Health for life

If you read my last post about cholesterol-lowering drugs, then you understand some of the problems that can arise from their use.  Statins can produce some nasty side effects.  But side effects aside, statins save lives right?  I mean, doctors prescribe them to just about everyone, they must be effective.  Not quite... the story is not as simple as it may seem.

When looking at the statin drug clinical trials, its important to keep a few things in mind.  Firstly, and most importantly... total mortality is more important than heart disease mortality.  If a drug prevents you from dying of heart disease but doesnt affect your chances of dying in general, then that drug is not worth taking.  Whats most important is whether or not the drug will extend your life.  Secondly, you must consider that different groups of people may respond differently to the drug.  Women, middle-aged men, the elderly, and those with preexisting heart disease may all respond differently to treatment. 

Id like to begin by talking about women... both because I like women, and because they dont respond well to statins.  Although many statin studies notoriously neglect to reveal the all-cause death data for women, there are a few studies that do.  Check out the Scandinavian Simvastatin Survivial Study (4S), which was one of the most positive trials to date.  The big pharma folks must have been partying it up when this one came out.  This was a secondary prevention trial, meaning that participants all had pre-existing heart disease (previous heart attack or angina).  For future erence, a primary prevention trial would be an experiment in which the participants did not have pre-existing heart disease.  So, half of them took simvastatin and half of them took a placebo.  The results were great across the board: heart attack numbers were reduced, along with deaths from heart disease and all-cause mortality.  But there was one group that clearly didnt benefit:  women.  Over the duration of the 5.4 years of the trial, 27 (6.6%) of the women taking the statin died, while only 25 (6%) of the women taking the placebo died.  So despite the rest of the data, which was very supportive of statins, there was actually a slight increased risk of death in women from taking the statin.  As youll soon see, this finding is consistent throughout all of the statin trials, yet it is completely ignored by mainstream medicine.  These drugs simply dont work for women.


Now, men are a bit of a different story.  Its important to split men up into two distinct groups:  those with diagnosed heart disease (previous heart attack or angina), and those without diagnosed heart disease.  In those without heart disease, statins appear to be largely ineffective.  Both the University of British Columbia and Dr. Graham Jackson in the UK have published review articles looking at many of the primary prevention statin trials.  These were both reviews of the existing research, and they did not pick and choose studies that would support one side or the other.  Heres a key statistic from the UBC paper:  "71 primary prevention patients with cardiovascular risk factors have to be treated with a statin for 3 to 5 years to prevent one myocardial infarction or stroke."  And heres one from Dr. Jacksons study:  "Long term use of statins for primary prevention of heart disease produced a 1% greater risk of death over ten years versus placebo when the result of all the big controlled trials reported before 2000 were combined."  Although both studies showed reduction of cardiovascular deaths in those taking statins, overall deaths were either the same or higher.  Oh, and they also found zero effect on cardiovascular deaths in women.  Sounds like statins arent so effective in those without pre-existing heart disease. 

And Ive got more.  In 2005, a study called ASCOT-LLA, which studied Lipitor on high blood pressure patients, was stopped early due to the supposed "massive" reduction in cardiovascular deaths experienced by the Lipitor group.  The researchers considered the benefits so great that it was unethical to continue to deprive the placebo group of proper treatment. This study is considered to be one of those landmark trials that proved once and for all the life-saving benefits of statins.  Well, lets look at the data... youll have to click to enlarge it.



In that first set of data, Id like to draw your attention to the "all-cause mortality" graph in the bottom right.  See that vertical line there that Ive drawn in?  Thats a little trick I learned from Dr. Malcolm Kendrick in his book The Great Cholesterol Con.  The reason that line is drawn in there is because the trial ended at 3.3 years.  The graphs, however, show data until 3.5 years.  If you look closely at the graph, at 3.3 years there is almost no difference between the Lipitor group and the control group, but for the last 0.2 years of the study, the two lines begin to suddenly separate.  WTF mate?  How does one acquire data for a study after the study has ended?  Something seems fishy to me...  tampering of evidence perhaps?  No way to know for sure, but I can say with certainty that there was no reason to shut down this study early.  Theres virtually no difference in the all-cause mortality data.  Oh, and that second graph... thats showing the effectiveness of Lipitor on cardiovascular mortality (note: NOT all-cause mortality).  Notice women in this trial had an increased risk of dying from heart disease on the drug.

To sum up the statin drug data, heres a convenient table copied again from Dr. Malcolm Kendrick:


You can see here that the 4S trial, which I discussed earlier, was overall very supportive of statin use.  This trial was purely a secondary prevention trial.  And I must admit that statins do appear to save lives in men with previous heart disease.  But that is the ONLY group for which they save lives.  Purely primary prevention trials, like EXCEL, actually showed in increase in all-cause death on statins.  And then there are trials like WOSCOPS, which was a mix of primary and secondary prevention, and those trials typically yield results somewhere in the middle of the extremes.  Even in the most positive statin data for those with pre-existing heart disease, however, the results are really underwhelming.  You would think that with all the hype surrounding these supposed "life-saving" drugs, the data would be a little stronger.  Even if you do have pre-existing heart disease, and are a man, you can only expect about a 3% reduction in the chance of dying over the next several years.  That is just unimpressive to me.

So despite the relentless pushing of these drugs by big pharmaceutical companies, mainstream doctors, and my Anatomy and Physiology professor, caul examination of the data shows a surprising lack of evidence to support their use.  Statins decrease the risk of dying of heart disease; thats good.  But they dont decrease the risk of dying overall in the majority of the population; thats bad.  So then, if heart disease deaths are decreasing but overall deaths are not, statins must be increasing the risk that youll die of something other than heart disease.  Im even going to go as far as to say that they cause these non-cardiovascular-related deaths. Unfortunately, most studies fail to specify exactly what these non-cardiovascular deaths are, but take a look at my previous post for an idea.  If youre a woman, statins wont even reduce your risk for heart disease, and they actually increase your risk of dying overall.  The only population for which statins can save lives is men with pre-existing heart disease, which is less than 5% of the population.  If youre one of those people, take your statin if youre so inclined.  But if youre anyone else, especially a woman, you are barking up the wrong tree.

Researchers at the Linda Crnic Institute for Down Syndrome and the University of Colorado School of Medicine have found that a single mechanism may underlie the damaging effect of cholesterol on the brain and on blood vessels.

High levels of blood cholesterol increase the risk of both Alzheimers disease and heart disease, but it has been unclear exactly how cholesterol damages the brain to promote Alzheimers disease and blood vessels to promote atherosclerosis.

Using insights gained from studying two much rarer disorders, Down Syndrome and Niemann Pick-C disease, researchers at the Linda Crnic Institute for Down Syndrome and the Department of Neurology of the University of Colorado School of Medicine found that cholesterol wreaks havoc on the orderly process of cell division, leading to defective daughter cells throughout the body.

In the new study published this week in the on-line journal PLOS ONE, Antoneta Granic, PhD, and Huntington Potter, PhD, show that cholesterol, particularly in the LDL form, called bad cholesterol, causes cells in both humans and mice to divide incorrectly and distribute their already-duplicated chromosomes unequally to the next generation. The result is an accumulation of defective daughter cells with the wrong number of chromosomes and theore the wrong number of genes. Instead of the correct two copies of each chromosome, and thus two copies of each gene, some cells acquired three copies and some only one.

Granic and Potters study of the effects of cholesterol on cell division included a prominent finding of cells carrying three copies of the chromosome (#21 in humans and #16 in mice) that encodes the amyloid peptide that is the key component of the neurotoxic amyloid filaments that accumulate in the brains of Alzheimer patients.

Human trisomy 21 cells are significant because people with Down syndrome have trisomy 21 in all of their cells from the moment of conception, and they all develop the brain pathology and many develop the dementia of Alzheimers disease by age 50. Earlier studies by Granic, Potter and others have shown that as many as 10% of cells in an Alzheimer patient, including neurons in the brain, have three copies of chromosome 21 instead of the usual two. Thus, Alzheimers disease is, in some ways, a form of acquired Down syndrome. Furthermore, mutant genes that cause inherited Alzheimers disease cause the same defect in chromosome segregation as does cholesterol, thus indicating the presence of a common cell division problem in both familial and sporadic (non-familial) Alzheimers disease.

The new research also found trisomy 21 neurons in the brains of children with what, until now, was thought to be an unrelated neurodegenerative disease (Niemann Pick type C), caused by a mutation affecting cholesterol physiology. This result suggests that neurodegeneration itself might be linked to chromosome missegregation.

Such a model is supported by the finding of Thomas Arendt, MD, and colleagues at the University of Leipzig that 90% of the neuronal cell death observed at autopsy in Alzheimer patients is due to the creation and selective loss of neurons with the wrong number of chromosomes.

Identifying the specific problem caused by cholesterol will lead to completely new approaches to therapy for many human diseases, including Alzheimers disease, atherosclerosis and possibly cancer, all of which show signs of defective cell division. Granic and Potter already have found a potentially simple approach to preventing cholesterol from causing cells to distribute their chromosomes unequally into their new daughter cells. Specifically, when cells in culture were first treated with ethanol, the subsequent exposure to bad cholesterol was without effect on cell division: Each daughter cell received the correct number of chromosomes.

Its been too long since Ive spoken about cholesterol, too long I tell you. For those of you who dont know, I would sum up my view on cholesterol like this: its the most overhyped risk factor for heart disease there is. All you hear in the media is "Watch your cholesterol!" or "Cheerios lower cholesterol!" or "This food is cholesterol-free, so its good for you!". Bollocks. Bollocks I say.

First of all, the cholesterol in the food you eat barely has any effect on the cholesterol in your blood, if it has any effect at all. And second, lets set the record straight on "high cholesterol"... please for the love of God, quit worrying about it. Your total cholesterol is just about meaningless unless its taken in context with your triglycerides, HDL, and LDL... even better, your LDL particle number. Despite having no real, accurate clinical implications though, "high cholesterol" has taken on this sort-of boogey man role, scaring every health-conscious person into Lipitor land.

Anyway, I came across something today that was just too good not to write about; this stuff needs to be shared. This study was designed to analyze lipid-lowering therapy, but thats not the part I want to talk about here; its the cholesterol levels of the patients that piqued my interest. The researchers examined 65,396 patients hospitalized for heart disease (heart attack or angina) across the United States. Below youll find a screenshot of the baseline blood lipid data, taken within the first 24 hours of admission. You would expect, based on what you think you know, that heart disease patients must have had high cholesterol, right?

Average blood lipid values upon admission among all study participants.

Nope. On average, their cholesterol was 170.1 mg/dl, well below the high limit of 200. If any of these people had visited the doctor for a check-up a week before their hospitalization, the doc would have looked at these numbers and said "Steve, your cholesterol is great! Keep up the great work!" Assuming his name is Steve.

But things werent great. Each of these people experienced an acute coronary event that required hospitalization and very well could have ended their lives. Its irresponsible that were putting so much stock into cholesterol values when they clearly are NOT a good indicator of heart disease risk.

Sometimes it only takes one little piece of data, like this one, to completely change your beliefs on cholesterol and heart disease. I hope this provided the baseball to your brand new home window.

But what does this mean??
Now, theres an excellent chance that many of these people were already taking a cholesterol-lowering drug. Theres no data in the study to show whether this is true, but since so many people are on them, its very likely. So lets say for a moment that they were on statins. Say their normal cholesterol levels are around 220 mg/dl, and the statins bring it down to a more friendly-looking 170. Well, this only destroys the cholesterol and heart disease connection even more doesnt it? First off, it doesnt say much about the efficacy of the drugs. But also, it shows that reducing cholesterol from "high" back into "normal", at least via these mechanisms, is useless.

Okay, let me say it another way... if high cholesterol is the cause of our problems, lowering it should reduce our risk, regardless of the manner by which we do so. If it is not the cause, and it is just an indicator of a problem, then pharmacologically lowering it will NOT reduce our risk. It will, in fact, just make things appear to be fine when they are not.

Its sort of like when we get sick and we get a fever. We may take over-the-counter meds to reduce the fever; it makes us feel better and it takes away one of the symptoms of our illness. But we forget that the fever is an important part of our bodys defense mechanism to fight a bacterial infection... bacteria dont like the heat. We may feel a little better, but we remain just as sick as we were before, and weve now likely prolonged our sickness by messing with our bodys natural defense mechanisms.

The fever is like cholesterol, the symptom. The bacterial infection is the root cause. Got it? Okay its not a perfect analogy, but you get the point.


What is the root cause of heart disease then? If not total cholesterol, what should we focus on? Well thats a big can of worms... there are many factors that go into it. Stay tuned next week for a comprehensive guide on how to prevent heart disease!

If youre active, watch your diet, and have been successful at maintaining a healthful weight, you may have managed to keep your cholesterol levels under control ... or not. Lifestyle wields control over your cholesterol response but so do your genes. Its quite possible that no matter how hard you work to keep your cholesterol levels down, the influence of your familys genes could thwart it.

A study due out in the July 8 issue of the American Journal of Clinical Nutrition found just that. Researchers tested the cholesterol response in identical twins (with identical genes), and found their levels were about the same - even though one exercised regularly while one was relatively sedentary, even though one ate a low-fat diet while the other ate a high-fat one.

Lifestyle matters, but its always a good idea to monitor and manage your lipid levels with your healthcare provider.

________
For a summary of the study:
Bad Cholesterol: Genes Make the Difference

For the study itself:
Concordant lipoprotein and weight responses to dietary fat change in identical twins with divergent exercise levels

Laurel Miller, via Salon.com, reviewed Mark Bittmans new cookbook, "Food Matters: A Guide to Conscious Eating With More Than 75 Recipes." (Bittman writes a food column for the New York Times and blogs for the NYTs at Bitten.)

How To Live What Michael Pollan Preaches, Salon.com, January 2009

Here are some excerpts from her article:

"[Bittmans book is] an unusual blend of manifesto, self-help manual and cookbook designed to convince people that they can drastically improve their diets with relatively little discomfort."

Bittmans formula: "Eat less of certain foods, specifically animal products, ined carbs, and junk food; and more of others, specifically plants, in close to their natural state."

"At 57, [Bittman had] gained 50 pounds over his college weight and had developed high cholesterol, high blood sugar (especially scary for someone with a family history of diabetes) and sleep apnea, a condition caused by his excess weight."

Bittmans specific tactics ...

"With a colleague, Kerri Conan, Bittman devised a plan they called "vegan until six." They ate almost no animal products at all until dinnertime, no simple carbohydrates and no junk food. (Simple carbs are sugars, white flours and other processed grains like white rice.) At dinner, they ate as they had before, although in time Bittman found that even his evening meals came to include more "vegetables, fruits, legumes and whole grains and less meat, sugar, junk food, and overined carbohydrates."

"It was easy, and in a matter of months hed lost 35 pounds, lowered his cholesterol and blood sugar, and had no trouble sleeping through the night. Most important, he continues to eat this way and is content to do so for the rest of his life."

________

A byproduct of cholesterol functions like the hormone estrogen to fuel the growth and spread of the most common types of breast cancers, researchers at the Duke Cancer Institute report.

The researchers also found that anti-cholesterol drugs such as statins appear to diminish the effect of this estrogen-like molecule.

Published in the Nov. 29, 2013, edition of the journal Science, the findings are early, using mouse models and tumor cells. But the research for the first time explains the link between high cholesterol and breast cancer, especially in post-menopausal women, and suggests that dietary changes or therapies to reduce cholesterol may also offer a simple, accessible way to reduce breast cancer risk.

"A lot of studies have shown a connection between obesity and breast cancer, and specifically that elevated cholesterol is associated with breast cancer risk, but no mechanism has been identified," said senior author Donald McDonnell, Ph.D., chair of the Department of Pharmacology and Cancer Biology at Duke. "What we have now found is a molecule – not cholesterol itself, but an abundant metabolite of cholesterol – called 27HC that mimics the hormone estrogen and can independently drive the growth of breast cancer."

The hormone estrogen feeds an estimated 75 percent of all breast cancers. In a key earlier finding from McDonnells lab, researchers determined that 27-hydroxycholesterol – or 27HC – behaved similarly to estrogen in animals.

For their current work, the researchers set out to determine whether this estrogen activity was sufficient on its own to promote breast cancer growth and metastasis, and whether controlling it would have a converse effect.

Using mouse models that are highly predictive of what occurs in humans, McDonnell and colleagues demonstrated the direct involvement of 27HC in breast tumor growth, as well as the aggressiveness of the cancer to spread to other organs. They also noted that the activity of this cholesterol metabolite was inhibited when the animals were treated with antiestrogens or when supplementation of 27HC was stopped.

The studies were substantiated using human breast cancer tissue. An additional finding in the human tissue showed a direct correlation between the aggressiveness of the tumor and an abundance of the enzyme that makes the 27HC molecule. They also noted that 27HC could be made in other places in the body and transported to the tumor.

"The worse the tumors, the more they have of the enzyme," said lead author Erik Nelson, Ph.D., a post-doctoral associate at Duke. Nelson said gene expression studies revealed a potential association between 27HC exposure and the development of resistance to the antiestrogen tamoxifen. Their data also highlights how increased 27HC may reduce the effectiveness of aromatase inhibitors, which are among the most commonly used breast cancer therapeutics.

"This is a very significant finding," McDonnell said. "Human breast tumors, because they express this enzyme to make 27HC, are making an estrogen-like molecule that can promote the growth of the tumor. In essence, the tumors have developed a mechanism to use a different source of fuel."

McDonnell said the findings suggest there may be a simple way to reduce the risk of breast cancer by keeping cholesterol in check, either with statins or a healthy diet. Additionally, for women who have breast cancer and high cholesterol, taking statins may delay or prevent resistance to endocrine therapies such as tamoxifen or aromatase inhibitors.

The next steps for research include clinical studies to verify those potential outcomes, as well as studies to determine if 27HC plays a role in other cancers, McDonnell said.

In recent years, the prescription of statin drugs to reduce cholesterol has soared through the roof.  Youve heard of them:  Lipitor (atorvastatin), Crestor (rosuvastatin), Zocor (simvastatin), and the like. The supposed benefits of these drugs, as your doctor will tell you, is that theyll reduce your cholesterol levels, hence lowering your risk of heart disease.  Im sure you all know by now how I feel about lowering cholesterol levels (see this)... but thats beside the point in todays discussion.  I will just say that statin drugs effectiveness may have been a bit overstated.  Today, though, Id like to focus on the dangers, or side effects, one may encounter in taking statins.

First, just a little information about how statin drugs work in the body.  Their main function is to block an enzyme called HMG CoA Reductase.  This is one of the enzymes that is involved in making cholesterol in the liver.  So through blocking this pathway, the drug has inhibited the bodys ability to make cholesterol molecules.  As a result, your blood cholesterol level goes down, your doctor is happy, and youre happy.  Weve finally won the battle against cholesterol!  Yeah... except cholesterol is needed in the body for all sorts of vital processes, like hormone production, vitamin D synthesis, cell membrane structure, and brain function, just to name a few.  Hopefully by the end of this, youll realize how ridiculous it is to think that blocking an important biochemical pathway like this one is a good idea.





Meet Dr. Duane Graveline.  Dr. Graveline is a family doctor with a high cholesterol level, who began taking statins several years ago.  Shortly after starting on statins, he suffered a serious and disturbing loss of memory, so he stopped taking the drug.  He had no further problems for a year while off statins, so his doctor persuaded him to begin taking them again.  That high cholesterol needed to be treated.  Shortly after returning to the meds, Dr. Graveline experienced a much worse episode of memory loss, during which he regressed into his teenage years, unable to recall his training as a doctor at all.  After getting off the statins, though, his memory returned again.  Interesting huh?  Well Dr. Graveline decided to tell his story by publishing a letter on a website called Peoples Pharmacy.  Almost immediately, he was flooded with letters from hundreds of other statin-takers who had experienced a similar problem.  Clearly, something about these drugs was causing serious impairment in the brain.

On a related note, there has been consistent data since the 1960s showing that people taking cholesterol-lowering drugs tend to die more frequently from violent deaths, such as car accidents, suicides, and shootings.  This information has largely been disregarded for lack of a plausible explanation.

But how about this... 25% of the cholesterol in the body is concentrated in the brain.  Until recently, we didnt understand the reason why, but new research by Dr. Frank Pfrieger shows that cholesterol is absolutely essential to neuronal communication in the brain.  Cholesterol is so important, in fact, that without it the brain would be almost entirely useless.  So, now we have a very plausible mechanism to explain the mysterious amnesia experienced by Dr. Graveline and others.  That also may explain the increase in car accidents; lapses in brain function lead to mistakes on the road.  Low cholesterol, not necessarily as a result of statins, has also been shown to lead to reduced serotonin levels in the brain.  Low serotonin is one of the key brain abnormalities involved in depression, and it has been linked to increased violence and aggression as well.  Heres an example of a study that linked low cholesterol levels to increases in school suspensions and expulsions.  According to the researchers, "the results of the current study are consistent with the majority of previous studies examining the associations between low cholesterol and various forms of aggression in adults."  Looks like its no accident that those with low cholesterol are more likely to be suicidal or violent.  Still think blocking pathways is a good idea?  Read on.

As I mentioned before, statin drugs act on the enzyme HMG CoA Reductase, inhibiting its action.  While this prevents cholesterol synthesis, it also prevents synthesis of another important molecule that shares the same biochemical pathway.  This molecule is known as coenzyme Q10 (CoQ10).  This vital substance is found in every cell in the body, and in particularly high concentrations in high-energy cells such as muscles, especially the muscle cells of the heart.  CoQ10 is an important part of ATP synthesis, meaning that it is needed for your body to turn food into useable energy.  If cells run out of ATP, they die... so yes, CoQ10 is seriously important.  Which cells did I say had the highest concentrations of CoQ10?  Ohh yes, cardiac muscle cells!  And what will happen if your cardiac muscle cells run out of CoQ10, along with ATP?  Heart failure.  Thats right, the medication that is supposed to be protecting your heart can cause heart failure.  Incidentally, while heart disease rates have actually been on the decline in America, there has been a recent sharp increase in congestive heart failure.  Theres no evidence to prove statins are causing this recent phenomenon, but its certainly an interesting coincidence.

You know, every time I write one of these blogs, I try my best to be as concise as possible so that I dont end up with something so long that nobody wants to read it.  But, here I am again with another research-paper-length post.  Anyway, in conclusion here, Id like to reiterate the problems with blocking the pathway that makes cholesterol.  Cholesterol is an important molecule with a number of vital functions in the body, not the least of which is to allow the brain to function.  Without it, the brain is useless.  Think about that (with your brain) next time you take your statin drug.  And dont forget about that whole car accidents, suicide, violence thing.  Low cholesterol levels, resulting from statins or not, increase your risk for depression.  Also, blocking the cholesterol pathway prevents CoQ10 production, which is vital to every cell in the body, especially heart cells.  Without it, youre at risk for heart failure (the irony kills me).

The take-home lesson:  While taking a statin drug will make your cholesterol numbers look better, at least in your doctors eyes, there are serious problems with inhibiting cholesterol synthesis.  Cholesterol is far more important throughout the body than most people give it credit for.  And while it may be a risk factor for heart disease in certain populations, it is not the true cause... where is the logic in treating the innocent risk factor??  Its clear to me that the path to health does not lie in working against your bodys natural mechanisms; we need cholesterol, not statins.

A heart-healthy diet helped men at high risk for heart disease reduce their bad cholesterol, regardless of whether they lost weight, in a study presented at the American Heart Association’s Arteriosclerosis, Thrombosis and Vascular Biology 2013 Scientific Sessions.

The 19 24- to 62-year-old men in the study had metabolic syndrome, which ers to three or more significant risk factors for heart disease and stroke. The risk factors included in this study were high waist circumference, high blood pressure, high levels of triglycerides and fasting glucose and low levels of high density lipoprotein or HDL “good” cholesterol.

For five weeks, the men followed a standard North American diet which is high in fats, carbohydrates, ined sugar and red meat. For a second five weeks, they ate a Mediterranean-style diet, which is high in fruits, vegetables and whole grains, and low in red meat. It also includes olive oil and moderate wine drinking.

The men then went on a 20-week weight-loss regime, then another five weeks of Mediterranean eating.

Regardless of whether patients lost weight, following the Mediterranean-style diet resulted in a 9 percent decrease in levels of low density lipoprotein (LDL) known as “bad” cholesterol. Similarly, blood concentrations of the protein part of the lipoprotein, called apolipoproteinB, dropped 9 percent after eating Mediterranean-style. Apolipoprotein plays an important role in lipid transport and metabolism.

“The Mediterranean-style diet, or MedDiet, may be recommended for effective management of the metabolic syndrome and its related risk of cardiovascular disease,” said Caroline Richard, M.Sc., study lead author and a registered dietician and Ph.D. candidate in nutrition.

I hate to say I told you so.  But I did.  Like a million times.  Yet, the fear of cholesterol continues.  What is it?  Is it the Lipitor ads?  Is it your cholesterol-phobic doctor, determined to get your cholesterol under 200 mg/dl at all cost?  Whatever it is, its about time we stopped worrying so damn much about high cholesterol.  This new study, entitled "Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid?  Ten years prospective data from the Norwegian HUNT 2 study.", shows us why.  Did anybody hear anything about this one in the media??  I didnt think so, not with a catchy title like that.  At least now the 3 people that read my blog will be aware of it.  The researchers followed 52,087 Norwegians aged 20-74 who were free of cardiovascular disease (CVD) for 10 years, then assessed the relationship of total cholesterol with total mortality, CVD mortality, and ischemic heart disease mortality (IHD).  (Just to be clear, CVD mortality signifies deaths from any disease of the cardiovascular system, while ischemic heart disease ers only to diseases involving restricted blood flow to the heart.)  Lets jump straight into the data then, shall we?  And another note:  since this study comes from Europe, the units for blood cholesterol are shown in mmol/L, rather than the mg/dL that we are used to.  The researchers classified the participants into four groups, based on their blood cholesterol.  Here are the converted unit values in mg/dL for the four groups...  <193, 193-229, 230-269, and >270


First, the least shocking data.  This graph compares the association between cholesterol levels and death from ischemic heart disease.  For the men, it looks like theres not much variation.  Deaths from heart disease rose slightly along with cholesterol levels, but nothing dramatic.  Women, on the other hand, yielded a much more interesting result.  Clearly, by a LARGE margin, cholesterol below 193 mg/dL was most predictive of death from heart disease.  All other groups, including the group with cholesterol over 270 mg/dL, showed significantly lower risk.  Yes, seriously.  On to the next graph!




This one here shows the association between cholesterol and cardiovascular disease, or CVD, which includes heart disease with stroke and any other disease of the cardiovascular system.  Again, lets begin with the men.  The lowest risk appears to lie in those with total cholesterol between 193 and 229 mg/dL, but a close second is the next range up, from 230 to 269.  If you know your erence ranges, you know that anything over 200 is considered dangerous.  Does anybody ever bother to check why this is considered dangerous, or do we just accept it without question??  Clearly, the data from this study suggests that a cholesterol level in men between 193 and 269 is optimal for CVD prevention.  As for women... oops, looks like they screwed up the data there!  They must have it backwards!  Except they dont... yes, the data shows that if youre a woman, the higher your cholesterol is, the lower your risk of death from CVD.  Id repeat it, but Ill be doing that again shortly.  Read on to all-cause mortality!


Here we are, all-cause mortality... the only statistics that really matter.  Deaths from IHD or CVD are cool, but not nearly as cool as all-cause mortality.  This one cuts through the bullshit.  Its not your risk of dying from one disease that really matters, its your risk of dying overall.  So, for men... the group with the HIGHEST risk of dying overall had the LOWEST cholesterol (below 193 mg/dL).  Even those with a cholesterol level over 270 fared better.  The sweet-spot, protective level here was shown to be 193-229, a level that, based on the current erence ranges, will likely get you prescribed a statin drug for being too high!  Its just not right I tell ya.  And for the women, we see another complete inverse relationship between blood cholesterol and all-cause mortality.  High cholesterol appears to be protective for the ladies!  Maybe I could incorporate that into a pickup line somehow... but I digress.

So, does this prove anything?  No.  Not really.  Although it happens to be in accordance with what I believe, its all just observation.  But this isnt the only study to show this kind of trend, just the most recent; there are at least 20 others like it if you just follow that link.  And it certainly makes a strong case for women... having low cholesterol, in the healthy erence range, mind you, just appears to be straight up deadly!  Despite the studys inability to conclusively prove anything, that didnt stop the researchers from letting loose a little on the drug industry.  And I quote from the conclusion of the paper... "Many individuals who could otherwise call themselves healthy struggle conscientiously to push their cholesterol under the presumed danger limit, coached by health personnel, personal trainers, and caring family members.  Massive commercial interests are linked to drugs and other remedies marketed for this purpose."  That may not seem so harsh, but for a group of researchers to say this and imply that massive commercial interests are wrongly influencing the clinical guidelines... thats a pretty strong statement.  And I agree wholeheartedly.  The guidelines need to be reassessed.

What does this mean, though, if having high cholesterol isnt a bad thing?  What are the implications?  Well, for one, maybe it will get people off these ridiculous statin drugs.  But even more significant, to me, are the implications for saturated fat consumption.  These days, everyone just "knows" saturated fat is bad.  But if I asked you, could you tell me why?  The standard answer is, because saturated fat raises your blood cholesterol.  Well... um... so what?  If you step outside of this cholesterol=bad paradigm for a while, things start to look a bit different.  What else is known about saturated fat?  Well, if you eat more of it, it makes up more of your cell membranes, and its highly resistant to oxidative damage.  So thats good, it protects your cells.  And... short-chain saturated fats like butyric acid, found in butter, are burned perentially as fuel and promote proper immune function.  And... saturated fats enhance calcium absorption, along with all the fat-soluble vitamins (A, D, E, K).  And dont forget, if youre a woman, having high cholesterol appears to be beneficial.  Wait a minute... could saturated fat be... healthy!?  So much for a French paradox...

The issue of cholesterol is complex, to say the least.  You might not realize it from watching cholesterol-lowering drug commercials, or even from talking to your doctor.  But there is way more to the story than simply keeping your cholesterol low.  This will probably be a frequent topic on my blog, as there are so many aspects of it to be explored, but for today Id like to focus on total cholesterol.

Check out this very eye-opening paper.  Its an outstanding review of some of the more intriguing cholesterol research, and one of the few papers that Ive actually found difficult to put down.  I seriously couldnt stop reading it.  And it blew my mind.

According to several studies, older adults with higher cholesterol live the longest. In fact, groups with the lowest cholesterol levels typically have the highest morbidity rate.  Heres the breakdown from a couple of these studies...  Dr. Harlan Krumholz found in 1994 that old people with low cholesterol were twice as likely to die from coronary heart disease than those with high cholesterol.  Another study of 92 women aged 60 or over found that those with a total cholesterol level of about 270 mg/dl lived the longest.  Those with the highest cholesterol, over 300 mg/dl, were only 1.8 times more likely to die, while the lowest cholesterol group, 154 mg/dl, was 5.4 times more likely to die.

Interesting stuff huh?  That review paper discusses 20 studies just like these, where blood cholesterol levels were either not associated with cardiovascular disease or all-cause death, or there was an inverse relationship.  This quote from the paper sums up the situation quite nicely...

"It is true that high t-C is a risk factor for coronary heart disease, but mainly in young and middle-aged men. If high t-C or LDL-C were the most important cause of cardiovascular disease, it should be a risk factor in both sexes, in all populations, and in all age groups. But in many populations, including women, Canadian and Russian men, Maoris, patients with diabetes, and patients with the nephrotic syndrome; the association between t-C and mortality is absent or inverse; or increasing t-C is associated with low coronary and total mortality. Most strikingly, in most cohort studies of old people, high LDL-C or t-C does not predict coronary heart disease or all-cause mortality; in several of these studies the association between t-C and mortality was inverse, or high t-C was associated with longevity. These associations have mostly been considered as a minor aberration from the LDL-receptor hypothesis, although by far the highest mortality and the greatest part of all cardiovascular disease are seen in old people."

 In case youre having trouble with the terminology, t-C just means total cholesterol, LDL-C means LDL cholesterol.  A couple of key points here...  if cholesterol is the cause of heart disease, then shouldnt it be a risk factor for everybody, regardless of age, sex, or ethnicity?  It should.  But its not.  While cholesterol levels can be somewhat predictive of ones risk of heart disease, cholesterol doesnt cause the problem.  The second bolded quote is very key as well.  Studies done in older adults, like these ones showing that those with high cholesterol have less risk of cardiovascular disease, should not be taken as an aberration.  By far the highest risk group is adults over 60, so if the conventional wisdom doesnt hold true for them, it doesnt hold true at all.  These studies should indicate that our current thinking about cholesterol is highly flawed.  Cholesterol simply cannot be the cause of heart disease when it is so notoriously unreliable as a predictor of heart disease in the most at-risk populations.  Its that simple.

If youre a regular reader of this blog, you may know that I love to talk about cholesterol.  You know about my many blog posts on the falsity of the lipid hypothesis, the idea that high cholesterol causes heart disease.  Its been by far the most covered topic on my blog (1, 2, 3, 4, 5, 6, 7, 8, 9, 10).  Its always been a major topic of interest to me, because I feel so strongly that people are being misled when it comes to cholesterol.  Its my view that high cholesterol (recognized by most doctors as higher than 200 mg/dl) is completely overrated as a risk factor for heart disease, and that cholesterol-lowering drugs are unnecessary/useless/potentially harmful for 95% of the population.  Everyone is always so damn worried about their cholesterol, and they dont need to be.  So Im "that guy".  Im the guy who scoffs at doctors when they prescribe statin drugs for women with cholesterol levels of 210.  Im the guy who shakes his head when an otherwise healthy person returns from the doctors office upset about having high cholesterol.  And Im DEFINITELY the guy who laughs when you start eating egg white omelets every morning to fix it.  Thats just hilarious in so many ways.
Second test
My diet had not changed that significantly from the first to the second test, in which my total and LDL dropped dramatically.  I began to increase my carb intake a little, and I cut back on the conventional fatty meat for sure.  I ate more full-fat dairy and eggs, as well as some rice and potatoes.  The macronutrient ratios likely didnt differ much from that of the first test:  55% fat, 25% protein, 20% carbs.

Third test
I would say my diet has changed more from the second to the third test than from the first to the second.  I now eat significantly more gluten-free grains like rice and corn, as well as potatoes.  I still eat around 4 eggs each day and drink whole milk regularly.  But of course, meat, vegetables, and fruits are still a major part of my diet.  Oh, and grass-fed butter.  What would I ever do without you.  I would estimate my diet at about 40% fat, 25% protein, 35% carbs. 

Theres no question that high levels of good cholesterol—also known as high-density lipoprotein (HDL)—seem to be protective against heart disease. Rather than depositing fat into the blood vessels the way the "bad" cholesterol (low-density lipoprotein (LDL)) does, HDL appears to carry cholesterol away from blood vessels to the liver. From there, the liver processes it for removal from the body.

However, adequate levels of HDL might not be enough. Several recent studies have suggested that many cases of heart disease occur in people with normal levels of HDL cholesterol. Consequently, some researchers believe that even if people have adequate amounts of HDL cholesterol, it might not work well. Such HDL may not fulfill this molecules other important duties in the body, such as reducing inflammation and acting as an antioxidant.

Because exercise has the potential to protect against heart disease in a variety of ways, Christian K. Roberts and his colleagues at UCLA tested whether HDL in men who weight trained regularly behaved in a healthier way than HDL in sedentary men. They found that the men who didnt exercise were more likely than those who weight trained to have dysfunctional HDL. Having faulty HDL was associated with numerous other risk factors for heart disease, including high triglycerides and a higher trunk fat mass. This finding held true regardless of the mens weight, which suggests that maintaining a "healthy" weight isnt as important for healthy cholesterol function as being active by regularly performing strength training.

The article is entitled "Untrained Young Men Have Dysfunctional HDL Compared to Strength Trained Men Irrespective of Body Weight Status." It appears in the Articles in PresS section of Journal of Applied Physiology, published by the American Physiological Society. It is available online at http://bit.ly/1eQgZ1u.

Methodology

The researchers worked with 90 men between the ages of 18 and 30 who already had established exercise habits. They separated these participants into three groups: lean men who weight trained at least four times each week, overweight men who also weight trained at least four times each week, and overweight men who had no structured exercise regimen. The researchers took some basic physical measurements from the volunteers, including height and weight, waist circumference, blood pressure, and body composition. They tested the volunteers muscle strength and their carotid artery thickness (a sign of heart disease), and they took a blood sample. The researchers analyzed that sample for a variety of different molecules present, including cholesterol, insulin, various markers for heart disease including triglycerides and C-reactive protein, and sex hormones. They also checked the volunteers HDL to see how well it functioned as an antioxidant, a sign of how well their HDL works in general.

Results

The study authors found that HDL functioned better in the participants who had a regular weight-lifting program, regardless of their weight—overweight exercisers HDL has similar effectiveness as an antioxidant as the lean exercisers HDL cholesterol. Both groups HDL performed significantly better than those who didnt exercise. Such dysfunctional HDL was associated with numerous other factors associated with heart disease, such as elevated triglycerides and trunk fat mass.

Importance of the Findings

These findings suggest that regular weight training might improve HDL function and protect against heart disease, even in those who remain overweight. Although indices of weight were associated with HDL cholesterol function, differences in fitness, the authors say, may be a better measure of who has healthier functioning HDL cholesterol, and theore, who is at risk of heart disease.

"The role of obesity in the risk of coronary heart disease may indeed be largely accounted for by differences in fitness," the authors say.

Reduce Cholesterol with Lime - Beside consume the drug from doctor, many natural way that can tried to reduce and lower the levels of blood fats. It is way is easy and you can get it easy.
- Take a fresh lime and wash.

- Orange juice split four, then thinly sliced.

- Add sliced lemon with its peel into a mug or glass.

- Pour hot water into it until full, then cover tightly.

- Wait approximately 30 minutes, then drink it down.

- Do it twice a day, every morning and at night before bed.

Please note, orange juice does not cause burning in the stomach. Lime is also not be peeled because the lime skin there is oil content required for treatment. Good luck

March 23, 2011 -- Cocoa, used throughout history as a folk medicine, may actually have significant health benefits, according to a new study by Harvard researchers.
Their analysis of 21 studies with 2,575 participants shows that cocoa consumption is associated with decreased blood pressure, improved blood vessel health, and improvement in cholesterol levels, among other benefits.
Eric L. Ding, PhD, of Harvard Medical School says the apparent health benefits come from polyphenolic flavonoids in cocoa that have the potential to prevent heart disease. Flavonoids are antioxidants that are commonly found in fruits, vegetables, tea, wine, and coffee.
Cocoa Flavonoids Good for Cholesterol
In addition to decreasing blood pressure and improving blood vessel health, consumption of flavonoid-rich cocoa decreased “bad” LDL cholesterol among people under age 50, and increased good HDL cholesterol, the analysis showed.

Flavonoid-rich cocoa consumption also was linked to reductions in risk factors for diabetes -- a major risk factor itself for cardiovascular disease.

Also, resistance to the hormone insulin, which helps regulate blood sugar, favorably dropped among people who consumed flavonoid-rich cocoa, compared to people in comparison groups.

Further, consumption of flavonoid-rich cocoa did not change triglyceride levels of study participants or make them obese. Triglycerides are a type of blood fat that have been linked to coronary artery disease when levels are elevated above normal.
More Research Needed to Nail Down Benefits of Cocoa

Most of the previous studies analyzed were short-term research projects using mostly sugar-free, dark chocolate.

Ding and his colleagues say in the new study that because most chocolate is high in added sugar and fat, more research is needed to determine the risk-benefit effect on the heart health of eating commercially available chocolate.

Though past studies by Ding and others have found that cocoa may reduce heart attack risk, the dosage necessary to produce this effect is not known, and further research is needed to shed more light on that question, as well as on cocoa’s direct benefits on preventing strokes and heart attacks, according to a news release.

The new research is being presented in Atlanta at the American Heart Association’s Nutrition, Physical Activity and Metabolism/Cardiovascular Disease Epidemiology and Prevention 2011 Scientific Sessions.

National guidelines recommend that at-risk women be screened for elevated cholesterol levels to reduce their chances of developing cardiovascular disease. But who is ‘at risk?’ The results of a study by investigators at the Centers for Disease Control and Prevention (CDC) to estimate the proportion of women young and old who have cholesterol levels that meet the definition of being at-risk are reported in an article in Journal of Women’s Health, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available on the Journal of Women’s Health website.

In "Cholesterol Screening for Women: Who is At Risk?" Cheryl Robbins, Patricia Dietz, Shanna Cox, and Elena Kuklina, from the CDC, Atlanta, GA, analyzed data for a representative sample of 1,781 U.S. women not previously diagnosed with elevated cholesterol.

More than half (55%) of younger women (ages 20-44 years) and 74.2% of older women (>45 years) were at-risk for high cholesterol as defined by U.S. Preventive Services Task Force guidelines. Nearly all of the women in both age groups had at least one risk factor that would make them candidates for cholesterol screening according to the American Heart Association risk definition. The authors suggest the need for future research to determine whether screening and treatment of young women with high cholesterol will help to decrease subsequent deaths due to cardiovascular disease.

“The high prevalence of dyslipidemia reported in this study even among younger women is striking and supports the need for increased education about the risks for cardiovascular disease in women,” says Susan G. Kornstein, MD, Editor-in-Chief of Journal of Women’s Health, Executive Director of the Virginia Commonwealth University Institute for Women’s Health, Richmond, VA, and President of the Academy of Women’s Health.

People who exercise along with taking statins to lower their high cholesterol levels can dramatically reduce their risk of dying, a large new study suggests.

"The reduction in death is independent; whatever statins do is independent of what exercise does," said lead researcher Peter Kokkinos, a professor in the cardiology department at the Veterans Affairs Medical Center in Washington, D.C.

"When you combine the two, you get even better results," he said. "If you are taking statins, your mortality is about 35 percent lower versus not taking statins, but if you exercise, your mortality level decreases as your fitness level increases to the point where you can reach a 70 percent reduction in mortality."

Kokkinos is talking about regular moderate exercise -- not vigorous workouts. "Thirty minutes a day of brisk walking -- not a whole lot," he said.

Statin drugs include Lipitor (atorvastatin), Lescol (fluvastatin), Pravachol (pravastatin), Crestor (rosuvastatin) and Zocor (simvastatin).

Some people cant take statins because of side effects, Kokkinos said. "For these people, exercise alone reduces your risk just as much, if not more, than statins," he said. However, he stressed, "we do not recommend that people do not take their statins."

Exercise works by stressing the body making it stronger, Kokkinos said. Its an evolutionary adaptation to protect the body from being overcome by changing stressors, he said.

"Get off the couch -- walk," Kokkinos said. "About 150 minutes a week of brisk walking is all you need."

The report was published online in the Nov. 28, 2012 edition of The Lancet.

For the study, Kokkinos team analyzed the medical records of more than 10,000 veterans with high cholesterol levels treated in Veterans Affairs hospitals in Washington D.C., and Palo Alto, Calif. Of these, 9,700 were men and 343 were women.

The researchers judged the fitness levels of the participants by looking at the results of standard treadmill exercise tolerance tests, which were given between 1986 and 2011.

Fewer deaths occurred among participants who were taking statins and were physically fit. Over 10 years of follow-up, those who were the most physically fit had the lowest risk of dying, the researchers noted.

These fittest people actually reduced their risk of dying by about 60 percent regardless of whether they were taking statins, according to the study.

These difference in death risk could not be explained by age, weight, ethnicity, gender, history of cardiovascular disease, risk factors for cardiovascular disease or medications, the researchers said.

According to the U.S. Centers for Disease Control and Prevention, about 71 million Americans have high cholesterol, which is an important risk factor for heart disease, the authors pointed out.

One expert familiar with the new findings cautioned that exercise is not a replacement for statins in those with high cholesterol. The best results are among those taking statins and who are the fittest, he emphasized.

"Cardiovascular disease remains the leading cause of death and disability in men and women in the United States," said Dr. Gregg Fonarow, a spokesman for the American Heart Association and a professor of cardiology at the University of California, Los Angeles.

"Statin therapy has been proven in multiple clinical trials to substantially reduce cardiovascular events and all-cause mortality in men and women with or at risk for cardiovascular disease," he said.

Some people have assumed that if they are engaging in regular exercise and are physically fit that they may not benefit from statin treatment and some physicians consider statin therapy only for patients who have failed attempts at lifestyle modification, Fonarow said.

This new study shows that at all levels of physical fitness, statin therapy was independently associated with lower risk of dying. The very best 10-year outcomes were among men and women taking statins with the highest fitness levels, he noted.

"These findings further reinforce the remarkable real-world clinical effectiveness and safety of statin therapy to prevent and treat cardiovascular disease," Fonarow said.

Earlier I mentioned resistant starch as a type of carbohydrate that may aid blood glucose control. Another carbohydrate that studies find can help manage blood glucose, as well as reduce serum cholesterol, is psyllium husk fiber (shown).

Following are two studies that appeared in the American Journal of Clinical Nutrition.

In the first¹, from October 1999, researchers found those who supplemented their diet with psyllium had reductions in serum glucose:

"Two doses of psyllium taken immediately before breakfast and dinner resulted in significantly lower [glucose] measurements. ... All-day and postlunch postprandial glucose concentrations were 11.0% and 19.2% lower, respectively, in the psyllium than in the placebo group."

They also found reductions in cholesterol:

"Serum total and LDL-cholesterol concentrations were 8.9% and 13.0% lower, respectively, in the psyllium than in the placebo group."

In the second², from June 2000, researchers documented reductions in cholesterol:

"In this study, dietary change and long-term use of a standard dose of psyllium (5.1 g twice daily) resulted in 5% lower serum total cholesterol concentrations and 7% lower LDL-cholesterol concentrations than did dietary changes and placebo."

Both studies supplemented with 5.1g of psyllium fiber twice a day.

________
¹ For the first study, from 1999:
Effects of psyllium on glucose and serum lipid responses in men with type 2 diabetes and hypercholesterolemia

² For the second study, from 2000:
Long-term cholesterol-lowering effects of psyllium as an adjunct to diet therapy in the treatment of hypercholesterolemia

A study presented at the American Physiological Societys annual meeting last year found that a daily bout of humor could affect very tangible changes in blood lipids and markers of inflammation.¹

Heres a short video that describes the studys findings:



In the study, 20 diabetes patients with hypertension and hyperlipidemia were assigned either to a laughter group or a control group. All received meds for diabetes (glipizide, thiazolidinediones, metformin), hypertension (ACE inhibitor or ARB) and hyperlipidemia (statins). The laughter group watched at least 30 minutes a day of a self-selected humor video. (Self-selected ... "Funny" is very subjective.)

At the end of a year:

• HDL cholesterol rose 26% in laughter group.
  
• HDL cholesterol rose 3 % in control group.
  
  
• C-reactive protein decreased 66% in the laughter group.
  
• C-reactive protein decreased 26% in control group.

C-reactive protein is a marker of inflammation. The laughter group also had lower levels of the inflammatory markers TNF-α, IFN-γ, and IL-6, as well as lower epinephrine and norepinephrine levels by the second month, which may indicate reduced stress.

"The authors conclude that mirthful laughter may thus lower the risk of cardiovascular disease associated with diabetes mellitus and metabolic syndrome."

One of the authors, Dr. Berk, added:

"The best clinicians understand that there is an intrinsic physiological intervention brought about by positive emotions such as mirthful laughter, optimism and hope."

________
¹ Mirthful Laughter, As Adjunct Therapy In Diabetic Care, Increases HDL Cholesterol And Attenuates Inflammatory Cytokines And C-RP And Possible CVD Risk, The FASEB Journal, 2009

American Physiological Society Press Release:
"Mirthful Laughter," Coupled With Standard Diabetic Treatment, Raises Good Cholesterol And May Lower Heart Attack Risk, April 2009