Did the monkeys get to vote? ;)

I would LOVE to read a response from the AHA!

Come on Doc, these statistics are obviously bias. That's like asking the readers of an vegan/animal-rights blog, "Do you think meat is murder?" and trying to transpose the results as being all encompassing.

I have to agree with Anonymous here. Nothing surprising in the fact that the majority of readers of a blog that regularly criticizes the AHA have a critical stance towards the AHA.

Move along, these are not the droids you're looking for.

I think you are being a bit generous to them. I certainly agree about the ADA. They seem to be in it for the money and they are getting plenty of it from drug companies. I am a physician and a diabetic and if I followed their advice my blood sugars would be out of control. As it is I am on a very low carb life style and in excellent control!
Thanks for your posts.

certainly it's not a random sample, but nonetheless, I would have to agree that all of these organizations and government agencies are losing credibility with the public and fast.  As a health professional myself, I can only hope my colleagues may begin to soften their stance before our credibility is completely shot with the public.

Tuck, the monkeys must make up the extra 18%.

Doctor, I truly appreciate your blog, read it religiously and follow much of your advice, but before forwarding to the AHA, you might want to check the numbers.

I think the AHA has done a lot of good in the treatment of heart attacks and keeping people alive.  However, I was thinking mainly of the "prevention" side when I voted "Tries to maintain the procedural and medication..."

Likewise, the ADA and other diabetes orgs are no doubt doing some good research into causes and prevention of type 1 diabetes, but their nutritional approach is a disaster.  Again, just maintaining the status quo for so long that they would be afraid to admit they were wrong if they finally did see the light.

Their heart is in the right place. In another 40 years scientists will be deriding the intriguing bloggosphere theories.

I just dislike these organizations jumping on a bandwagon d'jour, and trying to apply it to everyone blanketly.

People are not a " one size fits all " species!  When will the AHA, ADA, etc, stop aligning with big agriculture and pharma and think of individual people and their specific needs?  Is that just a pipe dream?

Real Food RD, I'm with you!

I was going to throw the other ADA in that stack too.  I've let them know several times how I feel about their corporate sponsors and partners.  Disgusted.

To be honest... after promoting such a lifestyle for so many years... wouldn't a sudden change in opinion open them to law suits?

How can they respond to that?

Great point Brian. I hadn't even thought of it.

Wouldn't it be the same with any condition that current medical research might up- end the treatment protocols?
ie..remember when patients with gastric ulcers were advised to drink milk and cream and avoid spicy foods etc?  
Then enter H. Pylori...albeit some 10 years after published studies and much derision from U.S. gastros. Treatment standards changed dramatically. Never heard of lawsuits over that.

Could people leave more than one response?  The percentages add up to more than a hundred.
Bob

OK, I did the math.  Apparently about 375 unique respondents, with 70 or so choosing more than one answer.

My impression is that 'disease associations' exist primarily to ensure their continued existance.

I have heard good reports on the Muscular Distrophy Assoc.

Dr D, I don't think the AHA is sending you a Christmas card this year

I don't know if this would qualify as an endogenous substance, but I've recently added the herb turmeric to my supplementation list. I take a capsule or two a day.  I'm on an e-mail list for supplement studies and marketing going on in health food circles, and it seems tumeric is receiving good press for its ability to help strengthen bones. Figure with the connection between brittle bones and heart disease, it's worth taking a little.

Dr. Davis,

You mentioned that estrogen is a natural substance that causes problems if administered at higher than physiological levels.

You do know, I hope, that all the data showing supposed problems from estrogen supplementation is from research studies where women were given MUCH too high doses. I've been using a dose of non-horse origen estrogen about 1/4 of what they used the studies and it makes a huge positive difference in my blood sugar, blood pressure, and weight with no negative effects on my endometrium (which my doctor has me get measured with ultra sound every so often.

I'm very grateful that I have a good gynecologist who didn't react mindlessly to the research showing negative outcomes from estrogen.

It appears to be protective against macular degeneration (which made my dad blind in his 90s) and for me it makes blood sugar control much, much easier.

But the usual dose given women is much, much too high, and it isn't adjusted for body weight or titrated by observing symptoms. And hence the whole idea of supplementation has been nixed.

That is interesting about the bones and tumeric. I recently added curcumin because my fibrinogen level was elevated. Maybe it will help with my bone loss too. That would be great.

What is the difference between tumeric and cucurmin? Does it matter which I take? I could not find tumeric but I did find cucurmin 500mg.

Hi Anne,

I guess it is the curcumin found in the spice turmeric that is receiving positive press.  As mentioned I've seen some on bone health studies but have also seen heart health and diabetes write-ups too.  I'll post below a recent small rodent research paper on diabetes benefits of curumin:

Curcumin may offer diabetes benefits: study
By Stephen Daniells

KEYWORDS

    * Phytochemicals, plant extracts

    * Diabetes

GET THE LATEST MARKET REPORTS

    * curcumin
    * diabetes
    * cardiovascular health

All market reports

30-Apr-2008 - Curcumin, the natural pigment that gives the spice turmeric its yellow colour, could have benefits for diabetics, suggests a joint Korean-American study.
A mouse model of diabetes was used to test the effects of curcumin on various variables and significant improvements were reported for insulin resistance and glucose tolerance, report the scientists from Sunchon National University and Kyungpook National University in Korea, and Columbia University in the US.

Curcumin has increasingly come under the scientific spotlight in recent years, with studies investigating its potential benefits for reducing cholesterol levels, improving cardiovascular health, reducing the risk of Alzheimer's, and potential protection against cancer.

If results of the new study, published in the journal Molecular Nutrition & Food Research, can be repeated in humans, it may suggest potential for the spice for diabetes management or prevention.

Promising results for diabetic mice

The researchers, led by Mi-Kyung Lee, used diabetic mice, so-called db/db mice, and non-diabetic controls, named db/+. The animals were fed diets with or without added curcumin (0.02 per cent) for six weeks.

They report that the diabetic mice supplemented with curcumin experienced lower blood glucose levels, than the controls. The animals also lost less weight.

Activity of the glucokinase enzyme in the liver was higher in the diabetic mice following the curcumin-supplemented diet than in the diabetic control group. This enzyme plays a key role in the conversion of glucose into glycogen, the body's main carbohydrate stores. This would blunt the glucose rise following the meal.

The spice was also linked to reduced activity for other enzymes associated with the production of markers of cardiovascular health, such as free fatty acids, cholesterol, and triglyceride were also significantly lower following curcumin supplementation in the diabetic animals.

Importantly, no effects were observed on blood glucose, plasma insulin, and glucose regulating enzyme activities in the non-diabetic animals, stated the researchers.

"These results suggest that curcumin seemed to be a potential glucose-lowering agent and antioxidant in type 2 diabetic db/db mice, but had no affect in non-diabetic db/+ mice," they concluded.

Potential market opportunities

Significant additional research needs to be performed before anyone can contemplate recommending curcumin for diabetics, but if further studies support these preliminary positive findings, this may offer help for the estimated 19 million people affected by diabetes in the EU 25, equal to four per cent of the total population. This figure is projected to increase to 26 million by 2030.

In the US, there are over 20 million people with diabetes, equal to seven per cent of the population. The total costs are thought to be as much as $132 billion, with $92 billion being direct costs from medication, according to 2002 American Diabetes Association figures.

Source: Molecular Nutrition & Food Research
Published online ahead of print 8 April 2008, doi: 10.1002/mnfr.200700184
"Effect of curcumin supplementation on blood glucose, plasma insulin, and glucose homeostasis related enzyme activities in diabetic db/db mice (p NA)"
Authors: K.-I. Seo, M.-S. Choi, U.J. Jung, H.-J. Kim, J. Yeo, S.-M. Jeon, M.-K. Lee

Turmeric is about 4% curcumin. Turmeric and curcumin need fat like Vitamin d to be best absorbed. Lecithin also improves absorption.

As much I know the large doses of cretin monohydrate are widely taken, particularly by athletes, as an endrogenic supplement; cretin supplements are also taken by patients suffering from gyrate atrophy, muscular dystrophy, and neurodegenerative diseases.
Physical Therapy Supplies

Amen, brother! This is the dirty little secret that proponents of the lipid-hypothesis of CAD continually try to sweep under the rug. Looks like the cat's out of the bag, though, thanks to the internet.

But what can be done about post-meal elevated triglycerides?  Would it be best to avoid fats too, and just eat fruits and vegetables, if one had the will power to do it?

Perhaps we should just give up eating altogether.

I think that worrying about post-meal elevated triglycerides is probably shortening your life more than post-meal elevated triglycerides.

so what does this mean?

"It also remains true if you chronically consume fats."

my understanding is that it is actually in support of normal metabolic functioning for us to "chronically" eat fat. low carb eating, in my lay-person's opinion, means therefore eating good fats (and i am of the un-pc standpoint that saturated animalfats are a-ok) , not just green veggies alone. low-car and low-fat would be no fun! but that's just my 2 cents.

I've had two non-fasting cholesterol tests performed in the last year.  My fasting triglycerides are around 40.  My triglycerides three hours after eating a meal with 10g carbs and 59g of fat were 91.  The time prior to that, they were 79 eight hours after breakfast and three hours after lunch (both were high-fat meals).

Yeah, they go up, but not that much.

So what about the other side of the equation? Decreasing the absorption rate of fat (or spreading it out over more meals) might not help any. But if you can optimize the deposition of fat where it really belongs, in subcutaneous fat tissue-- that is, if fat is deposited in fat tissue where it belongs until needed, at a rate close to the rate at which new dietary fat is absorbed into the bloodstream-- then there shouldn't be a problem.
Interventions that raise HDL generally increase adiponectin. Eating less wheat, beer, fructose, or adding in fish oil, niacin, vitamin d, even being born a woman. And they also associate with less wheat belly.

http://www.springerlink.com/content/dpy09vbc0r8jxnm9/

-----------------------------------
Conclusion/interpretation. These data suggest that adiponectin concentrations are determined by intra-abdominal fat mass, with additional independent effects of age and sex. Adiponectin could link intra-abdominal fat with insulin resistance and an atherogenic lipoprotein profile.
--------------------------------
Maybe they've got cause and effect reversed here? I read a study in mice that were leptin-deficient. Adding extra adiponectin made the mice fatter. So adiponectin is probably not so much a reaction to deposited fat as it is a promoter, maybe a facilitator of proper fat storage.

?

Thanks, interesting post. Just wondering: what about proteins?

So if I eat cheese slices with butter as snacks all day, my triglys will be chronically high and I can get heart problems?

Does this mean that intermittent fasting is very important if you eat low carb/paleo style?

Where Oh Where can I find a Doctor like Doctor Davis in the New Jersey area?

My doc who is a cardiologist referred to by local medicenter when it was found out my Trigs were 235 and Total Cholesterol were 295, LDL 195, HDL 57, promptly put me on 5 mg Crestor to lower trigs and LDL, never discussed diet or anything with me. His office plastered with Pfizer Lipitor posters and Crestor bags given by pharma reps.

Heres the kicker, this was all done with blood work that was NON-FASTING. I had blood drawn an hour after I had eaten eggs and bacon. This was also around halloween time too when I was over indulging on ALOT of Sub sandwiches and bread and lots and lots of candy. I love peanut butter cups. But I know 5 a day is excessive, which was my intake.  Was I getting a DOUBLE Whammy increasing my Trigs?

Since I found this blog, I've been taking my Crestor which I don't want too. But have taken up the no wheat diet and HFC out of my diet that Dr Davis suggests. Dropped 18 pounds in a matter of weeks.

Took my own cholesterol with one of those home machines after 4 weeks of Crestor. Doctor wants to test after 3 months. But my Total Cholesterol was 151, calculated LDL 87, HDL 50 and Trigs 69. I wonder how much was the Crestor doing the change or the change in my diet and 18 pound weight loss?

Sorry for the rambling, but Dr. Davis your blog does give great info and brings peace of mind to me.

Anonymous,

Absolutely not. Having elevated triglycerides immediately after a meal is not a dangerous thing. It's only when they are chronically elevated that you are in danger. Same thing with insulin. Chronically elevated levels are the problem.

Both of these are caused by excessive sugar/carb consumption.

-Bryce Lee

Bookmarked this. Sometimes non-standard due to you after sharing. Positively value my time.

Dr. Davis: a friend of mine recently had triglycerides trending up to 700 and more. I pointed him to your blog, recommended low carbs and fish oil, and after *one month* his TGs are around 200.

Kudos to you.

Interesting series of posts. But keep one thing in mind: Excess blood glucose is converted to palmitic acid by the liver...a saturated fat.

(This fact alone should give the anti-saturated-fat crowd pause...if the body could have evolved to convert glucose to any type of fat, why did it evolve to produce a saturated fat? Can't be too bad for you...)

Anyway, if the body through DNL produces a saturated/healthy fat after only a very brief (and normal) spike in blood glucose - after which the glucose returns to a normal fasting level - then high starch (not fructose) diet appears to be quite healthy. This would answer the question of why a rice-base culture can maintain good health while consuming a diet high in starches...in effect, they are eating a high saturated fat diet.

If they don't eat continuously, allowing their bodies time to eliminate the excess blood glucose and the attendant insulin spike before the DNL triglycerides (palmitic acid) hits their blood stream, then there is no insulin-driven storage of the fats. Instead, they have elevated blood-borne fats that remain available for a consistent energy source of over time, of a type that their body prefers and has evolved to produce.

Can you get the same effect from eating saturated fat in the first place? Yes. But to assume that this is better than the starch-driven approach you have to accept that higher levels of ANY saturated fat in the bloodstream is unhealthy. Which runs counter to the viewpoint of paleo and low-carb eaters.

As Stephen has pointed out, there is no evidence that post-prandial glucose spikes are dangerous to someone with a healthy metabolism (i.e. not a type I or II diabetic). So, if there is no evidence of danger from a post-starch-meal spike, why would your body care where it got its saturated fat? Either dietary or liver-produced, it’s all the same once it is in your blood.

Following the chain of reasoning further, a high-starch diet that leads to DNL production of palmitic acid would be healthier than a high fat diet composed of vegetable oil or other undesirable fats.

We have to be very careful about quickly latching onto bits of "evidence" that confirm our biases. Remain scientific, think it through. The human body is an amazingly complex organism; when we begin to isolate its responses to prove our points, we can start down a path that leads to conclusions that may satisfy our dietary worldview, but are not entirely accurate.

Scott W

Note: If we are being carefully scientific in our approach, we should be careful to distinguish our descriptive terms for non-fat and non-protein calorie sources. "Carbohydrates" is too general. It encompasses fructose, which as a much different effect on the liver than glucose. My discussion above focuses on starches for a reason; they break down to glucose, which the body has evolved to handle efficiently, even in large quantities. It can handle fructose, too, but did not experience it in large quantities prior to modern times. Even using the term "sugar" is inaccurate, since it is half fructose and half glucose. By extension of my discussion above, eating pure glucose powder (dextrose) would be as healthy for a rice-based culture as eating white rice itself. You are simply giving the body the end product of rice digestion (glucose), from which it can produce palmitic acid.

There's no question that postprandial triglyceride-rich lipoproteins are causally related to atherosclerosis, regardless of whether they were fat-driven or carbohydrate-driven.

However, these brief posts are NOT meant to endorse low-fat diets. They are meant to show that a simple low-fat vs. low-carb approach is too simple-minded. There are other aspects of diet that count for substantial effects. Postprandial phenomena are one important class of effects that cannot be fully controlled by just controlling carbohydrate or fat content of the diet.

You still haven't explained why the chart in your previous post (Di Novo Lipo-what?), where normoinsulinemic people have lower DNL on a high-fat diet, is in marked contrast to the chart of Gretchen in the post before that (Gretchen's postprandial diet experiment II) when she was eating high-fat.  From those two posts, it seems that peoples' postprandial triglyceride level is dependent on the amount of insulin they produce (and obviously how sensitive they are to that insulin).  Therefore a high-fat diet is not problematic unless one is also hyperinsulinemic.

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.

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

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.

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.

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).    

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."

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?

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.

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.

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

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.

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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.

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.

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.

Sorry, meant to say Apo-E cases.

[...] sensitive to dietary fat, particularly saturated fat, as well as carbohydrate. William Davis MD has found that for these individuals, moderation of both fat and carbs is necessary to avoid elevations in [...]