There are foods, which can easily lower the LDL. You should consume fishes. They are considered to be the greatest source of omega3 fatty acids. They can easily lower LDL levels and increase good cholesterol levels. In order to discard heart diseases, it is always advisable to eat high soluble fibers. You should consume lots of green colored vegetable, fruits and cereals to reduce LDL.

Thanks Dr. Davis. This is definitely very interesting. Would it be plausible that higher omega 3 levels are protectorant solely because omega 6 intake and cellular AA is so astronimically high?  

I ask if you've considered this because there is a sect of researchers that believe, when both omega 6 and 3 levels are low, an even more beneficial and anti-inflammatory PUFA is produced in its place called Mead Acid.  

Just wondering if you've encountered these ideas, and if so, why you've written them off in favor of achieving a high omega 3 level.

My guess is the other biggest cause of variation in omega-3 index, after omega-3 consumption, is omega-6 consumption. Inversely of course. Dr Bill Lands writes extensively about this on his essential fatty acids education (efaeducation) web site hosted by the NIH.

Does the omega-3 index likewise have the same striking correlation with stroke incidence?

Dr Davis,

  Is there any issues with international orders for the O3 Index kit?  For myself, Canada specifically.

Also, I'd be interested to hear your thoughts on *over* consumption of omega-3s and the potential health hazards, if any, in a future post.

I'm kinda fuzzy on the interaction between omega-6 and omega-3. Would lowering omega-6 consumption increase the Omega-3 Index as well?

I've lost over 40 pounds so far with diet and exercise.  I blog at Fitness Achievement

Harris and v. Schacky proposed omega-3 index in 2004 as a novel physiologically relevant, easily modified, independent, and graded risk factor for death from CHD that could have significant clinical utility
http://tinyurl.com/ybxmor4

In my view it is impossible to reach a 8-10% omega-3 index just by increasing intake of fish and other seafood. One needs fish oil as dietary supplements.

The role of LDL cholesterol in atherosclerosis is a major misunderstanding. The mechanism of the disease is mainly chronic low-grade inflammation, and omega-3:s are excellent anti-inflammatory agents. JELIS demonstrated it nicely. The effect goes beyond cholesterol.
http://tinyurl.com/ye55mfr

E-EPA (1.800 mg/day), as dietary supplement, prevented angina pectoris, clinical myocardial infarctions and new cases of coronary heart disease in Japanese population, although they eat 5-6 times more fish and Americans.

And even more important: keep the Omega-6 low. One you do that, you won't have to worry so much about additional intake of omega-3.

If fish oil does turn out to be the fountain of youth it will be bad news for the fish.

Leptin receptor polymorphisms interact with polyunsaturated fatty acids to augment risk of insulin resistance and metabolic syndrome in adults. This study shows how low omega 3 status and/or high omega 6 status exacerbate genetic risk of hyperinsulinemia and insulin resistance and changing to a high omega 3 low omega 6 status abolished that risk factor.

In response to Medical Answering Services  may I remind readers farmed fishes, such as Tilapia, may provide more omega 6 than omega 3 and may be equivalent to eating donuts or burgers.

Omega 3 and omega 6 should in a 1/1 ratio. In order to maintain that you need a low carbs diet and supplement with about 3.000 mg of fish oil per day.

Commercial fish is loaded with omega 6, so is most of the meat you buy at the supermarket.

So, in the real world you have to cut all grains, grain oils and take some omega 3 supplements.

If any of the readers is interested in reading about omega 3 in spanish, please go to http://www.omega-3-fish-oil-wonders.com/omega3.html

Best wishes,
Alfredo E.

While fish oils are a viable source for omega 3 fatty acids, reports indicate krill oil may be a more suitable supplement for cholesterol lowering strategies.  

A recent study on neptune krill oil and cholesterol found patients taking 500 mg. per day of Neptune Krill Oil experienced total cholesterol decrease of 19%, LDL cholesterol decreased by 44% and HDL cholesterol increased by 33%.  Study subjects who took 3 grams a day of fish oil supplements experienced Total cholesterol decrease of 6%, LDL cholesterol decrease of 4% and HDL cholesterol increase of 4%.  

Fish oils do offer cardiovascular benefits, but it may appear Neptune Krill Oil could be a more suitable supplement for patients seeking more aggressive cholesterol lowering treatment.

What a great resource!

I ate fishes but fried them in sunflower oil but there was no benifit

Here is the latest article written by Prof Clemens von Schacky about Omega-3 Index
http://20.fi/3779

Dr Pentti Raaste and yours truly have just published a small leaflet for prevention and self treatment of cardiovascular diseases http://20.fi/3780

30-Days of High Omega-6 Diet--Stiffens Arteries and Increases Belly Fat

I was shocked to see what happens when someone with a good omega 3 status changes to an omega 6 rich diet for a month.

Now consider what happens when people have been consuming too much omega 6 in relation to omega 3 from  conception and throughout their entire lives.

The data suggest that, while an omega-3 index of 7.3% is associated with reduced risk for sudden cardiac death, a higher level of 10% or greater is associated with less risk for heart attack. Surprisingly, fish consumption and fish oil intake account for only 47% of the variation in omega-3 index.

That graph really shows how healthy omega 3 is. It is just a very amazing thing. I think taking omega 3 regularly will keep our body healthy.

I discovered the powers of omega-3 when I was diagnosed with rheumatoid arthritis. of course, that didn't cure me but I'm really better now on omega-3 supplemts. It's not eliminating fats what we need to be healthy (as many would say), it the RIGHT fats. I'm glad the healthy fats topic is getting more and more popular.

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.

Hi Dr Davis, nice post

The parallels you describe so neatly become self explanatory once you realise that niacin acts on the beta hydroxybutyrate receptor. Even without full blown ketosis, LC diets raise the level of the natural ligand for the receptor that niacin, at pharmacological dose rates, stimulates. And no flush from LC.

Regarding LC diets as a means to weight loss alone misses their intrinsic health benefits.

Peter

Nicotinic acid receptor subtypes and their ligands.
Soudijn W, van Wijngaarden I, Ijzerman AP
Med Res Rev. 2007 May;27(3):417-33

Thanks, Peter. I wasn't aware of that.

In your experience have you seen a lipoprotein benefit to a wheat-free diet in people where there is little excess weight to lose, say 5 to 10 lbs?

Yes, though the magnitude of benefit is usually less. In this case, small LDL in particular is largely genetically driven. You can only hope to suppress it to a minimum.

as soon as I started lc, after about three months my hdl went from 40 to 68 and stays there, I don't excercise much so its not due to anything but lc I assumed.

However,my score from scan went from 183 in '04 to 390 in 07 so that alarmed me but my doc said if I didn't lc, as I lc most the time, calcium score could have been way higher.lc is not only great for weigh loss but bg and craving control
Thnx for comparison list, wish ADA would recognize this.

Chickadee North - While I am a believer in reducing/eliminating processed carbs especially for people who have metabolic syndrome, are diabetic and/or overweight, you still had an increase in calcification of 30% per year.  That outcome is consistent with the results that occur when there is no intervention in terms of diet/drugs/lifestyle.  Thus, I am somewhat skeptical that the low carb diet kept you from having an even greater increase in calcified plaque.

There are other benefits from low carb that you don't see with niacin. Lower BP, lessening (at minimum) of symptoms of many chronic diseases, lower blood sugar and insulin levels...all very important in today's world!

Can you please comment on this article:
http://in.reuters.com/article/health/idINWRI08496320071210
"In middle-aged and older women considered to be at low risk for heart disease, calcium build-up in their heart arteries, an indicator of artery-clogging plaque, predicts the development of heart disease and heart-related events like chest pain, heart attack and stroke, new research shows."
Doesn't plaque and calcium build up in the heart indicate heart disease?

Yes, excellent points!

I believe that study is yet another piece of evidence that heart scans (for coronary calcium and plaque quantification) are vastly superior to risk factor analysis, such as that in the Framingham equation. As the study points out, the Framingham risk equation mis-classified a substantial number of people as low-risk.

Incomprehensibly, the report quotes some reviewers as saying "There is not enough evidence to support coronary artery calcium screening in low-risk women and they call for further studies to better identify who would benefit from such screening."

This is another study among many that have shown similar results.  How many people have to die or have heart attacks needlessly before the deeply entrenched habits of the status quo are broken?

Re: "In middle-aged and older women considered to be at low risk for heart disease, calcium build-up in their heart arteries, an indicator of artery-clogging plaque, predicts the development of heart disease..."

I think this relates to Dr. Davis orignal post on low carb.  Since glucose metabolism involves a lot more calcium than lipid or ketone metabolism then perhaps excessive calcium build up may be a proxy for excessive glucose metabolism?

  It may explain a curious fact that anything that switches metabolism away from glucose (e.g. niacine acting towards ketone b., vitamin D3, fasting or L.C. diet) would also at the same time act protective against the coronary heart disease?  Interesting!

Stan (Heretic)

But my question is....If there are already calcifications doesn't that mean there is already Heart Disease?

So the women with calcium plaques would HAVE heart disease, not be AT RISK of developing it?

"...calcium build-up in their heart arteries, an indicator of artery-clogging plaque, predicts the development of heart disease..."

Somewhat unrelated question:  
Angiotensin II inhibitors like Benicar apparently have the additional effect of dramatically lowering Vitamin D 1,25D in the body, and some think this is useful for people with Lyme disease and chronic fatigue system ("Marshall Protocol" http://snipurl.com/1v5s6). [Adherents of this protocol believe that in these diseases, opportunistic bacteria thrive on the additional Vitamin D.]

However, for hypertensives who don't have CFS or Lyme disease, does this trait mean that drugs like Benicar, while reducing blood pressure, might be increasing coronary blockage by interfering with Vitamin D?  (I guess my questions are, Am I concerned with the right form of Vitamin D?  If  so, are angiotensin II inhibitors problematic for blocking Vitamin D?  Do they make Vitamin D supplementation pointless? If so, what's a better drug for hypertension?)

Anyway, if this question is too far afield, ignore it, and thanks for a great blog.

A few things we don't know about chickadee north;

1 her age. (did she just enter menopause or premenopause?
2 when she started her low carb diet.
3 how often her heart was scanned between 2004 and 2007.
Without knowing these, I think we have to give her doctor the benefit of the doubt.

Cindy--
Yes, you are absolutely right.

In arteries, calcium = atherosclerotic plaque, not risk for plaque. It is a risk for coronary "events" like heart attack, however.

The Benicar/ARB and vitamin D connection is interesting. I've never heard of it. Do you have any data or references?

Honestly, I'm a layperson and can't comment intelligently on it other than to suggest you look at marshallprotocol.com

Some of the things that jumped out at me were Benicar's (and to a lesser extent, other angiotensin 2 inhibitors) ability to block  at least one D3 variant, the idea that chronic fatigue/fibromyalgia/etc are the result of infection by a new form of bacteria that survives by hiding within immune system cells, the concept that because of this, D3 actually protects the bacteria in these patients, etc.

It's all wayyyy out there, but fascinating, and I thought you'd be interested.  (At the very least, it might affect your choice of hypertension med.)

I am 57 and am menopausal since 04, have lc since 03 and fell off wagon for almost a yr,was in extreme grief with death of kid sis and other significants in my life and neglected me.

Had one scan in 04 at 186 and then second scan in 07 ( 2 weeks ago) and it was 390, so yes about 30% a yr.

I assumed dropping A1C from 8 to 5.8 would have a bearing, no wheat products and eight loss of 80 lbs, way lower bp mostly about 110/68 or so would have given me less of  score.

For 5 months in yr I run a B&B and work hard enough to make a sweat and in winter I walk.

I only knew about Vit D and fish oil since coming here, few weeks back,  so take fish oil, its harsh to do as I have that HP bacteria and the fish oil makes allot of heartburn and distaste. I am waiting for the softgel Vit d 3 as can only get the dry form here, as well the l'arginine was ordered as well.
My ldl is 97, my hdl is 68 and trig are 78.Ratio is 2.5, have not got advanced lipid profile back, should all be back this week and CRP and lip protein  were all low and within norm levels.

I've been diabetic since 94 and needed insulin which I no longer need. I tried to use Actos as I read it reversed some plague so asked a doc for some, but it caused some chest pain and side effects so after 3 months I quit it.

Stress has been a factor with husbands illness, many deaths and just finished testing for lung cancer( on my recent heart scan the radiologist noticed something in my lungs???? and suggested the rule out cancer??)(never smoked a puff in my life but my mental health patients smoked in my office for a few decades until I put a stop to it in 1980 and got my wrists slapped for doing that).

Now I know I have no lung cancer am assuming my stress will decrease,husband being tested for asbestoses etc so lots of anxiety,I know thats not good for heart either,  typically I handle stress ok and use alot of humor in my life.

So now you know more and can make some impressions. This doc doesnt really know me but felt had I continued with my program from Cdn Diabetic assc which was hi grains I would have had a higher score and my A1C couldn't get under 7.8 on insulin and I needed 158 units of humalog a day to keep it there so now I am not as insulin resistant , since lc, so maybe I would have a higher score if hadn't lc.

I am only assuming and am only learning all about the TYProgram, I tried to introduce some oat bran daily but it spikes my BG way too much and I am aiming for AC under 5 so will stick with ground flax

Anyone have some insight let me know, oh yes my vit d blood level was low as was DHEA, hormone levels of progesterone and all estrogens very low too from saliva test so using bio identical progesterone cream.

I am assuming I will start on Niaspan to drop trig.

Hi, Chickadee--

I believe that you are on the right track. I encourage you to stay in contact through the Forum, where we can discuss your issues in more detail, along with feedback from other members.

Yes I plan too and once all blood work back I am hiring you to do a consultation via scanner, how new age is that!!!

I have had one diet pop a day as a treat for a sweet taste but am stopping that now too since reading about carbonation on the forum, lots of good info there for sure and dedicated membership

Lipoprotein(a) in 2004 was 0.21g/l and in 2007 June was 0.09g/l.....so there is hope for me yet
I should have new NMR results in few days.

This 04 one I had only been low carbing for one yr.So maybe prior to that it was higher, but never had it checked ??

I am exited to know that and now to try your ideas as if I could do that without supplementation and often off the statins....then who knows whats next

Thnx soooo much for all your insights

chickadee-

That's curious: a big drop in Lp(a) with low-carb diet. Although the diet clearly works, I've never seen such a a dramatic effect on Lp(a). Was there anything else you did?

Yes I went off insulin, cozzaar,lipitor, slowly lost 80lb, ate only nutrient dense foods, more meat,eggs, only low gi veg,salads, olive oil daily,I am worried what if it was an error, will know in 2 days what new results are.
Oh I ate a ton of ground flaxseed, .....my chol went up &, and HDL went from 40 to 68 and stayed there,LDl went up in that time frame and Dr Westman from Duke said its probably big fluffy good ldl stuff as typically thats what occurs with people doing low carb and getting into ketosis...could higher hdl  move out sticky lipoprotein???

Hi, Chickadee--

If you're asking whether higher HDLs are more likely to reverse plaque, the evidence would suggest that it does. HDL is probably crucial for plaque regression, since it acts as a "scavenger" of cholesterol in atherosclerotic plaque.

...so if I add excercise then my hdl should go even higher right?

Yes, and the effect can be substantial if you're starting from a sedentary lifestyle.

...was thinking what I did, I also used a full dose adult ASA daily as read in (Edtmn Protocol( the ones who do the stem cell transplant for diabetes type I) that diabetics should use a higher dose of ASA, so have used that and folic acid 1 gr OD since 03. Dont know if this accounts for it.
I am not sedentary from May to Oct as run a busy B&B and bust my butt but in winter I only curl and quilt and my Christmas gifo to myself is a gym membership, keeping in mind I have a terrible mind set about excercise so am working to change thatMaybe I will get addicted to exercise rather than carbs.

The primary function of niacin, vitamin B3, is to metabolize fats, which can then produce a usable form of energy. Niacin, also known as nicotinic acid, is one of the B- complex vitamins, the water soluble vitamins, that all work together to covert the carbohydrates in our body into sugar, for the production and metabolism of our body's energy.

just found this site. I don't have any sign of heart disease as yet but my HDL is 6.

I never met anyone with HDL that low, so that is why I'm taking niacin, 250mg split into thirds cuz the flushing and rash are awful, though brief.

Already on low carb 35 - 45g per meal and lost 22 pounds since I was newly diagnosed diabetes 3 months ago.

Question: how long to take niacin to see a rise in HDL? I don't want to take this stuff for more than 12 weeks.

Thanks a lot for this nice informative post keep posting and updating the blog on regular basis....


Smith ALan