Super size me in little bits and pieces



Alvin came into the office for consultation on his cholesterol values: LDL 198 mg/dl, HDL, 43 mg/dl, triglycerides 143 mg/dl. He says that he doesn't really try to choose healthy foods but he restricts his overall calorie intake by following the Weight Watcher's exchange approach.

Every morning, 7 days a week, Alvin eats a Sausage McMuffin for breakfast. He justified this by skipping lunch to make up for the 450 calories in the Sausage McMuffin, and not eating anything until dinner.

Can this work? Can you eat foods with unhealthy ingredients but make up the excessive calories by cutting back elsewhere?

The nutritional composition of McDonald's Sausage McMuffin includes 27 grams of total fat (10 gm saturated); 255 mg cholesterol; 950 mg sodium; 31 gm carbohydrate; 2 grams fiber. In other words, it's essentially the same as butter with sugar on it--pure fat, processed wheat, with little fiber or nutritive value.

For Alvin, this is an extremely unhealthy way to eat. His lipid patterns are just the tip of the iceberg: multiple hidden factors are also at work to create heart disease, atherosclerosis in other territories outside the heart, diabetes, high blood pressure, and cancer.

I think the effects are not much different than what Morgan Spurlock achieved in his Super Size Me documentary, but in little bits and pieces. Eating at McDonald's "restaurants" three times a day yielded frightening changes in his lipids, liver function, kidney function, not to mention his appearance and the way he felt. Alvin is doing the same thing, though in less dramatic fashion.

I see this very frequently: people mimicking the experience of Spurlock, just a little at a time, with overindulgence in processed fats and starches.

When you seen a set of Mcdonald's golden arches (or any fast food restaurant, for that matter), run as fast as you can in the other direction. Such indulgences, even in small bits and pieces, still creates a mess of your health.

View from the precipice


Many people, upon first learning of their CT heart scan score, feel like they're on the edge of a sharp drop. It can feel like you're facing a vast, unknown abyss. At the bottom, all those dreaded things that can happen to you: heart attack, heart failure, hospitals, even dying.

I've encountered this "deer in the headlights" look many times. It truly can be frightening to hear that your heart scan score is 300, or 500, or whatever.

What I find truly frightening, however, is when your score prompts the usual array of misinformation commonly dispensed by physicians: "That's so bad you need a heart catheterization", "Nobody knows why people get calcified plaque", or "Reversal is impossible". All absolute bunk.

Let your fear motivate you to do something about your risk for heart disease. Aim for reversal of your coronary plaque and seek out the tools to achieve this. It is possible and, in fact, we do it all the time. I can't claim 100% success, but the majority of people who engage in an effort like the Track Your Plaque program to reverse coronary plaque succeed. Even a substantial slowing of plaque growth from the expected 30% per year is better than submitting to the conventional approach.

At the very least, get both LDL and HDL cholesterol around 60 mg/dl. This alone is a major plus in reducing the risks associated with your heart scan score. It doesn't guaranteee reversal, but it sure tips the odds in your favor.

Organic Rice Krispies?



Breakfast cereal manufacturing giant, Kelloggs, is launching a line of three cereals that will carry the "organic" designation: Organic Rice Krispies, Organic Raisin Bran, and Organic Frosted Mini-Wheats.

This reminds me of the advertisements I've seen for "fresh fried chicken", or "fresh from the can", or "contains only pure cane sugar". How about organic tobacco? Would that make cigarettes healthier?

The TV ad ends with the slogan "Childood is calling!" Oh, those marketers are a shrewd, clever bunch. I worry that they're so clever that most people will fall for these ludicrous tricks.

Don't fall for these thinly-shrouded marketing shenanigans. Organic? Who cares. These foods remain unhealthy whether or not they contain pesticide residues. Take a look at the nutritional composition: Rice Krispies, organic or not, is sugar to your body. It is the sort of food that creates pre-diabetes, diabetes, makes us fat, and fans the flames of lipoprotein patterns like small LDL, VLDL, and postprandial particles, all of which is like throwing cow manure on the weed patch of your coronary plaque.

Nuts as functional foods

Food manufacturers gave nuts a bad name when they started adding evil ingredients to them. "Party mix", "honey-roasted", mixed nuts, etc., are made with added hydrogenated oils, salt, sugar, excessive quantities of raisins, or other added ingredients that turned a healthy food--nuts--into something that made us fat and hypertensive, raised LDL, dropped HDL, and raised blood pressure.

But nuts themselves are, for the most part, very healthy foods. The very best are nuts with a brown fiber coating like almonds, walnuts, and pecans. Nearly all nuts also come rich in monounsaturated oils similar to that in olive oil. Although calorie-dense, nuts tend to be very filling and slash your appetite for other foods. I have never seen anyone gain weight by adding raw nuts to their diet. In fact, I find adding raw nuts cuts craving for sweets.

Nuts are also among the most concentrated sources of magnesium, containing around 150 mg per 1/2 cup serving. As most Americans are at least marginally if not severely deficient in magnesium, this really helps. Magnesium deficiency is a prominent aspect of "metabolic syndrome" and resistance to insulin.




Some nuts have added benefits like the l-arginine content of almonds or the linolenic acid content of walnuts. However, I think the real health "punch" comes from the fiber and monounsaturate content.

Add 1/4-1/2 cup of raw almonds, walnuts, or pecans per day to your diet and what can you expect? The effects that I see every day that are relevant to plaque control/heart scan score-reducing efforts include:

--Reduction in LDL--usually a 20 mg/dl drop, sometimes more.

--Reduction in triglycerides, especially if nuts replace processed carbohydrate calories. This may be because the fiber and monounsaturate content of nuts reduces blood sugar and the effective glycemic index of any accompanying foods.

--Modest blood pressure reduction.

--Though somewhat inconsistent, partial suppression of the dreaded small LDL particle pattern. We struggle with turning off the small LDL pattern in some people, and raw nuts can provide a real advantage.

If that isn't enough, the fiber content also makes your bowels regular.

Unless there's some reason to avoid nuts (e.g., allergy), nuts should be a part of your heart scan score reducing program. Shop around, as prices can vary wildly. I've been paying $12.99 for a 3 lb bag of raw almonds from Sam's Club, though I've seen almonds elsewhere for up to $12.99 per pound.

For additional commentary, go to one of my favorite Blogs, http://fanaticcook.blogspot.com. The Fanatic Cook's recent post, The Season for Walnuts , provides additional discussion on walnuts and the recent study showing how they improve "endothelial function". The nutritionist behind this Blog has fabulous insights into food, including the concept of "functional foods", i.e., using foods as a treatment tool. She is also unfailingly entertaining.

Can you tell the difference?

Stan is 55 years old. He feels fine, is in moderately good physical condition. His LDL cholesterol is 135 mg/dl, HDL 43 mg/dl, triglycerides 167 mg/dl, total cholesterol 211 mg/dl.

Can you tell me whether Stan has heart disease or not?

How about Charles? Charles has an LDL cholesterol of 127 mg/dl, HDL of 44 mg/dl, triglycerides of 98 mg/dl, and total cholesterol of 191 mg/dl. He is also reasonably fit and feels fine. Can you tell whether Charles has heart disease?

If you can't, don't feel bad. Neither can your doctor. But this is the folly of using cholesterol for risk prediction.

Stan's heart scan score: 0

Charles' heart scan score: 978

Look even more closely at Stan's and Charles' cholesterol numbers. Is there some fine distinction we overlooked? What if we calculated total cholesterol to HDL ratio? Or LDL/HDL ratio?

No matter how you squeeze it, shake it, beat it with a stick, you simply cannot use cholesterol numbers to predict heart disease in specific individuals. Yes, the higher your LDL cholesterol and lower your HDL, the higehr your total cholesterol to HDL ratio, the greater the likelihood of heart disease. But you can simply cannot tell in a specific individual at a specific point in time. If you've seen your doctor puzzle over the numbers, understand that he/she is trying to make sense out of something that doesn't make sense, no matter how hard he/she tries.

You simply need to measure the disease itself: get a CT heart scan, the only measure of atherosclerotic coronary plaque that you have access to.

By the way, if you haven't seen it yet, go to the Track Your Plaque website (www.cureality.com) to see the news piece reporting the American Heart Association's much overdue position statement on CT heart scanning. The AHA has finally released a statement which, in effect, provides their "official" endorsement. Blocked by political shenanigans behind the scenes for several years, the guidelines finally made it to press. The only real difference it makes to me is that my patients may finally get their heart scans paid for by insurance, once the insurance companies realize that it's getting tougher and tougher to dodge their responsibility.

Statin agents and muscle aches

How common are muscle aches with the statin drugs?

It depends on who you ask. If you ask the drug manufacturers, they will tell you no more than 2% of people who take them. They back this up with the experience in tens of thousands of people in published clinical trials.

What if we ask people who take them outside of clinical trials. How many then? I estimate, from my large experience, over 80%! In other words, muscle aches are inevitable in nearly everyone who takes them. The longer you take them, the higher your dose, the more likely muscle aches are going to be.

Why the disconnect between published data and real-world experience? I really don't know. In some instances, the differences are dramatic. The ASTEROID trial, for instance, in which Crestor, 40 mg, was given for two years, only resulted in 8% of people dropping out because of side-effects. My experience: everybody--nobody can tolerate this dose for any length of time.

Let me qualify what "muscle aches" mean. It means achiness and/or weakness, usually mild, occasionally moderate to severe, worse upon awakening and less with use. It can affect many muscles or it can involve only one. Rarely is it incapacitating but it is commonly annoying and frightening. It commonly shows up as gradually diminishing strength with exercise. Strength usually returns promptly upon stopping the offending drug.

"Rhabdomyolysis", or true muscle destruction is, fortunately, very unusual in otherwise well people. People with abnormal kidney function, diabetes, and other concurrent illnesses are somewhat more prone. But in reality, rhabdomyolysis is unusual. I've personally seen it twice, both in people sick for other reasons.

Coenzyme Q10 (CoQ10) supplementation has been a godsend for us. At least 4 out of 5 people who require statins and develop muscle aches respond favorably, but it requires 100 mg per day. The preparation must be oil-based to work, not powder in a capsule which exerts no effect. Some people get by with less; some require as much as 300 mg per day. I've had favorable experiences with the CoQ10 from Sam's Club, GNC, Vitamin Shoppe, and Life Extension (www.LEF.org).

The Track Your Plaque target for LDL cholesterol is 60 mg/dl. Many people do indeed use statins to achieve this level, the level of LDL that amplifies your chances of heart disease reversal, i.e., reduction of heart scan score. The only drawback that I'm aware of with CoQ10 replacement is cost. Beyond this, it's a benign supplement that even supplies higher energy for some people who take it.

More catheterizations would make me happy!

I received this fax today from a cardiologist seeking a position:

"I would prefer to perform as many interventions [stents, angioplasties, etc.] as possible..."

That about sums it up, doesn't it? The goal of this young man, trained in major universities including Columbia University, Harvard, and Emory, is not to pursue an avenue of investigation or healthcare that yields real answers. His goal is to perform as many procedures as possible.

This attitude is deeply ingrained in cardiologists. It's also shared by all procedural medical specialties: the drive to do more and more procedures. It's not because it does more good for the public, but it fulfills a primitive impulse to spread your influence, enlarge your territory, and--of course--make more money.

Personally, I find this impulse repulsive. The fact that this young cardiologist looking for a position is willing to make this statement out in the open demonstrates how widely accepted this attitude is. Imagine your cancer surgeon, looking for a new job, said, "I'm looking to remove as many tumors as I can."

My colleagues have lost sight of the fact that we're trying to reduce or eliminate disease, not enrich our pockets or service some primitive impulse to beat others at our game.

"I hate fish oil!"

I get this comment occasionally, usually from the fishy belching that can occur, rarely because of other crazy effects like rash, fishy body odor, etc.

In the vast majority, fish oil is a benign but wonderfully effective agent. Track Your Plaque followers know that fish oil, starting at 4000 mg per day of a standard 1000 mg capsule preparation, dramatically reduces triglycerides and thereby raises HDL, partially suppresses small LDL, and is the best agent available for reducing postprandial (after eating) abnormalities like IDL and certain VLDL fractions.

However, an occasional person (about 1 in 20) just doesn't like the effects. Are there alternatives? Fish oil packs such a wallop of beneficial effects that can not be replaced by any other single agent or lifestyle practice. For this reason, we have a number of easy strategies to enhance your tolerance for fish oil. (Of course, if your and/or you doctor determine that you're allergic to fish oil, then you should indeed avoid it; thankfully, this is rare.)

Helpful strategies include:

--Refrigerate fish oil capsules--this cuts back on fish belching.
--Take only with meals. This also may increase fish oil's benefits on suppressing after-eating lipoprotein abnormalities.
--Take an enteric-coated preparation--this delays breakdown of the tablet/capsule, making fishy belching less of an issue. Sam's Club has an inexpensive preparation.
--Take liquid fish oil. Usually orange or lemon flavored, liquid fish oil may be a faint fishy taste and odor, but usually not as prominent as the capsules. There's also less stomach upset.
--Coromega--a paste form of fish oil available at health food stores or through http://www.coromega.com. Coromega tastes fruity and comes in little squeeze envelopes.
--Frutol--Pharmax, a British company, makes another fruity fish oil that is non-oily and tastes like apricot. It's actually fairly reasonably priced, too. However, it is hard to find. The only way I know to get is to go online at www.pharmaxllc.com. You may have to actually order through a health care provider.

When using any preparation of fish oil, the best way to determine your dose is to add up the EPA and DHA content. For instance, if you use a fish oil liquid that contains 320 mg EPA and 240 mg DHA per teaspoon, you will need two teaspoons a day to achieve the equivalent of our starting dose of 1200 mg of EPA+DHA, usually provided by 4000 mg total in 4 capsules. Note that some lipid and lipoprotein disorders will require higher doses, e.g., 1800 mg EPA+DHA for high triglycerides (>200 mg/dl) or high IDL.

Sudden death in athletes

A recent report in the Journal of the American Medical Association details how a group in the Veneto region of Italy cut back on the incidence of sudden cardiac death in athletes by a simple screening program.



You can read the abstract of the article at http://jama.ama-assn.org/cgi/content/full/296/13/1593.

Although sudden death in athletes is still a rare event, it is especially tragic when it happens. In this population, the incidence was 3.6 deaths per 100,000 athletes aged 12 to 35 years. By implementing a simple screening program that involved only a physical examination and an EKG, an astounding 89% reduction in sudden death was documented.

What lessons does this hold for those of us interested in coronary plaque reversal? Beyond the obvious lesson of pointing out the great benefit of simple screening of athletes, I believe that it tells us the value of simple screening tools for heart disease in general. It is my strong belief that, if we were to implement CT heart scans among the broad population of men 40 years and over, women 50 years and over--without regard to cholesterol or other relatively lame risk identifiers--we could slash the risk for heart attack and death 90% or more. Putting CT heart scans into the hands of the public makes your coronary risk obvious. It takes the guesswork out of risk predictors like cholesterol and high blood pressure.

But heart scans are already available, you say! Yes, of course they are. But the lack of insurance reimbursement continues to be a restricting factor for many people, despite the number of lives that could be potentially saved and the money that would be saved in the long run by reducing need for major heart procedures. The continuing resistance to prevention by my cardiology colleagues and the persistent ignorance of primary care physicians also remain major impediments.

But it's getting better. You don't have to be chained by ignorance. Put your CT heart scan to good use.

My heart scan was wrong!



Tom came into the office ready for a confrontation.

Tom's wife insisted that he see me to discuss the implications of his CT heart scan score of 459. At age 50, this was clearly bad news that placed Tom in the 99th percentile (worst 1% of men in his age group).

But Tom had already undergone a stress test. There had apparently been a small abnormality, and a heart catheterization had been performed by another cardiologist. "They told me they didn't need to do anything. No stent, no ballon, no bypass, nothing!"

I asked, "Did they tell you that there was any plaque or blockages seen?"

"Yeah, but he said it was nothing. So the heart scan was wrong!"

I've been here many times before. I explained to Tom that, no, his heart scan was not wrong. All the tests he'd undergone siimply provided a different perspective on the same disease. You could say:

--The stress test, being a test of blood flow, may have been abnormal because of the abnormal constrictive behavior of arteries containing plaque, known as "endothelial dysfunction", because the inner lining of arteries (the endothelium) control the tone of the artery. Abnormal constriction in arteries with plaque is quite common.

--The catheterization simply showed that no plaque had collected in a configuration to block flow, thus no stent, etc., since flow was normal. But there was indeed plaque.

All three tests were right; none were wrong. They all provided a little different perspective on the same process. Of course, I favor the heart scan as the means to identify, precisely measure, and track the atherosclerotic plaque in your arteries. The stress test is too crude and only measures flow, the catheterization is not something you'd want to undergo year after year. Catheterization also is too crude a measure to precisely track plaque growth or reversal.

So I explained to Tom that, even though a stent or similar procedure was unnecessary, he remained at substantial risk for heart attack due to plaque "rupture". In fact, Tom's heart attack risk was 5% per year, or approximately 50% over the next decade. That is, indeed, substantial. In fact, you might say that, of the three tests Tom underwent, only the heart scan revealed his true risk.
When MIGHT statins be helpful?

When MIGHT statins be helpful?

I spend a lot of my day bashing statin drugs and helping people get rid of them.

But are there instances in which statin drugs do indeed provide real advantage? If someone follows the diet I've articulated in these posts and in the Track Your Plaque program, supplements omega-3 fatty acids and vitamin D, normalizes thyroid measures, and identifies and corrects hidden genetic sources of cardiovascular risk (e.g., Lp(a)), then are there any people who obtain incremental benefit from use of a statin drug?

I believe there are some groups of people who do indeed do better with statin drugs. These include:

Apoprotein E4 homozygotes

Apoprotein E2 homozygotes

Familial combined hyperlipidemia (apoprotein B overproduction and/or defective degradation)

Cholesteryl ester transfer protein homozygotes (though occasionally manageable strictly with diet)

Familial heterozygous hypercholesterolemia, familial homozygous hypercholesterolemia

Other rare variants, e.g., apo B and C variants

The vast majority of people now taking statin drugs do NOT have the above genetic diagnoses. The majority either have increased LDL from the absurd "cut your fat, eat more healthy whole grains" diet that introduces grotesque distortions into metabolism (like skyrocketing apo B/VLDL and small LDL particles) or have misleading calculated LDL cholesterol values (since conventional LDL is calculated, not measured).

As time passes, we are witnessing more and more people slow, stop, or reverse coronary plaque using no statin drugs.

Like antibiotics and other drugs, there may be an appropriate time and situation in which they are helpful, but not for every sneeze, runny nose, or chill. Same with statin drugs: There may be an occasional person who, for genetically-determined reasons, is unable to, for example, clear postprandial (after-eating) lipoproteins from the bloodstream and thereby develops coronary atherosclerotic plaque and heart attack at age 40. But these people are the exception.

Comments (17) -

  • Might-o'chondri-AL

    4/8/2011 12:21:11 AM |

    I don't know how individuals with mis-sense SNP for gluco-kinase regulatory protein (ex: GCKR rs780094) fit into the pattern. They get more liver steatosis (fat build up) with attendant elevated LDL and triglycerides, despite less fasting glucose and less fasting insulin numbers; while their 2 hour blood glucose runs high (GCK gene is very determinate of 2 hour glucose levels), showing down-regulation of the homeostatic model for Beta cell function (HOMA-B).

    Normally GCKR regulates triglycerides and determines persons glycemic traits by governing how glucose is stored and how it is dispersed. GCKR also geneticly regulates the availablility of substrate used for de-novo lipo-genesis.

    Gene SNP of protein phosphatase 1regulatory (inhibitor) subunit 3 B (PP1R3B rs4240624) manifests increased liver steatosis  and both elevated LDL and elevated HDL; with low fasting glucose. PPP1R3B codes for controling protein and modulates the break down of glycogen (storage glucose moleccule).

    Together PPP1R3B and GCKR are integral to blood sugar dynamics and the levels of lipids in circulation.

    If Doc's regimen counter-balances individual missense genetic workings, like those above, then that is impressive corrrection achieved through intervention . I presume for people with liver steatosis missense mutations (ie:  SNPs like above) elevated LDL treatment using statins would be bad for their liver.

  • Dr. John

    4/8/2011 1:10:14 AM |

    Statins might be helpful if you have bacterial pneumonia:
    http://www.bmj.com/content/342/bmj.d1907.extract?sid=f762e55c-1a0b-4ef3-81c4-f31cc472a372

    That's because the rapidly growing pneumococcal bacteria are very susceptible to HMG-CoA reductase inhibitors (statins). The bacteria have similar cholesterol compounds (hopanoids) in their membranes, essential for their membrane function. With the statins blocking the hopanoids, they die....very quickly.

    All bacteria have a mevalonate pathway.  The HMG-CoA reductase enzyme is inhibited in bacteria and are VERY toxic to bacteria. So thus, you have a "statin-benefit" because it kills the bacteria, before it kills or injures the patient.

    Statins can essentially inhibit biological life forms.
    Dr. John

  • Dr. William Davis

    4/8/2011 1:11:01 AM |

    HI, Might--

    As usual, you've come out of left field with a totally unexpected issue!

    I'm not sure how this genetic variant fits into this argument. It is, to my knowledge, a very rare diagnosis.

  • Might-o'chondri-AL

    4/8/2011 6:40:15 PM |

    I don't envy Doc trying to sort out who needs what treatment. Genetic high cholesterol entails over 50 amino acid variations out the jumble of 692 amino acids assembled into relevant complexes.

    Pro-protein convertase subtilisin/kexin-9 (PCSK9)is involved in familiar hyper-cholestemia. Those who make too much PCSK9 (in the liver and small intestine) rapidly degrade their cholesterol receptors and can't pluck much LDL out of circulation; plasma cholesterol rises.

    Should one's genetics foster making too little PCSK9, then cholesterol receptors don't degrade. This promptly shunts cholesterol into the liver lysosome (an organelle inside a cell)for break down; thus they  measure low cholesterol in the blood.

    I speculate Doc's diet, in "normal" genetic people up-regulates cholesterol reception. Which means his program has the epigenetic effect (from diet dynamics) on "normal" liver/small intestine genes in a way that less PCSK9 is expressed

    The caucasian anglo-saxon PCSK9 D374Y mutation causes 4 times the normal cholesterol in patients. Their risk factor for pre-mature death is 10 years earlier than even more benign PCSK9 mutations; so Detective Doc Davis is willing to prescribe statins for people like them.

  • Anonymous

    4/9/2011 2:59:55 AM |

    I might be one of these poor souls.

    Eating a strict diet, one Dr Davis would be very proud of... I'm lean as can be, feel great, but my cholesterol shot through roof (while HDL dropped).    

    Frown

  • Might-o'chondri-AL

    4/9/2011 4:53:48 AM |

    Hi Annon.,
    Internet self-diagnosing shouldn't replace a good medical consultant. My comments are not qualified medical assesments; am a layman.  

    My favorite cousin has had her cholesterol testing well over 300for several decades, and is now in her late 70s. Like Doc chided me earlier, there are "genetic variant" being "very rare diagnosis."

  • Lucy

    4/9/2011 11:47:29 AM |

    What do you think about KIF6?   I was tested and found to be a non-carrier, and I was subsequently told that statins would likely not benefit me as much as diet/lifestyle changes (I'm ApoE 3/4 as well).  Does that also mean that niacin would not help?

  • Anonymous

    4/9/2011 12:52:56 PM |

    To say the least, I am very disappointed in Dr. Davis' stance regarding ApoE 4 & statins. There is abundant evidence suggesting statins are counterproductive to brain health, which is much more pronounced in Apo E4's who are already at high risk for alzheimers disease. It isn't only about lipids, there is a larger picture to consider. The brain requires cholesterol.  Also, high cholesterol levels are associated with longevity in the elderly.

  • Might-o'chondri-AL

    4/9/2011 7:44:42 PM |

    Alzheimers and the relationship of ApoE4 is different than other ApoE isoforms (like ApoE 2 & 3). In normal people ApoE is integral to clearing amyloid Beta from the brain; it forms a conjugate (ApoE/AmyloidB)that is moved out across the brain blood barrier by LRP-1 (lipo-protein related protein 1).

    ApoE4 is acted upon (cleaved) in brain neurons, yielding rump fragments with unique Carbon- terminals; and,  ApoE4 degrades easier than ApoE 2 &/or 3. These ApoE4 fragments, when in a brain cell's cytosol, influence that cell's mitochondria hydro-phobic pattern of lipid binding.

    The ApoE4 fragment properties  do 2 unwanted things to the brain cell mitochondria. It decreases the mitochondria ability to perform tasks involved in glycolysis (glucose energy). And is antagonistic to PPAR gamma; PPAR gamma is what would otherwise promote adequate mitochondria bio-genesis.

    ALzheimer lesions show higher amounts when measured in individuals with concurrent Type II diabetes and the ApoE4 isoform. The ratio of insulin in the cerebro-spinal fluid to the amount of insulin in the blood also shows a difference depending on the specific ApoE geno-type.

    Alzheimer brains are using less glucose; patients show less receptors for insulin-like growth factor and insulin, as well as less insulin degrading enzymes. It is postulated that depending on the individual's ApoE variation there is a different amyloid Beta response to brain insulin.

    Normally one goes from glucose intolerance to hyperglycemia and then elevated insulin circulating as become diabetic. Yet experiments show that giving insulin improves diabetic neuro-pathy in the brain; it seems to be a way peripheral insulin resistance causes different tissues to respond.

    In Alzheimer experiments with supplemental insulin (nasal, etc.)administration cognitive function improved. This response was more significant in those with the ApoE4 allele (compared to other ApoE types with Alzheimers, who also improved cognition ).

    So, the Alzheimer enigma seems to involve energy format dynamics for ApoE isoforms more than specific levels of cholesterol. This is not a comment on ApoE homo-zygote genes relationship to cardio-vascular risk factors, or brain lipid metabolism.

  • homertobias

    4/11/2011 3:36:34 PM |

    Mito
    You sound like Suzanne Craft.  I like her work.

  • Medicomp INC.

    4/12/2011 4:06:52 PM |

    You make an excellent point here:

    ...eat more healthy whole grains" diet that introduces grotesque distortions into metabolism

    We are encouraged by transient sources that this is almost always the best alternative for other fattening foods, yet people never really delve deep into the cons of this transition either.  It truly does take dedication to be well-informed about the dietary changes you make in your lifestyle.

  • Anne

    9/18/2011 5:58:38 PM |

    I had a body scan a few years ago, and my plaque count was 1050, when they told me that 150 was considered high, I thought  I would implode at any moment, I went to a lot of different cardiologists and had all kinds of tests and they said to exercise and not  worry about the plaque. One Dr. put me on lipitor and 3 days later I could hardly walk from the muscle pain, he told me to stop taking it and I tried niacin and red rice with the same results. I don't know how to reduce the plaque, the Dr's all said it was hereditary . I am open to any advice.

  • Dr. William Davis

    9/20/2011 12:43:37 PM |

    Hi, Anne--

    Note that this is the blog that accompanies the Track Your Plaque program that focuses on just this issue. It means 1) identify all causes of plaque, then 2) correct them, preferably using natural means.

  • JK

    10/30/2011 4:52:34 PM |

    Dr. Davis,
    I don't know if you have already addressed this topic in prior posts but allow me to suggest that in lieu of consuming statin drugs, even for the aforementioned outliers, it is possible to achieve reduced LDL cholesterol and increased HDL cholesterol by supplementing with magnesium.
    (All the ensuing statements below I humbly attribute to Mildred S. Seelig and Andrea Rosanoff, "The Magnesium Factor," pages 139-147.)
    1. Statins (Lipitor, Zocor, Baycol, Mevacor, etc.) are designed to lower cholesterol by inhibiting HMG-CoA reductase, which is the enzyme responsible for the synthesis of cholesterol.
    2. These drugs when studied, not only lower cholesterol, but also reduce total mortality, cardiac mortality, the total incidence of heart attacks, angina, and other non-fatal cardiac events. (p.140.)
    3. They also made the blood platelets less sticky, they slowed the progression of plaques and stabilized them, and they reduced inflammation in the blood vessel tissue. (ibid.)
    All these results, and more, Seelig further informs the reader, are a result of reduced mevalonate in the cells, which is the direct result of an inhibited HMG-CoA reductase, which is the enzyme that statins are designed to inhibit.
    Now stay with me for a second because here is where it gets interesting.
    4. Magnesium is a natural inhibitor of HMG-CoA reductase. Here magnesium and statins are comparable (p. 141.)
    5. Magnesium also acts on two enzymes, phosphatase reductase and phosphohydrolase which reactivate HMG-CoA reductase. By its effects on these enzymes, which contrast one another, magnesium can either stop cholesterol formation or allow it to continue depending on the body's needs.
    6. Magnesium also activates another enzyme, lecithin cholesterol acyltransferase (LCAT) which, through this action, converts LDL cholesterol to HDL cholesterol -- increasing HDL and reducing LDL.  (Statins cannot do this.)
    In the interest of brevity, I'll conclude by saying that whereas statins are known to reduce cholesterol and perhaps achieve other cardiovascular benefits, this is due in large part to their suppression of mevalonate, brought about by their inhibition of HMG-CoA reductase.
    In contrast, magnesium not only inhibits HMG-CoA reductase, meaning that it would achieve the same results as statins in "1, 2, and 3 above," but it also converts LDL cholesterol to HDL cholesterol, achieved by its activation of LCAT, which is something that statins do less consistently.
    Further, instead of poisoning HMG-CoA reductase as statins do, magnesium inhibits it in ways that can be reactivated by other (magnesium dependent) enzymes so that the body can naturally make the mevalonate and cholesterol it needs.
    This is important because vitamin D is synthesized from cholesterol (when using the sun's rays), and cholesterol is also the precursor to testosterone, estrogen, and other steroids.
    So I encourage you to consider using Magnesium for those Apo-B cases that cannot be addressed by carbohydrate restricted diets.

  • JK

    10/30/2011 4:58:10 PM |

    Sorry, meant to say Apo-E cases.

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