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cholesterol

How Much Do We Know About “Good” Cholesterol?

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When it comes tocholesterol, we’ve viewed things in black and white.  Total cholesterol is bad.  LDL is bad.  HDL is good.

When drugs to lower total cholesterol and LDL cholesterol failed miserably (yes—the statins), the drug companies tried to make a drug that raised HDL cholesterol.  Ironically enough, the money for research and development likely came from the money from sales of the near-worthless statin, atorvastatin (Lipitor).

Torcetrapib, the first drug of its time made by Pfizer, indeed did raise HDL cholesterol but ended up killing patients 60% faster in phase III clinical trials so the drug was scrapped.

So what happened?

For some reason, the drug companies still don’t get it.  They don’t seem to understand that it’s not about the NUMBER, it’s about what the number represents.  Any number on your blood work, whether it’s total cholesterol, HDL, fasting glucose, HbA1c or liver enzymes, are merely the snapshot of the entire picture.  You see water leaking from 10 different locations in your house; do you plug all the individual leaks and throw down towels?  Or do you figure out what the problem is (like maybe the roof…) and fix it??

While this seems so obvious with home repair, it seems to have escaped the realm of common sense in medicine.  We find some type of lab value and latch onto it like a toddler with a new toy (or rather, a toddler with the box from the new toy…).  Then we put all of our focus into that lab value and build an entire approach to a disease based on this single lab value.

Back to the HDL issue.  HDL is not a single molecule.  Rather, as this particular study points out, it is actually made up of at least 85 different subtypes of proteins.  85.  So which ones are the best of the best and which ones are irrelevant as far as your risk of heart disease?  Many prescription drugs are designed to target a very specific pathway.  In the example above given for Torcetrapib, it is highly likely that the drug only affected a very small number of the 85+ types of HDL molecules.  Given that we don’t even understand how each of these types of HDL molecules work in concert, messing with only one could potentially lead to disaster, which is what happened.

Contrast this with lifestyle.  Lifestyle changes do not affect a single pathway.  It is likely that the right lifestyle changes geared towards lowering your risk of heart attack and moving you away from diabetes will lead to alterations in a large number of these HDL protein molecules.  Some will shift lower, some will shift higher, all moving in the direction they are supposed to go to protect you from chronic diseases.  Picture the most elaborate concert you have ever heard; each instrument orchestrating beautifully among one another to produce the perfect outcome.  THAT is what lifestyle does.

Pharmaceutical drugs, on the other hand, would be like throwing 2 or 3 toddlers with bats into the percussion section of a philharmonic orchestra.  Not pretty.

This same reason is why, despite the near universal salivation by the drug companies to create a drug that raises HDL cholesterol levels and magically lowers the risk of dying from a heart attack (while at the same time miraculously boosting profits), it will never happen.  Too many variables at play.  Stick with GMO-free soy, exercise and nuts to raise your cholesterol levels instead.

CRP Concentrations Correlate With the Severity of Atherosclerosis – (07-24-00)

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CRP Concentrations Correlate With the Severity of Atherosclerosis

C-Reactive Protein is a marker for chronic inflammation in the body. Many experts believe that inflammation is a major contributor to heart disease. Make sure that CRP levels are checked with your cholesterol if you are at risk for heart disease.

Eur Heart J 2000;21:958-960,1000-1008 Dr. Mira-Christine Tataru from Herz- und Gefassklinik, in Bad Neustadt/Saale, and colleagues analyzed the relationship between plasma C-reactive protein levels and the severity of atherosclerosis in 1,112 male and 299 female survivors of acute myocardial infarction and in 326 male and 138 female age-matched controls without coronary disease. Confirming prior studies, Dr. Tataru and colleagues report that plasma C-reactive protein levels increase with age and are higher in smokers than in nonsmokers. Additionally, they report that C-reactive protein concentrations are higher in coronary heart disease patients than in control patients. Among survivors of acute myocardial infarction, C-reactive protein levels correlate with the angiographically detected severity of coronary heart disease. It is also noteworthy, the authors say, that C-reactive protein levels were higher not only in patients with clinically manifest atherosclerosis, but also in patients with preclinical stenoses of the pelvic and leg arteries as well as the extracranial arteries supplying the brain, or aneurysm of the abdominal aorta.

Enhanced Progression of Early Carotid Atherosclerosis & C pneumoniae – (04-12-01)

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Enhanced Progression of Early Carotid Atherosclerosis & C pneumoniae

We are starting to see more and more evidence that an infectious etiology plays a part in heart disease. I believe that this is a big reason why mainstream medicine has such a problem with heart disease; there is no “one cause, one cure.” Inflammation, hyperinsulinemia, hypertension, oxidation of cholesterol, high homocysteine, infections…the list is quite long. An approach to heart disease prevention needs to be comprehensive and address all these factors. Putting on blinders and lowering only high blood pressure or cholesterol is not good enough.

Circulation — Abstracts: Sander et al. 103 (10): 1390

Read entire article here

CRP–Mediated Low Density Lipoprotein Uptake by Macrophages – (03-22-01)

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CRP–Mediated Low Density Lipoprotein Uptake by Macrophages

I may need to clarify what this article is talking about. First, it is current theory that macrophages become foam cells once they take up LDL cholesterol from the bloodstream. These foam cells are what lead to the buildup of plaque on the arteries. This article is suggesting that CRP (a marker of chronic inflammation) increases the attraction (“opsonizes”) between the LDL and the macrophages. Low level chronic inflammation can come from so many different sources; and can in turn lead to a multitude of chronic diseases.

Circulation — Abstracts: Zwaka et al. 103 (9): 1194

Read entire article here

The “Soy is Evil” Saga Continues: 7 Effects on Prediabetes

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For those of you that read my blog post on soy a few weeks ago and still think I’m off my rocker and being paid under the table by the soy growers association, I present exhibit B.

With the usual caveats of non-processed and non-GMO soy, the research is overwhelmingly in support of soy as part of a healthy lifestyle.  I’ve read the arguments stating that soy was only recently introduced into the human diet maybe 75 years ago, but much like all the other misconceptions about soy, this is untrue and, in this case, the authors are only maybe 5,000 years off (and, in the timeframes of the universe as well as carbon dating techniques, this is merely a rounding error).

In this particular study, authors looked at the ability of genistein (the protective isoflavone found in soy) to help improve prediabetes.  120 women with prediabetes were given 54 mg genistein (about the amount found in a serving of soy) for 1 year.  Here’s what they found:

  1. With genistein use, fasting glucose and fasting insulin dropped.
  2. HDL-C increased an average of 10 mg/dL.
  3. Increased adiponectin levels (an anti-diabetic hormone produced by the fat cells).
  4. Decreased total cholesterol, LDL-C down 30 points, triglycerides and visfatin (another fat derived hormone that drives inflammation and chronic disease).
  5. Homocysteine levels dropped as well (an amino acid linked to heart disease and stroke).
  6. Systolic and diastolic blood pressure was also reduced.

To top it all off, genistein users complained of no more side adverse effects than the non-users in the study and did not discontinue the study at any different rate.

Looking at the drop in LDL cholesterol and triglycerides coupled with the increase in HDL, the risk of heart disease is going to plummet with this as well.

Compare this to statins, the wonder drug that I love so much, which ONLY effects one single blood marker (LDL) and will actually LOWER HDL.  So, a drug with loads of side effects (which can be perused ad nauseam in my eBook, which can be found on the eBooks page by clicking here) that has almost no effects on heart disease or stroke rates is not even in the same ballpark as a serving of soy at protecting your heart.

Much life the proverbial death match between the HR Block accountant and the ninja warrior.  Too bad the accountant has billions of dollars backing him up.

Markers of cumulative biological risk: studies of successful aging – (05-10-01)

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Markers of cumulative biological risk: studies of successful aging

This article reviews the use of allostatic load (AL) to determine biological risks of aging. AL is an index that uses 10 parameters of biological functioning to give an overall level of risk. I have seen computer programs that attempt to give a biological age to the patients. I have very little faith in these because they do not address real questions (they ask for seat belt use, check BP and cholesterol, exercise levels…). Ironically, none of the 10 factors in AL are used on these questionnaires. I have to mention one more thing for those of you that just read my comments…6 of the 10 factors are associated with Syndrome X. Go figure…a disease state that most of the medical profession is unaware of, a disease state that is highly modifiable with nutrition and natural medicine, and one that contributes to 60% of aging? And we wonder why medicine in the US is ranked so poorly.

PNAS — Abstracts: Seeman et al. 98 (8): 4770

Read entire article here

Cholesterol from eggs increases the ratio of total cholesterol to HDL – (05-28-01)

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Cholesterol from eggs increases the ratio of total cholesterol to HDL

It is very likely that all the press about eggs being fine for cholesterol levels was promoted and propelled by the egg industry. I’ve never been a great fan of eggs and this does have a tendency to solidify my opinions. However, egg whites are a very good source of high quality protein, along with whey, soy and certain rice proteins. If you do like eggs, try to eliminate the yolks and keep the whites.

AJCN — Abstracts: Weggemans et al. 73 (5): 885

Read entire article here

Dietary cholesterol is secreted over several subsequent meals – (05-28-01)

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Dietary cholesterol is secreted over several subsequent meals

This is truly a insightful article that may help us better understand how the food we take in can affect our overall health days after we eat. These researchers determined that, when the participants ate cholesterol, it took up to 48 hours for that cholesterol to show up in the bloodstream. Each successive meal “pushed” the cholesterol from the original meal into the bloodstream. This study shows that dietary constituents do not always show up directly in the bloodstream. Too many times mainstream medicine does not look beyond the most immediate meal.

AJCN — Abstracts: Beaumier-Gallon et al. 73 (5): 870

Read entire article here