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

Dr. Davis,

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

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

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

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

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

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

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

Hi Anne,

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

Curcumin may offer diabetes benefits: study
By Stephen Daniells

KEYWORDS

    * Phytochemicals, plant extracts

    * Diabetes

GET THE LATEST MARKET REPORTS

    * curcumin
    * diabetes
    * cardiovascular health

All market reports

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

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

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

Promising results for diabetic mice

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

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

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

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

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

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

Potential market opportunities

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

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

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

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

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

The NMR Lipoprofile test provides LDL particle counts, and the VAP test provides Apo-B measurement.
Is there a direct conversion factor to determine Apo-B for a given total LDL count, and vice versa?

Hi Dr. Davis,
Is there an advantage to ordering the VAP along with the NMR Lipoprofile?  Does the information from one or both of these two tests greatly improve on measuring the apo B and apo A ratio?
Thanks,
John

Hi, Arnoud--

Apoprotein B and NMR LDL particle number are roughly correlated with a difference in units by a factor of 10. An LDL particle number of 1000 nmol/L is approximately equal to 100 mg/dl apo B.

By the way, apo B is calculated on VAP, not measured.

LDL does not cause atherosclerosis. Thus, there is no possible gradient such as "most likely". It might look like a semantics argument but I'm really just exposing the flawed hypothesis behind the semantics.

What is truly most likely, is that whatever causes atherosclerosis also causes small LDL.

Carry on.

Hi Dr. Davis,
Is there an advantage to ordering the VAP along with the NMR Lipoprofile? Does the information from one or both of these two tests greatly improve on measuring the apo B and apo A ratio?
Thanks,
E. John

I was previously unaware of this information; thanks for the heads up.

Dr. Davis,

I've been following your dietary advice for a few years (low carb, little to no wheat, lots of nuts and flax) and all my biomarkers are excellent... Except.. my serum phosphorus, which tends to be either above the normal range or at the very high end of the normal range... this isn't an issue with my kidneys since all other markers are optimal... I wonder if you've seen similar results before with this nut/flax rich diet?

Thanks,
David

I had an ApoB of 43 mg/dl, an LDL particle number on NMR of 593 nmol/L, and an LDL on NMR of 78 mg/DL with particle size of 21.6 nm.  My ApoB seems much lower than my LDL particle number (even after adjusting for the factor of 10). Weird?

Glycosaminoglycan (dermatan sulfate form, a bi-glycan) and ApoB together make the type of plaque that is rupture prone.

The enzyme hyaluronidase increases glycosaminoglycan synthesis when lack ApoE. In animal models the aorta collagen increases, plasma volume drops, proteinuria rises, endothelium degrades and atherosclerosis begins.

The poly-anion hyaluronate is available (water soluble) in a pectic polysaccharide as hyaluronic acid in fruit of Abelmoschus esculentus; "okra" is the plant in English.

This may partiallly explain the autopsy analysis of the differences seen in arteries of Africans (who eat okra) & Westerners. Maybe the okra hyaluronate "uses up" the excess enzyme hyaluronase, which effectively "neutralizes" the Apoliprotein risk factors (ApoE deficiency & hypothetically here the ApoB excess).

My hunch is apo-b is correlated with oxLDL, but I've seen no papers that show that small LDL or apo-b count is more predictive than oxLDL.

We know that high carb yields high blood sugar and that alone is oxidative of LDL. What if apo-b is correlated with oxLDL because both are driven by high BG?

Unless this is separated out,  we might be wasting money on expensive apo-b tests instead of cheap oxLDL tests or even cheaper postprandial BG testing.

This is interesting as there are reports of okra water reducing some people's fasting blood glucose.

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

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

Perhaps we should just give up eating altogether.

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

so what does this mean?

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

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

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

Yeah, they go up, but not that much.

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

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

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

?

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

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

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

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

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

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

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

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

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

Anonymous,

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

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

-Bryce Lee

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

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

Kudos to you.

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

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

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

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

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

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

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

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

Scott W

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

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

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

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