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.

More info about modern vaginal surgeries , can be fond on
vaginal repair

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 [...]

The government advice to "eat more healthy whole grains" is not off-base.  But that's not what Americans did.  Instead they ate more fructose and replaced saturated fats with more polyunsaturated fats.  This is totally fundamentally different than eating a low-fat, high-carbohydrate diet like that of the rural Zulu tribe studied by T.L. Cleave or the Africans studied by Denis Burkitt and Hugh Trowell that were diabetes and obesity-free.  

Americans are still not even coming close to the grain consumption of a century ago, when such diseases were exceedingly rare.

This video is very good:

"Vitamin D and Diabetes-Can We Prevent it?"

http://www.youtube.com/watch?v=wTtmvMvgfl0

At this link you'll find the slides of a short presentation on
The Influence of high vs. low sugar cereal on children's breakfast consumption.
There are some surprising findings.

I found it at Cerealfacts.org website

The situation in the UK is much the same. The breakfast cereals most likely to find at discounted prices are those with the most sugar.

It's  often the case the choice of cereal going into the trolley is made by the child rather than the parent. There should be more restrictions on the promotion of pre-sweetened cereals to kids.

In my early 60s I notice that I don't get much "kick" out of sugary foods as I might have earlier.  I've gotten to the point where I can't believe the amount of sugar in say cookies or ice cream...which I no longer buy.  

I do now take several phyto-extracts...pomegranate...blueberry...cocoa...resveratrol...green tea...grape seed...etc.

Pomegranate at least has been shown to moderate insulin response and maybe reverse atherosclerosis.

http://www.lef.org/LEFCMS/aspx/PrintVersionMagic.aspx?CmsID=114814

Great post!
I've just blogged about my eating history too...  years of low-fat, high starch, high fruit eating led me to the brink of diabetes. I'm amazed I survived childhood!

Interesting, but this leaves out neogenesis within the pancreas. Assuming that glucose intake is reduced, wouldn't new beta cells be undamaged and have full functionality? [Unless progenitor cells are also damaged...]

Wouldn't this be more along the lines of adult onset type 1 diabetes (insulin dependent)?  It seems like that is growing too but the real swell seems to be in Type 2 diabetes where you produce copious amounts of insulin but your tissues are resistant to it.

"Interesting, but this leaves out neogenesis within the pancreas. Assuming that glucose intake is reduced, wouldn't new beta cells be undamaged and have full functionality? "

That explains why my obese elderly mom has normal blood sugars even though she has always eaten diet high in simple carbs.

Dr. A, your previous diet was indeed low fat and starch based but there was not much actual, real food in it!  I am missing the connection both here on this thread and in your blog, between people eating manufactured, food like substances that don't have much fat in them and are loaded w/ refined/highly processed starch carbs w/ almost zero fiber or nutrients in them, and the eating of actual whole grains, either fully intact or minimally processed.

"Wouldn't this be more along the lines of adult onset type 1 diabetes (insulin dependent)? It seems like that is growing too but the real swell seems to be in Type 2 diabetes where you produce copious amounts of insulin but your tissues are resistant to it."

If you haven't already, check out Jenny Ruhr's blog, Diabetes Update, and her related website, Diabetes 101.  Type II is being subdivided according to short and long-term beta cell function and insulin resistance.  Different genes cause different impairments.  Emerging is MODY (mature onset diabetes of the young), or type 1.5.  A defining characteristic is that the ability of the pancreas to secrete insulin declines slowly over time, rather than suddenly as in type I, but it declines no matter what the treatment.

I am a Ketosis Prone Type 2 diabetic and it isn't necessarily true that glucose toxicity leads to permanent loss of pancreas functioning.

Typically, we will lose all pancreas secretion and will go DKA, at that point we are essentially type 1's. We need insulin to survive but after 2 to twelve weeks of normal blood sugars we can be taken off insulin and we will have near normal blood sugars.

Weird, yes, but there are thousands of us out there so this isn't uncommon.

Narrative Review: Ketosis-Prone Type 2 Diabetes Mellitus
http://www.annals.org/content/144/5/350.abstract

My blog has more information, if you are interested.

We seem to be severely intolerant of carbs so I too wonder what would have been the case, if years ago the carbs were taken out of my diet.

Michael Barker - your blog is fascinating. Thanks for the pointer. Will you be allowing comments?

What a great resource!

Matt Stone said...
"The government advice to "eat more healthy whole grains" is not off-base. But that's not what Americans did." The public were conned. Manufacturers turned whole grains into dust and formed the dust into junk. Because everything that was in the grain was in the junk, they called the junk "whole grain".

Sadly, this is what happened to me. I had glucose problems by age 15, but they told me for years I was fine. There was less information available in those days. I stopped all soda and junk, but it was too late, my fate was sealed. My pancreas and teeth were damaged. Somehow I managed to eat fruit without getting headaches years later, so I thought fruit in moderation was healthy. I though my fatigue was from my mercury fillings, but now I realize some of my fatigue was from fruit sugar. I blame society and my parents, although I forgive my parents. I was fed tons of soda and every type of high glycemic junk food you can imagine.

Amen. As someone diagnosed with heart diease in the last few weeks, I have a lot to learn, and your materials appear a healthy and informative way to approach the topic.

Hi Dr. Davis,

I searched for that reference but I wasn't able to find it.  I found two papers from Austin et al. in 2000 but neither contained that graph.  Would you mind giving a more detailed reference for it?  I'd like to have that paper as a reference.  Thanks!

HI Dr. Davis--

Since I have been having my cholesterol levels checked, my triglyceride level has always been on the very low side...ave. around mid 30's.  My hdl  and ldl are generally around low to mid 80's.

Could you say something about the people who have low triglycerides...is this healthy or a concern?

My doctors usually think this is great , but I wonder.
Thank you.

Hi, Stephan--

Here's the URL for the abstract on Pubmed: http://www.ncbi.nlm.nih.gov/pubmed/2372896

I also see that I got the year wrong: It was 1990. (Now corrected.)


Anon--

Low triglycerides are wonderful. Your values are at the biologically perfect range.

This is from Anon , who wrote you about my very low triglycerides-in the 30's.  Thank you so much for responding--I had been concerned there was something wrong with me!  
  
I do not think my levels are due to genetics as my siblings have cholesterol issues. I think it is my diet and ex.

Do you see many people with tri's in the 30's?  
Thanks again!

I must be doomed; even with vlc diet (less than 30g per day), fish oil and niacin, my triglycerides have never been under 103. They started at 440, so that's progress, but I suspect I have familial hypertriglyceridemia, as I can't get them to budge lower after two years.

I tried going off niacin at one point, and they rose to 140 again. So I continue with the fish oil (1200mg of EPA and 900mg of DHA), niacin (1500mg 1x day) and vlc diet.

Triglyceride (Trig.)clearing relys on the enzyme lipo-protein lipase being able to function at the capillary endothelium. If a Trig can get into a cell it is not taken out of circulation.

Trigs move around in the circulation bound to lipo-proteins, and one natural component (among several components) of the lipo-protein molecules that carry Trigs is identified as Appoliprotein (Apo) C III. When there is an un-naturally high proportion  of Apo C III involved  this inhibits the working of the enzyme lipo-protein lipase, which is an essential enzyme for clearing Trigs from the blood stream (note: this is not discussing how Trigs get formed).

Apo C III blocks the lipo-protein lipase enzyme from functioning at the capillary endothelium; Apo C III doesn't actually bind to the lipo-protein lipase enzyme.  It (the enzyme) can't get to work at that capillary inter-face when Apo C III over-abundant; so, there is less lypo-lysis (ie: Trig cleaving off) done to the Trig carrying lipid molecules (ie: VLDL, IDL and chylomicron lipids burdened with Trigs).

So, what complicates the natural process when there is no underlying genetic cause obstructing Trig clearing from the blood stream ? If you said "insulin" you are correct; insulin signaling has a distinct regulatory affect on the APOC3 gene expression, which encodes for Apo C III.

Docs interventions keep Trigs down in the obvious manner of setting up less substrate for Trig formation. What contiues to intrigue me is how insulin is involved in metabolic signalling beyond text book role of "driving" glucose into cells.

edit last comment (mine) 1st paragraph, 2nd sentence to read:
" If a Trig can NOT get into ...."

When I had my last lipid analysis, I had been fasting for about 36 hours.  I frequently do intermittant fasting. My numbers were very contradictory and I wonder if my LDL levels were artificially increased due to the extended fast. My triglycerides were 69, VLDL were too few to be measured, but the number of small LDL particles was very high.  Thank you for addressing this issue.

might, as I understand it, as VLDL loses trigs, it becomes IDL, and after further loss of trigs and all apolipoproteins except ApoB, it becomes LDL. I have been wondering if receptors in the LDL family are part of the process whereby VLDL and IDL and LDL lose trigs to cells throughout the body. Is this the way it works, or are receptors of the LDL family all or  mostly in the liver?

Anonymous, would you mind sharing your typical diet and lifestyle practices, including exercise?  I'm sure all curious minds could benefit!  Thank you.

Adam M--In response to your question about my regimen. There really is nothing extreme about it so I have been baffled for years with my cholesterol results esp. the tri's in the 30's.

For the past 20 yrs. I have almost totally avoided processed foods.Basically no junk food at all. Most of that time I ate no red meat. I have probably not eaten enough food...I  have always been a light eater and on the thin side. Lowish bmi but def. not anorexic or any eating disorder . I haven't eaten butter, though I do drink no-fat, or low fat milk and eat yogurt  daily as well. I use olive oil as much as I care to have, and eat walnuts and almond butter.I don't drink alcohol except on the very rare occassion--maybe a few times a yr.

No special supplements...but fish oil over the past 8yrs. and a good level vit d. for the past few years. I was probably vit d deficient most of my life before supplementing vit d.


For the past 10 years, I have walked briskly at least 6 days a week 4-6mi. I lift weights  (dumbbells #15-3-4 days a week. Do some tai chi.

So you can see ...nothing too special but I do think vastly different than most Americans.

My guess is that I am reaping the benefits of some good habits from the past 20 plus years. As I said my siblings take bp meds and statins....I don't take either. I think they have bad eating habits, don't exercise consistently and drink alcohol . Though 2 siblings have fairly decent diets, don't drink much and still need a statin and bp meds.

I am female in my late 50's and siblings a bit older and a bit younger, male and female.

Hope this helps. Anon.

Hi Harry,
The liver exports most Trigs bound to VLDL; when measuring fasting Trigs these are mostly complexed to VLDL. IDL (intermediate density lipo-protein) is really a spin off phase of a VLDL remnant, and is itself short lived (ie: IDL degrades quickly).

When measuring fed (post-prandial) Trigs these are some appearing in VLDL (ie: liver exported) and some Trigs the chylo-microns carry (ie: from the intestine, a different source of Trigs); a relatively minor amount would be Trigs carried by IDL. When fasting (ex: overnight) there are very sparse amounts of Trigs associating with chylo-microns and IDL would be neglibible.

HDL also has to carry Trigs; it (HDL) brings them back to the liver, which hydrolizes (cleaves) those Trigs for the liver to "play" with again. The HDL Trigs are not scavenged from the long enduring VLDL lipo-protein; but are Trigs HDL had picked up (ie: from the peripheraly circulating short lived IDL & chylo-microns).

My understanding is that it is not the LDL receptors that are key to how & when Trigs physically get "off" of any molecule that is carrying a Trig. The Apo C III (detailed previously) is one of several proteins ( Apo C molecules exist in different iso-forms, do so simultaneously and sometimes as mutations); a lot of sub-groups get "bundled" to the Apo B complex.

Apo C III component having excessive expression is what interfers with the enzyme  (lipoprotein lipase) involved in cleaving off Trigs. LDL receptor dynamics only add mitigating circumstances to how/where/when a circulating Trig is coming to be (or not be) presented for cleaving off.

At least 50% of my caloric intake consists of fat, mostly saturated and monounsaturated from grass-fed tallow, ghee, butter, cheese, coconut, olive oil, almonds, avocados, and one tsp. fish oil... I get plenty from organ meats, wild salmon, free-range eggs, chicken, and beef too.  Not to mention I avoid grains, starch, and sugar as though they are poison.

I'm a 50 y.o. male, and try to perform at least three apposing compound weight resistant exercises every day (bench-presses, pull-ups, squats, military-presses, rows, lunges, dead-lifts, power-cleans, or clean-&-jerks.)

I've been doing this for a couple years.

Along with very (visibly) favorable body comp muscle/fat ratios, my last 12 hr. triglyceride measurement came in at 52 mg/dl.  I think I'll stick with what I'm doing.

Dr Davis,

I'm a bit confused about number 4. You suggest that a postprandial value of greater than 88 is dangerous, but accept levels of up to 90 in your program. Are you sure the figures are correct?

Also, are the 4 points in the order you intended?: you move from fasting triglycerides being too high (1), to being low (2), then to being too high again (3), then you move to non-fasting triglycerides in 4, starting with quite a very low figure (88), and suddenly jumping to 400+. How about more typical non-fasting figures in the 100+ or 200+ ranges?

I must really be screwed. Even on six fish oil caps a day and a gram of niacin, I'm at 292.. my all time low was 157. I'm on even more fish oil and cut out breakfast cereal and other sources of high fructose corn syrup. What I need is a whole new genotype....

Dr. Davis,

While I understand that your target audience are probably Americans, as a European, I would be very grateful if you would also post values of the tests you speak of in the measurements used on the other side of the Atlantic. Here we speak of triglycerides in mmol/L, not in mg/dl, so whenever I read your posts I have to sit here with a conversion sheet and calculator, and considering that I can't make notes on other people's websites, I have to do so EVERY time I read your posts, even for the second or third time. It would be very helpful (and probably not too much work for you) if you could post values in both measurement systems, so I can put down the calculator and conversion sheet in the future and put all my attention to the contents.

Thanks for listening.

To ' I must be screwed up, VLC diet may be working for , so you  may want to try a different approach, eg. low fat plant based diet, do some fasting, also may need some attention to your liver.

@Alex: +1

Australia uses mmol/L also as it's the SI standard.

Perhaps a converter on your site or quick reference table?

"I must really be screwed. Even on six fish oil caps a day and a gram of niacin, I'm at 292.. "
If you didn't do this, you may try exercising, sesame butter and soy lecithin.

@Alex:
  +1
We need M measure too. I have to convert each read, too.

Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role. That will be an issue for another day.

Interesting point. Many people think that fat is the most important part of a diet to assess, other factors definitely play a role in heart complications.

Exertion (ex: manual work, breathing harder exercising, endurance training, etc.) improves insulin resistance; the
sedentary, overweight, obese and Type II diabetics are told to actively exercise. Less insulin lingering in circulation means less insulin signals to ratchet up the Apo C III level; Trigs can clear out of circulation (as detailed above).

Lipo-protein lipase enzyme can then robustly cleave of circulating Trigs for then getting into cells. In the cell the Trig must be processed into a "droplet" molecule for storing inside the cell; up to 1% of our genome is suspected to be involved in the biochemistry of achieving fat "droplet", which reflects it's importance.

Fat Storage-Inducing Transmembrane Protein (FITM) in the cell's endoplamic reticulum make this conversion of Trigs into droplets (again note: this is not how Trigs are initially assembled). FITM uses the enzyme di-acyl-glycerol O-transfer-ase
to do the job; then the droplet is rendered into the storage form called di-acyl-glycerol.

FITM 1 is what exists in skeletal muscle endoplasmic reticulum to make muscle stores of di-acy-glycerol. When we exert ourselves and run out of glucose to burn the muscle takes back off the acyl-CoA fractions
from stored di-acyl-glycerol; then it cobbles back together tri-acyl-glycerol molecules (note: this is the same molecule as a tri-glyceride, the more commonly used term just skips mentioning the acyl group) to burn and meet the demand for energy.

Quite conveniently, for those who exert themselves, sustained activity also induces more di-acyl-glycerol transferase enzyme production; it is positive feed back augmenting the rate at which muscles can access their stored "fat" to burn (ie: training increases endurance).

With muscle fitness burning up the on site reserves of di-acyl-glyceride the muscle can then take up more Trigs from the blood stream. Thus Trigs readings are lower for most geno-type individuals who regularly exert themselves (there are a few instances, mostly disease related, where low circulating Trigs are due to the liver holding on to too many Trigs).

Our fat (adipose) cells' endoplasmic reticulum are the other site of a lot of lipid droplet processing for storage; there the adipose cells use FITM 2. When there is no exertion (ie: muscle cells have made no room for more stored di-acyl-glycerides) the Trigs slowly  get into the adipose cells(and some other tissues); so for the sedentary individual burning off that fat "reserve" is extremely difficult.

Might, have you seen Mendivil's paper "Metabolism of VLDL and LDL containing apolipoprotein C-III and not other small apolipoproteins" It's at

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2818784/

It seems to me that there must be some docking involved when a VLDL or LDL particle sheds trigs either in the liver or elsewhere in the body. Maybe it's not receptors of the LDL family that do the docking, but as I understand it, lipoprotein lipase isn't carried by the ApoB containing lipoprotein, but rather, is a component of the receiving cell that facilitates transporting the trigs through the receiving cell wall. The process may not involve full endocytosis, where the whole ApoB-containing particle is engulfed by the cell, but it seems to me that there must be some sort of adhesive or attractive region on the cell to trap the VLDL or LDL at least for a while so that the trig can be unloaded. Any idea how this works?

From what I've read, it appears that the longer half-life of LDL in the circulation, vs that of VLDL and IDL, is due to ApoE being contained in VLDL and IDL, but not LDL. Since ApoE can attach to LDL receptors as well as or better than ApoB can, this results in more rapid clearance of VLDL and IDL than LDL.  

As a result of this discussion and some references like Mendivil's paper, it appears that ApoC is involved also. Since LDL carries only ApoB, maybe that also contributes to the longer half-life of LDL.

Might, have you considered joining Dr. Davis' Track Your Plaque (TYP) forum? I'm a member, and we have many interesting discussions of CHD issues. There is a small fee involved, but we discuss many things before they make it into the Heart Scan Blog. For example, we discussed the subject of this blog thread about a year ago, and as a result, I purchased a cardiochek meter and did a postprandial trig test. My fasting trig level was 57, and I then drank 6 oz of heavy cream. My trigs peaked 4 hours later at 69, which showed that my low-carb diet (30 g/day) had acclimated me to rapid removal of trigs. We learn a lot from each other's experiences.

Anyway, your knowledge of cellular and molecular processes would make a great addition to the TYP forum. There are a number of ApoE3/4, E2/4, and E4/4 people there as well as E3/3's, and We sometimes discuss posts you have made in other fora. I hope you will consider joining us. And by the way, I'm not connected in any way with the TYP forum other than being a member who likes to get into the nitty gritty of CHD issues.

Might o'chondria:

I am enjoying your posts, though they are quite technical and mostly go over my head. It seems you are a very knowledgeable contributor here.
I have one request: You'd be of service for many, if you could add some "behavioral" recommendations or at least sensible things to do/to avoid after you analyze/report/explain physiological parameters and biochemical findings.

A simple sentence, like: Because of this, it would make sense to do this... or that.... or avoid this...would be much appreciated.
Thanks.

Renfrew

Hi Renfrew,
This is Dr. Davis' blog so it is my feeling that specific health
recommendations be his; and he does make them (some here & apparently more specifics  elsewhere). I am not a medical doctor, and do not follow
all his recommendations (as I know them)for that matter.

The fancy words I use are there because contemporary science has coined them to describe the complex details researchers keep finding. A lot of the hyphens (ex: "...-...-...") in words are inserted by me; this breaks up technical words into their component parts. I chose to do this so readers might identify some of the key parts  researchers coined that word from and not just tune out because of the jargon.

To Frank Hagan (I Must Be Doomed) and Anon (I Must Be Screwed) - It does not seem like either of you take enough fish oil.  I visited Doc a month ago and he moved me from 2,400 mg DHA & EPA per day up to 3,000 mg per day - and I my Trigs were in the upper 70's.  Have not tested since.

My understanding of TYP dosages is that you start around 3000 mg per day (DHA & EPA) and you go up from there, as high as 6,000 mg per day until your triglycerides are under 60.

Whatever happened to KRILL OIL ? Has it been forgotten?

I have read that KRILL oil is far more bioavailable than fishoil and chemically more stable, thus less prone to go rancid. Also because we are talking about phospholipids here which are absorbed much btter than ordinary fishoil, I would assume KRILL is the better choice.
Unfortunately there does not seem to be much science on this. Probably because big pharma cannot make a buck out of this.
I'vew been taking Krill oil for a year now and my trigs went from 250 to 56 in about 1 month. Stable since then. Unfortunately it does not seem to reduce LDL or raise HDL.
Any experience, comments or details on KRILL?
Renfrew

Hi Frank-

I am exactly the same way.  Mine started over 1000 then to 769.  On fish oil, VLC, and Tricor (200mg) the lowest I have been able to achieve is 229.  My HDL is very low <25.  Neither of my parents have issues.  Very frustrating.  I am hoping my body/metabolism is healing and it my tri's will come down with time.

Hey Anon-- you ain't the only one! my triglycerides are always around 31. I always thought they were too low as well because they flag low for the lab range.

@Renfrew

No offense, but Might-o's valuable contributions here are clear to me on what specific behavior would be a healthy one.

It can be summed up in one word... move. Well, maybe two more words would be clearer... lift something.  You would literally have to be blind and deaf not to notice all the effective programs  to help reach your goals. I particularly love Erwin Le Corre's Movnat - http://movnat.com/

Our distant ancestors didn't have cars, automated climate controlled houses, refrigerators, cooking stoves, grocery stores, TV's, computers, game consoles, or various other modern conveniences that relieved or distracted them from having to go do physical work... just to survive.

Combine that with today's widely available, tasty, cheap high carb food sources, you have a perfect synergistic formula for diseases of western civilization.

MCA:

You are my bochemistry reference guide and I really appreciate your posts. Please keep posting because you have the ability to answer why.
Moving ones body has got to be one of the best investments in physical and mental health. I would rather do that then obsess or stress-out about numbers on a lab test. Get out in the woods and mountains and cover a lot of miles. I am fortunate because I live in Montana and have the wilderness in my backyard.

10 mg/dl  =    0.555 mmol/L
10 mmol/L =  180.0   mg/dl

Maybe this scale of 10s will help those who need to do quick conversions.

Put me in the genetically hopeless camp.  Tri's are 150 despite vegetables being my only source of carbs and intense activity 3 x's per week (about 1.5 hrs total), body fat and natural musculature that could have me as a paleo-bod model.  I feel hopeless on the blood lipid front.

Easy to confuse....
Chol.LDL&HDL are on a different scale than TRIGS.
To convert mmol/l to mg/dl multiply by 39 for cholesterol.
For TRIGS multiply by 89.

@Might-o'chondri-AL said...
" 10 mg/dl = 0.555 mmol/L
10 mmol/L = 180.0 mg/dl"

When you are doing molar conversions there is a different factor for every chemical. Glucose, triglycerides, ...whatever. All have VERY different figues.

Since removing bread and starch from my life my values have never been so good.  I do *very* occasionally have some rice or soaked beans or lentils...but my fasting triglycerides were 33, my total cholesterol 221, my HDL was 94 and LDL 121.  Just posting in case you are collecting data

My fasting triglyceride level fell from 81 to 46 over a 9 month period.  During this time, I doubled my exercise from 30 mins a day to 60 mins a day (every day of the week).  I believe that this is the cause.  For those trying to cut out animal fat, I have to report that I eat chicken skin and pork fat and this does not affect my cholesterol levels.

I think Might-o'chondri-AL was giving us the conversion factors for glucose.

My triglycerides went from 118 pre-Atkins to 43 after a few years on it. No change in exercise; I just cut out the carbs.

Thanks M. Goroncy & Stargazey,
for correcting my mistake; I do make them, so anytime welcome errors being pointed out.

"Curiously, while fat intake (i.e., triglyceride intake) plays a role in determining postprandial triglyceride blood levels, it's carbohydrate intake that plays a much larger role."

I exercise moderately daily, HIIT and resistance. Eat Fuhrman's ETL diet so I get about 30% calories from fat (raw nuts and seeds)and get about 250-300 grams carbs per day (zero refined carbs though).  My fasting trigs just read at 56.  High dose fish oil can elevate trigs, refined carbs also. Not so much apparently for whole foods, unrefined carbs.

Well stated Paul Mcgrath!

Dr. Davis,

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

I have lower fasting triglycerides since going on a low carb, higher protein and fat diet similar to what you suggest (they dropped from about 100-120 to 60-90). Yet, when I've had an NMR Lipoprofile done, it shows that I have high amounts of small LDL particles (in particular 850 nmol/L of small LDL-P and 1720 nmol/L LDL-P). I'm disappointed both that my triglyercides don't seem to be consistently low and that my small LDL-P is high. I'm otherwise healthy, not obese, no signs of insulin resistance, and eat primarily meat, eggs, dairy, and leafy green vegetables (with some starchy vegetables and fruit).
I recognize you suggest this may be partly genetic, but what does this mean for me and is there anything I can do about it? Have you written about this elsewhere that I can't find? Thanks!

Travis- This might help ApoE.

ApoE 4/4 have to be more selective in their fat selections and amounts than an Apo 3/3.

This may be just 1 genetic marker that can account for your numbers.

2 years ago, when I had a case of the flu, and it didn't go away for 3 months, my doc ordered me a blood panel. My fasting triglycerides were 240mg/dL.

Of course, i also suffered from the typical symptoms of metabolic syndrome: high BP, high cholesterol, obesity (40" waist), diabetic level of fasting blood glucose, low HDL... He told me to eat more "healthy whole grains" and cut out all fat and eat no red meat, to which I answered "that is exactly how I have been eating for decades!"

Google then revealed to me Marks Daily Apple, I cut out all forms of sugar, grains, legumes, partially hydrogenated oils, and most dairy. Added in more grassfed beef, wild fish, coconut. Exercise sessions are short but as intense as physically possible.

2 years later, I'm 40kg (88lbs) lighter, my waist is now 29" (smaller than my mom and I'm a man!), no more high BP, no more high cholesterol, HDL is 90+mg/dL.

Triglycerides? 38mg/dL.

Good thing I didn't listen to my doctor and take a heap of pills which he said I have to take for the rest of my life.

Fascinating NYTimes article (4/13): "Is Sugar Toxic" by Gary Taubes. LINK

Brent, thanks for the comment re: fish oil dosage. I am at 3,900mg of EPA&DHA combined (specifically 2400mg of EPA and 1500mg of DHA).

I have a blood test coming up in June; I may increase to 5,200 mg to see if that has more effect.

Ensues, you might check with your doctor about using niacin (not sure if there's an issue taking it with Tricor so I would check with him; I couldn't continue on Tricor due to an allergic reaction to it).

My lowest triglyceride reading was when I was combining VLC, fish oil at 3,900mg EPA & DHA daily and 1,500mg of niacin.

Dr. Davis has a lot of info here on niacin, including recommendations for using SloNiacin (over the counter) instead of the prescription version (Niaspan, I think) to save money. And he has some tips to avoid the flusing most of us get (what works for me is a regular aspirin 30 minutes before taking the niacin, and drinking plenty of water.)

I notice some comments about large doses of fish oil (3+ grams daily) in order to reduce triglycerides.

Any concerns over immune suppression at these doses? Or even 1-2g doses?

I recall one pubmed study showing close to a 50% reduction in NK activity at a rather paltry EPA dose of 720mg/daily.

http://www.ncbi.nlm.nih.gov/pubmed/11237929

3+gm of fish oil might scare me a bit, longterm, if that study is correct.

I agree with your last statement that carbohydrates are a much bigger culprit to high triglyceride levels than fat intake. Looking forward to that post.

Thank you for all of this information, it was really helpful for one of my classes.

Hi Annon,
NK, a type of lymphocyte cell, is mostly effective against circulating and metastasizing tumors; solid tumors are much less vulnerable to NK action against them. I failed pursuing your link so couldn't read the study, yet the premise that EPA inhibits NK is sound; EPA works  partly because it does keep lymphocytes from getting into tissue cells. Other very common factors that inhibit NK are fats, alcohol and steroids.

EPA is showing itself to be useful against cancer; I seem to recall several types of neoplastic growths are less with EPA  supplementation. The EPA incorporated into a tissue cell's lipid membrane come into play through a series of steps; benefit is not as the EPA  molecule is being carried through the circulatory system.

Might-o'chondri-AL: can you please do us all a favour and start your own blog? I have started reading the comments section of many blog posts simply to see what you have written. All your posts are incredibly interesting, please keep up the good work!

Thanks for the info Frank.  I had indeed read up on niacin.  I started taking 500mg a couple months ago and then bumped to 1000mg after about a month.  I have not had a blood test yet to check the results.  I am hopeful though.  As for flush.  I have tolerated extremely well with really no problems except for one night.  After 2-3 months of no issues I experienced what I would call a crazy severe flush.  My skin was burning so bad I wanted to get it off.  Head to toe, hot and painful.  Not the "mild annoyance" I have read about.  It was nuts.  Lasted maybe an hour and a half.  Drank as much water as I could and a couple of aspirin.  Resumed 1000mg the very next day and have not had an issue since.  Very strange.  Thanks again for the comment.

Be very careful when taking Niacin.  I can not tolerate even the small amount in a B-complex. My blood sugar increases, but even worse I become irrationally angry at the slightest provocation.

Question regarding the reduction in NK cell activity ... could it pose a problem longterm?

Would it possibly lead to a greater chance of infections (as some rodent studies have shown)?

If someone had a metastasizing tumor, wouldn't fish oil then be contraindicated? I seem to recall DHA having some immune suppression activity too (not via NK however), but perhaps Vit E would counteract that.

And then there is also that fish oil/rodent/colon cancer study:
http://www.emaxhealth.com/1275/fish-oil-increases-risk-colitis-colon-cancer-mice

Which seems to indicate DHA may be implicated negatively with colon cancer (in mice).

And finally... I also recall the study testing oxidation values in people, using increasing doses of DHA (which is a bit of a messy way to test, but... whatever).

http://www.futurepundit.com/archives/006499.html

Somewhere between the 800mg and 1600mg levels of DHA, urinary isoprostane increased, which probably isn't such a good thing.

I'm not anti-fish oil, as I take it myself. I am just wondering if too much (2-3+ g), may have some negative consequences longterm.

Hi Anon,
I have no suggestion on how to dose fish oil; I'd like to hear
Doc's limitation on use for high
trigs. This is for orientation on what you are discussing, as I understand things.

Rodent and human models for chronic disease (inc. cancer) involve immune systems that are dissimilar; thus no cancer treatment has (to my knowledge) come from rodent results. That Michigan Univ. (2010) study fed mice that were geneticly pre-disposed to inflammatory bowels, in addition to fish oil, corn and safflower oils; those other oils can be converted into Arachidonic Acid, which is itself pro-inflammatory in some instances.

Isprostanes in the urine are a bio-marker of oxidative activity; their existance is not automaticly evidence of damage to healthy cells. Some isoprostanes are also carried in an esterified form by our good old HDL.

Isoprostanes come in several forms; they are mostly (but not exclusively) by-products of our natural anti-oxidants glutathione and glutathione peroxidase activity.  In other words when see isoprostanes in the urine it shows not only that the body had/has oxidative "stress", but that the body did something about it (ie: glutathione was busy doing it's job).

DHA apparently works to increase the apoptosis (cell suicide/programmed death) of cancer cells, including bladder cancer. One of the theories explaining this effect is that fish oil integrates into the cancer cell lipid membrane; then it becomes part of a cascade of events that along the way produces levels of endo-peroxides
(made inside the cell hydrogen peroxide).

A threshold (ie: high enough
dose)of fish oil must be reached to sustain a level of hydrogen peroxide that the cancer cell will take as a signal (ROS are internal cell signal molecules)
to go into apoptosis. While all that hydrogen peroxide is being spun off, again and again, the cancer cell's innate anti-oxidant glutathione is trying to
keep apace and neutralize it; so an endproduct (but not the endgame of the apoptosis dynamic that can "kill"
developing cancer) is more isprostanes showing up in urine.

When talking about dosage for fishoil what are we actually talking about?
Milligrams per pill or mg for DHA/EPA.
I am reading here 2-3 grams of DHA/EPA. So are we talking about the pure DHA/EPA content?
1000 mg of fishoil is surely different from 1000 mg of DHA/EPA.

Renfrew

Renfrew: amounts of EPA/DHA.

Total content of a fish oil capsule, which is typically 1g, is meaningless without concentration numbers.

So when 3g is mentioned, it's 3g of EPA/DHA, not simply 3, one gram capsules. 3g of EPA/DHA could be up to ten capsules.

Thanks for the clarification.
How about minimizing the number of capsules in taking KRILL oil?
Krill oil is a lot more bioavailable (phospholipids), compared to ordinary fish oil capsules. Less capsules for the same bioavailable amount of EPA/DHA.
It also contains Astaxanthin which is good for brain, eye and prostate health.
The ORAC test results in much higher anti-oxidant capacity.
Why aren't we all taking krill oil??

The reasons against krill oil:

It's not cost-effective nor is it less capsules for an equivalent amount of EPA/DHA (in fact, it's many more).

I know of one comparison study which did show krill oil being about 50% or so more bioavailable that fish oil. But krill oil is like 5-10x the price of fish oil (based on EPA/DHA dosing). So one can do the math there.

And there is also the fact that krill oil has been much less studied than fish oil has.

Astaxanthin is interesting and one day I'd love to see Dr. Davis touch upon it on this blog, state if any of his patients use it, etc. But if you want astaxanthin, I'd think it'd make more sense and be a lot cheaper just to buy astaxanthin (from algae). I've seen it going for as low as $8 for 120, 4mg caps and even non-sale prices are like $10/60 caps. Much cheaper than krill oil.

I have considered krill oil as i am very intolerant of anchovies and most fish oil caps contain it.

Tried the Salmon oil, but ewww...nasty!

Need the benefits of fish oil, but not the side effects.

Thoughts? Time to take the Krill?

Hey Dr Davis

Have a look at Gary Taubes' latest post with blood lipid test results:

http://www.garytaubes.com/2011/04/before-sugar-were-talking-about-cholesterol/

Nina

Any reason to be concerned with very low trigs? Below are my latest blood test results and the trigs seem to be very low. Does this indicate anything?


Glucose = 68.4 mg/dl
HDL = 59 mg/dl
LDL = 98 mg/dl
Triglycerides = 17 mg/dl

A little confused
Before I had my latest blood test I thought having low trigs and a good TC/H ratio was the best indicators of CVD. Thanks to Dr. Davis I discovered the NMR LipoProfile and Vitamin D tests and  added them to my panel.

The good part:
Trigs: 50
Total Chol: 198
HDL-C: 70
LDL-C: 118 (slightly elevated)

That gives me a TC/H of 2.8, which I assume is excellent.

But now, the surprising not so good news:
LDL-P: 1410 (High)
Small LDL-P: 613  (High)
Vit D: 31.4 (Low)

So, how can I have trigs below 60 and have a high LDL particle number and 43% of them small LDL-P?

Can anyone help me interpret these results? BTW, I am  a 50 yo man in good shape and weight.

Thanks in advance

Hi, Dr. , please check your email system, I have not been recieving my emails since you moved to this new site.

THanks

The text
"1) When fasting triglycerides are 133 mg/dl or greater, 80% of people will show show at least some degree of small LDL particles.

2) When fasting triglycerides are 60 mg/dl or less, most (though not all, since genetic factors enter into the picture) people will show little to no small LDL particles.

3) When fasting triglycerides are 200 mg/dl or greater, small LDL particles will dominate and large LDL particles will be in the minority or be gone entirely.

4) When triglycerides are 88 mg/dl or greater after eating, then risk for heart attack is doubled. Non-fasting triglycerides in the 400+ mg/dl range are associated with 17-fold greater risk for heart attack."
does not appear to be sourced from the sole referenced article in this blog post. The referenced article (Austin et al, 1990) is examining a specific human genetic phenotype in regards to triglyceride, HDL and LDL levels. Is there another source of this information, or are there specific page(s) I can read of the article to derive the same information?

Just got back from the docs and have mixed feelings as she prescribed a daily statin! However reading up on the low carb sites and on this blog it might not be all bad news! Fasting Triglycerides were 1.1 (96) and TC was 7.1 (6.22) I'm in the UK and hope I hope I've converted properly. I eat low carb, avoid cereals and am reasonably active, in addition to intermittently fasting. I think I've lost weight, that was one of the reasons I went to see the doctor as I thought my weight loss had stalled, but my BMI was down to 23 from 25/6. Its slow but getting there but I did read on some of LC forums that Triglycerides might be elevated whilst actively loosing weight. Clearly there is more work to do and I'm tempted to get a second test. I won't be taken a statin even though its free (provided on the NHS).

I know very little about Krill Oil. There had been a bunch of posts regarding Krill oil Brand on the various forums and blogs. After doing all research on internet, i came across with Krill oil Professional, this brand product is awesome. I ordered it online from there website at very competitive pricing. And now iam feeling very much relaxed from my Arthritis joint pain/stiffness relief.

How would those of us who have had valve repair and bypass surgery track our plaque if blood tests don't provide the whole picture ?

This is a problem area. One possibility is carotid ultrasound. Though less precise and an indirect measure of the body's burden of atherosclerotic plaque, it's the best that I am aware of once the heart's arteries have been changed or distorted by bypass.

I've been wondering about heart scans and plaque burden.  I have a  vested interest in this as I have a strong family history of early CHD. (FWIW, my CCS is 29 at age 41; not dramatically bad, but I believe that places me somewhere around the 90th percentile for my age; or potentially with the plaque burden of a 54 year old).

Once a person is old enough -- or has sufficient calcification of the plaques -- then there is a very good correlation between plaque burden and CCS.  That is my understanding as to why heart scans are not generally recommended for people under 40 and to some degree even for people in their early 40s.

So, in my case I worry that my low score may actually be an under indication of my burden.  The only way to figure that out though would be angiography or maybe carotid IMT, right?

Which leads me to my second questions: I think what you are doing here is fantastic, but have wondered, is the reduction in CCS a reduction in the plaque burden?  Or is it simply a reduction in the calcium in the plaques?  And how does that impact the stability versus the instability of the plaques?

Whew!

Unfortunately, too much to cover in a Blog. That's why we have an entire website devoted to this topic. You are invited to go to www.trackyourplaque.com to read further. You raise important issues that simply cannot be covered in a few sentences.

Hello Dr Davis,

Interesting post about hard and soft plaque.  I recently had a discussion with my GP regarding my serious increase in scan score (Jan 2006 = 235, Nov 2007 = 419).  

After the first scan we started aggressively going after my LDL, HDL and Trig.. 196,59,221

And have them down to 103, 65, 92 - we still have a way to go to 60/60/60 -

So the increase is a suprise, but my doctor said that the increase could in part be cause some of the soft plaque had been converted to hard plaque and the scan would show that conversion.

Does hard plaque register more than soft?

Thanks for what you  are doing.

Hi, Dave--

I'm glad your doctor is working with you on gaining better control over your plaque growth.

However, there is no such thing as soft plaque converting to hard plaque to increase calcium scores.

Think of it this way: Calcium is a surrogate measure of TOTAL plaque, both soft and hard. In the majority of settings, there is little advantage to characterizing soft vs. hard.

To seize better control, don't neglect: 1) hidden lipoprotein patterns, 2) vitamin D. Also see  our report "10 steps to take if your heart scan score increases more than 10% per year" at http://trackyourplaque.com/library/fl_02-006tensteps-2.asp.

Good luck!

Dr Davis,

Thanks for the response.

  I wonder if you are seeing any trends that indicate a "flywheel" or momentum in the creation of plaque.  I notice you have some patients that take two years or more to stop the growth.  

Starting point Jan 06 - score=236
Quit smoking - Jan 06
Vitamin D - taking 1200
Lost 20 #'s (5'11)=195
Exercise 40min 4x
Fish Oil = 1600 DHA+EHA
Crestor = 10mg
baby aspirin
Basic good diet - no processed foods
Oatmeal and blueberries/raisins everyday.

This month = score=419

After last scan
just added Zetia
Just quit all wheat products
Considering quiting redwine - I tend to have 3-4 glasses versus the recommended 2
Doctor is still saying no to L-arginine (not enough studies)
Considering Niaspan

Any comments?

Thanks again - Dave K

P.S. One more question... maybe this should be a separate post.  Do we know the exact connection between smoking and plaque?  Does it lower LDL size, lower HDL - iritate the lining of the vessels? Is it just elevated blood pressure?  What did my thirty years of smoking do to my heart (versus lungs)?

Hi, Dave--

I'm afraid there's too much to cover in this Blog. You will need lipoprotein testing and almost certainly require more than a baby-dose of vitamin D to gain better control over plaque growth. This rate of growth, however, is very concerning.  

I would invite you to look at the hundreds of pages of discussion on the www.trackyourplaque.com website devote to just this question.

Thanks Again Dr Davis,

I have poured over your website and I'm still reading.  I plan to make your list of turn around "stars".

BTW - here is the comment from my GP - sounds exactly like the cardiologist you mentioned in the original post.

"Remember that although your coronary calcium score has gone up, this does not mean that you are at greater risk than you were a year ago.  Remember that the most dangerous plaque is the not-yet calcified soft plaque, which will not show up on an EBT.  It is only the safe, calcified plaque that can be measured with the EBT.   For your score to go up like it did, while your lipids came down so much, what had to happen was that lots of dangerous unstable plaque was converted to stable, calcified plaque.    There are no accepted guidelines for interpreting changes in calcium scores over time, because the scores tend to go up as treatment converts dangerous plaque to safer plaque.    We do know that aggressively lowering LDL reduces both unstable and stable plaque, and we know that risk can be further lowered by adjuvant therapy such as I listed above. "

Sigh . . .

It's amazing what a simple reading of the literature by your doctor would reveal to him/her.

In near future, I will be posting some blogs that summarize crucial studies in the heart scan literature in an effort to provide better weapons in your fight.

Dr Davis,

Thanks again for all you are doing and I look forward to whatever you can post.  I plan to challenge some of my GPs positions.  Your data certainly is of enormous value.

Dave K

P.S. I going to 2000 vit "D" tomorrow.

Also - have you thought about a "track-your-plaque" certification.  Something to indicate that our Drs are at least up to speed on the latest in *preventative* proceedures...?  I would switch.....

Hi, Dave--

Yes, excellent thought.

It is something we'd like to aim for, but over the long term, since right now there are too few to make a difference. One by one, they are declaring themselves and separating from the "pack."

Stay tuned for more on this issue. In the meantime, I continue to try and inform my colleagues about what is right, what is wrong, what is preferable for patient safety and yields truly empowering information, and try to impress on them that the practice of cardiology is not just about enriching their retirement accounts.

You know, I have always made the assumption that our ancestors' teeth didn't rot because they weren't exposed to refined sugars and carbohydrates. I know accessible fluoride wasn't around then, but then again, I'm hearing that even fluoride may not be the best thing for teeth or bones (or humans) anyway.  What about Weston Price's research?
Good post!
Adam

I agree with DietKing...everything I've read has indicated that dental carries were seen only after the start of agriculture. I've also read several studies that indicate that early man more likely made a big kill and then fed off it for several days....kinda like wild cats do today. I agree that it often took several days to make a kill, but once done, it fed them for more than just 1 day.

Otherwise I agree....get back to natural as much as possible and you'll fare much better.

We are very much least we are slaves to our ancestors dna.

ironic that modern "progress" intended on increasing our survival is in fact killing us. We have built an impressive civilized society but it is not really compatible with our genetics. Maybe we need a genetic software update, nature tries to update our dna by natural selection but we have done everything possible to try to stop it either because of emotions or greed. (democrats or republicans)