease.

No, I am not tricking you by misrepresenting high HDL (good cholesterol) as part of this number. Many of these people do have higher than average good cholesterol but they also have LDL bad cholesterols that would prompt any self-respecting family doc, internist or cardiologist to whip out the ubiquitous prescription pad and start writing for statins and more statins.

OK, so it must be genetics or epigenetics, right? Somewhere, buried in the Eskimo and Japanese genome, there is a magic allele (a variant of the typical gene) that allows these people to stave off heart attacks in spite of too much bad cholesterol, right!?

Wrong!

The whole thing is very simply the effect of their diet because when you take these populations and stick them on our food pyramid or “traditional Western Diet” they develop heart disease and all the other things we get, at exactly the same rates, if not more.

Bottom line: the risk of heart disease in any population is directly related to the Omega6/3 levels.  The higher the tissue levels of Omega 3 (and yes, the blood levels as well), the lower the risk of heart disease.

I tell people to shoot for 1 to 1 Omega 6 to 3, but most of these populations are closer to .85. In other words, they are Omega 3 dominant.  And no, they don’t bleed to death (unless you shoot them), they don’t smell like fish, and the LDL particles that are supposedly causing harm in this situation either go away after a few months on a highly dominant Omega 3 diet or, as in the case of the above populations, they don’t matter.

LDL may wander into an inflammatory lesion and get oxidized but the toxic effects are caused by high Omega 6 levels unbalanced (e.g. in the presence of low Omega 3 levels) in the first place.

The real culprit is free fatty acid release from the liver, which must take place in order for cholesterol to be released as well. Free fatty acid release is caused when the liver gets too many calories in a single bolus to handle them, so it sends them out into the blood where they, along with the Omega 6’s, do the damage.

The cure for free fatty acid release is:  Don’t eat so damn much at one sitting!

So heart disease could be reduced by several hundred thousand people a year by combining the following:

1)         Reduced Omega 6 intake

2)         Increased Omega 3 intake

3)         Smaller meals and, if needed, small snacks in between

You can do most of this with diet alone but the majority of people, myself included, like to eat with other people socially and are more “omnivorous” than we might need to be. Secondly, I don’t really like fish all that much and I do not want all the mercury and other toxins that are in many different fish species, even though the FDA says a little mercury won’t hurt.

There are absolutely no long term studies on “a little mercury consumption”.  My way of thinking is a little over a long period of time can be very deadly, especially since mercurial dementia is not a typical part of the differential diagnosis of Alzheimer’s.  Also I do not want to count on today’s breed of ADD doctors to remember to check for mercury toxicity in a demented 80-year-old?! NO thanks! I will just avoid mercury.

I can’t count on them to chase the right rabbit!

This is why I have my fish oil purified to parts per trillion.

Doc

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Lengthen Telomeres With Your Food Choices

veggies and telomeresOne of the most vexing problems I face as an expert on telomeres and telomerase activation is the issue of diet and telomere length.  The problems come in many forms such as using vaguely related or truly unrelated studies to support an eating agenda, using poorly designed studies with inadequate measurements to claim positive results, and the complete lack of 3rd party verification to support  statements.

Examples of these in order include: Paleo or Raw Food Veganism, claims made for Multi-Vitamins and telomere length and resveratrol as a telomerase activator. Each and every one of these things could be a blog in itself but for now let’s just stick with what we know about diet and telomere length.
First a diet rich in anti-oxidants supplemental or otherwise has been suggested as a good addition to any anti-aging program. But defining the specifics of that diet has not yet been done.  And as usual  there is contrasting results depending on who has done the study. Bottom line: makes sense but not proven.
Fortunately a recent study in Finland may help clarify this a bit more by tying fruit and vegetable consumption with telomere length. In women, vegetable intake was positively associated with white blood cell telomere length. Men consuming the most butter and least fruits had significantly shorter telomeres than those consuming the lowest amounts of butter and highest amounts of fruits.
Here is what they found:  “ In women, vegetable intake was positively associated with LTL (P=0.05). Men consuming the most butter and least fruits had significantly shorter telomeres than those consuming the lowest amounts of butter and highest amounts of fruits.”
They also found that total fat intake and especially Saturated Fats were associated with short telomere length.  They tried to find an association with meat consumption ala the China Study but did not find it to be a dietary villain here.
It would be truly wonderful to do a full blown randomized placebo controlled study on diet and telomere length but this is almost impossible.  Getting people to live in a bubble for 12 months is going to cost you big time and the line of volunteers wouldn’t be very long.
Until then we have to live with the same old boring advice of eat more veggies, maybe some more fruit and avoid saturated fats.  This looks like it will slow down telomere loss and reduce the speed of aging.
This coupled with the reversal of short telomere length by TA-65 is a pretty compelling way to live longer and healthier!
Doc
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Your control over cancer

I hope I am not confusing you with my stance on epigenetics.  Ever since we wrote our book The Immortality Edge (Wiley 2010) I have stressed the role of things like diet, meditation, supplementation, exercise and sleep regulation, as a way of influencing your future health, wellness and longevity. In my Longevity Now talks last year, I reviewed how these things affected epigenetics and predicted, at that time, epigenetics would be the hot topic to come.  And now it is.

There is good news and bad news. Bad news first. Epigenetic study is probably not going to reveal a whole lot of new human behaviors that will modify your future.  Again, reference our book. One commenter, on Amazon, noted that “eating right, exercising and meditation are hardly new”, whining that he/she wanted “new” stuff.  Sorry, my friend, what has worked since the dawn of man will continue to work at a micro (telomeres and epigenetics) and macro (your health and wellness) level.  Additionally, the bad news is we know less about the epigenome than the genome. What I wrote about two years ago and spoke about last year, is becoming apparent: we know less about something that may be far more important than our genes in determining our fate!

Final piece of bad news: in spite of what the usual suspects are telling you, we do not know all that much (other than eating right, meditating, exercising, and supplementing) about how to create really favorable epigenomes, out of not so favorable ones. So while “yoga for epigenetics” or “Our diet or diet pill for epigenetics” or “exercise programs for epigenetics” makes sense, they are as yet unproven, so the claims are to be taken carefully, please.

The good news is that there is tremendous interest (funding) for all that and because of ever increasing computer power and global connectivity, the answers will come flooding in over the next few years, faster than ever!

What is likely to happen first is the disease based model we have lived with in medicine for centuries. Scientists will be looking to develop tests and drugs, to combat unhealthy epigenomes – while Mother Nature has already supplied the answer!

Cancer is one area where there is a flurry of epigenetic research and colon cancer, my personal greatest fear, is tops on the list, as of today, with breast cancer a close second.

A recent article, referenced below, has identified something called VELs, Variant Enhancer Loci that can be used to predict the risk of colon cancer. These are not part of the genome, but rather the epigenome.  They represent methylation gains and losses in thousands of histones (proteins attached to DNA – histones really are the major physical arbiters of epigenetics!) spread across the entire genome.  Since this pattern of changes is strongly predictive of colon cancer risk, it will surely be developed into a “pre test” for said cancer, allowing us to see a person at risk, long before a polyp or cancer develops.  And of course it then allows for follow up testing and a chance to change that epigenetic expression by the doctor and the patient. It does not alter your genetics and if you have high risk genes, you can’t change that. But, by far, most people succumb to their epigenetics, not their genetics, so you really can change the balance of these epigenetic marks, from sickness to health.

In case you are wondering about the role of telomeres here, an increasing percentage of short telomeres is almost always found in these situations, so therapy there may also help reverse the damage.

You will soon see profiles for other types of cancer, heart disease and diabetes, as well.  All of these are markers for accelerated aging, in my book, so I am going to predict a significant overlap in these epigenetic marks. Further, I am going to predict that the central clearing house for these effects will be the telomere.

Speaking of books, if you want to know what you can do to clean up your epigenetics, make sure you read our book, The Immortality Edge,  because everything that helps the telomere helps your epigenetics as well!

Stay tuned to the newsletters and blogs so you can get the developments in honest, unadulterated fashion.

Doc

Science. 2012 Apr 12. [Epub ahead of print]

Epigenomic Enhancer Profiling Defines a Signature of Colon Cancer.

Akhtar-Zaidi B, Cowper-Sal Lari R, Corradin O, Saiakhova A, Bartels CF, Balasubramanian D, Myeroff L, Lutterbaugh J, Jarrar A, Kalady MF, Willis J, Moore JH,Tesar PJ, Laframboise T, Markowitz S, Lupien M, Scacheri PC. Source

Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH 44106, USA.