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

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

Perhaps we should just give up eating altogether.

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

so what does this mean?

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

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

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

Yeah, they go up, but not that much.

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

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

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

?

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

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

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

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

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

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

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

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

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

Anonymous,

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

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

-Bryce Lee

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

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

Kudos to you.

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

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

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

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

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

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

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

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

Scott W

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

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

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

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

Man oh man I wish I lived closer and you were my doc!!!!

I try nicely to get docs to think that low carb and being off insulin is ok, that not being on a statin may be ok even though my ldl goes up but my lipoprotein a is low.....I don't know what to do about this new doc I am seeing as don't want to turn her off but want to turn her onto TYP.

Unfortunately we all do have to be our own advocates... thanks for giving us the means and tools to do so for our family and friends (and patients)!

The article you mentioned about MMPs (tissue metalloproteinases), CRP and D3 deficiency was quite frankly phenomenal.
Q J Med: 2002;95:787-796.
Cirgulating MMP9, vit D and variation in the TIMP-1 response with VDR genotype: mechanisms for inflammatory damage in chronic disorders?

Again, I think you are correct, the implications revealed here and elsewhere are blatant omissions from discussion in the ATP guidelines (the 'bible' when I was in pharmacy school).  

One-yr Post-supplementation with intra-muscular Vitamin D(from pre-8 to post-14 ng/ml) produced statistically reduced MMP9, as well as decreased CRP (another marker for chronic inflammation). These are all increased in acute MIs and unstable angina and in active arterial plaques. (unfortunately they did not raise the 25(OH)D levels sufficiently 50-70 ng/ml otherwise perhaps they might've seen substantial primary CAD prevention at the 5yr followup -- *bummer!*).

Thank you for the info on Doxy. I remember reading > 10yrs ago how doxy helped in arithritis.  It makes sense now!!!

With the role of D3 emerging that it's vital and affects all organ systems, do you think your TYP program is also treating and preventing ALL chronic conditions? Are you aware that you may be creating an immortal human subpopulation *ha haaa haa*. But alas, we are human...

Do you think that perhaps since D3 is a steroid structure, D3 may be depleted in cortisol-driven activities (ie, chronic stress -- physical, mental, genetic)?  Perhaps a cascade of events occurs, triggered by (let's conjecture) a marginal reduction in sunlight (since we obtain naturally about 99% of D3 activation from sunlight) which leads to broad widespread decline in D3-dependent cellular activities. Unfortunately D3-dependent cell functions appear to me (from your blog and the literature) to be literally ALL functions...

Immune cells--flu, infections, MS, lupus, asthma/copd, T1DM, RA
Thyroid & parathyroid--TSH and PTH irregularities (then eventually Graves/Hashimotos), osteoporosis
Bones/GI system--without D, GI incapable of absorbing calcium (absorb more Hg, Pb? ...autism spectrum?)
Colon--cancer, mortality
Cerebral arteries--migraines
Brain--depression, less euphoria
Nerve endings--peripheral neuropathy
Kidney/renin--hypertention, pre-eclampsia (during pregnancy when E2 and P hormone production is ramped up)
Pancreas/beta-islet--Metabolic Syndrome, glucose intolerance, Type 2 diabetes
Liver--PPAR changes, high TG/low HDLs (less HDL to scavenge out LDL)
Adipose--insulin resistance, weight gain
Coronary arterial plaque--CAD, MI
Nephrotic atherosclerosis--CKD, dialysis
Cerebral vasculature--stroke
Ovary, breast--infertility, PMS, cancer
Prostate--cancer
Hair follicles--male pattern baldness(?)
Overused joints--osteoarithritis

In the literature, D supplementation (sometimes with calcium, but I don't think it's necessarily relevant) improves all these chronic conditions. Is it all more interconnected then we suspect? I see all these conditions in the primary care setting, and I find that recently I'm giving the same 'dog-and-pony show' to all pts (migraines, perimenopause, T2DM, HTN, CKD, etc). 'fish oils, nuts/seeds, oat bran, relax, exercise, get some sunlight midday, low GI foods, Ezekiel bread, and on and on'.
I wonder now...wouldn't it be just easier to put 'the D' in the water?  There are so many challenges in overcoming the havoc caused by MMP and other inflammatory constituents(ie,'target organ disease').  The TYP plan truly seems to offer vitality... and immortality! Another medical genius said ( Hippocrates) "your food is your medicine, and your medicine your food."  He was so right, after all these centuries. Keep up the strong work and don't stop the rhetoric!

BTW, is there any tissue that is devoid of VDRs (vitamin D receptors)? toenails?  THANKS!!

Additionally...i forgot several disease states...so embryonic tissue in utero are affected too. does calcium modulation make such a difference at age 'zero'? there appears to be evidence. perhaps even for heart disease?

Skin--psoriasis (treated w/Dovonex a D analogue)
Maternal D nadirs--schizophrenia (in summer babies; see Oprah Nov's issue! *HA HAAA HAA*), Type 1 DM
Brain--Alzheimers (D improved cognition, cheaper than Aricept)
Muscles--chronic pain syndromes, fibromyalgia

do you have a cure for addiction to reading about disease reversal?

G--

I've had the very same thoughts.

Every day, I witness some new aspect of vitamin D replacement that I had not appreciated before. All of this needs to be systematically recorded and reported. Our first report on the effects of vitamin D, along with the Track Your Plaque program in all other aspects, will be reported next spring in the scientific literature.

I'm seeing so many fabulous effects. We will follow our initial report with more on these issues, though little by little. That's how it works, though I tell you about these things before the official report hits the press.

Curious thing, G: You will see accelerated growth of toenails and fingernails with vitamin D supplementation!

LOL!

Well, the enormous abyss of ignorance among physicians on these issues is a sobering thought.

That's funny. You are so right again! I've always noticed my nails always grower faster in the summer!

Did you get a chance to see Planet Earth on the Discovery channel?  AMAZING! Do you now what they focused on?!!!

The sun and the earth...'Sunlight is the engine of life... whether on land or sea, sunlight shapes life... it triggers birth and death...'  

I guess it's NO SURPRISE that VDRs are hinged next to other steroid receptors estrogen, progesterone,  and thyroid receptors (and possibly glucocortocoid and retinoic acid).
(is that why TAN MUSCULAR athletes probably procreate more than cardiologists and pharmacists? *ha haaa haaa*)

You notice and document here the tremendous disease reversal with testosterone, E2, vitamin D and DHEA...
It A-L-L makes sense!!!!!

can u translate?  I know this must mean something...

Heterodimers of Retinoic Acid Receptors and Thyroid Hormone Receptors Display Unique Combinatorial Regulatory Properties
http://mend.endojournals.org/cgi/content/full/19/4/863

There is an interesting discussion about PPAR and other nuclear steroid receptors. I think that Actos and Fibrates improve HDLs and TG and hence plaque reversal with their PPAR activities (gamma- and alpha- respectively).  Do you think that are other nuclear steroid receptors that can be explored for plaque reveral and ultimately reduction in chronic inflammation?

my health food store nutritionist recommends cod liver because it includes Vitamin A which is a cofactor for D (he said) compared with D3 alone. I'm hesitant because I've read that A can block (perhaps through competition) D activity. I had a *bad* reaction with Chicken liver pate once... ate a whole chunk then drank ONE sip of beer and had the WORSE etoh-dehydrogenase reaction!  I worry about vitamin A toxicity... it also had worse mortality for lung CA patients.

I wasn't aware of the proximity of those genes. Thanks, G.

Hi, G-

I'm afraid you've exceeded my scope of experience with that one.

However, I know of no such vit A/vit D interaction. I prefer single supplement preparations, in general, because it allows independent adjustment of doses.

I think you'll like this.  Bruce Ames discusses keeping mitochrondria happy (and preventing DNA damage and antagonistic pleiotropy). Vitamin D deficiency is mentioned as well.

http://www.pnas.org/cgi/content/short/0608757103v1?rss=1

Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage

Bruce N. Ames *
Nutrition and Metabolism Center, Children's Hospital of Oakland Research Institute, 5700 Martin Luther King Jr. Way, Oakland, CA 94609



Contributed by Bruce N. Ames, October 6, 2006 (sent for review September 20, 2006)

Inadequate dietary intakes of vitamins and minerals are widespread, most likely due to excessive consumption of energy-rich, micronutrient-poor, refined food. Inadequate intakes may result in chronic metabolic disruption, including mitochondrial decay. Deficiencies in many micronutrients cause DNA damage, such as chromosome breaks, in cultured human cells or in vivo. Some of these deficiencies also cause mitochondrial decay with oxidant leakage and cellular aging and are associated with late onset diseases such as cancer. I propose DNA damage and late onset disease are consequences of a triage allocation response to micronutrient scarcity. Episodic shortages of micronutrients were common during evolution. Natural selection favors short-term survival at the expense of long-term health. I hypothesize that short-term survival was achieved by allocating scarce micronutrients by triage, in part through an adjustment of the binding affinity of proteins for required micronutrients. If this hypothesis is correct, micronutrient deficiencies that trigger the triage response would accelerate cancer, aging, and neural decay but would leave critical metabolic functions, such as ATP production, intact. Evidence that micronutrient malnutrition increases late onset diseases, such as cancer, is discussed. A multivitamin-mineral supplement is one low-cost way to ensure intake of the Recommended Dietary Allowance of micronutrients throughout life.