I had the lipid test at Berkley about four years ago..and I was told two things..that I had a clotting problem and that I should avoid omega fats..that I had the type cholesterol that omegas were not good for.
I can't get into see my records at berkley and my cardiologist died a couple weeks ago and I can't get any response on my records. My current doctor and I am midwest instead of south east now..is asking about these and I don't know how to answer him. Why would omega be bad?

sorry I sent the question about omega fats and cholesterol. danellerene@ymail.com

Dr. Davis,

I have tried  "bioidentical" female hormones from a compounding pharmacy and ended up with sky high blood pressure and blood sugar. I do very well on the pharmaceutical yam-based estrogen. So I would caution people not to assume these hormones are benign.

I also have supplemented pregnenolone for a while and had to stop as I also started to see bad results with blood pressure and a hint of masculinizing.

So I would warn older women to be very careful with these hormones. The doses seem to be set very high and some of them may be optimized for males.

Dr. Davis, do you recommend any particular brand of pregnenelone?

Dr. Davis,

Ordinarily I would have no interest in the ultimate " bioidentical" hormone" but, my daughter is going through her changes and is having a bad time with them.  Could pregnenelone be used to alleviate problematic symptoms? She is dead set against hormone therapy because she has a fear of  cancer.

Bioidentical hormones have been a godsend for me... after "toughing out" a particularly long and difficult perimenopause I was in pretty dire straits.  I found a doctor who uses both mainstream Big Pharma hormones and bioidenticals in his ob/gyn practice, depending on the patient and their needs.  He is board certified, highly skilled, and compassionate.  After some trial and error and numerous blood tests, we arrived at compounded estrogen and progesterone as the best for me.  Gone are many horrible symptoms, so of course I would be very upset if the FDA were to "crack down" on "bioidenticals" in favor of manufactured Big Pharma products.

That being said, if the FDA is so inclined... I will roll with it.  There are several prescription estrogen products, both oral and topical that could meet my needs.  They are for the most part manufactured from soy (as are most bioidenticals).  There are also some progesterone products manufactured by Big Pharma companies... and I am betting we can figure out how to get to the combination and dosage I require to feel good and normal.

What won't I take?   Well Premarin and Prem-Pro for starters.  They're not bioidentical... in fact they are foreign to the human body.  Equilin,  derived from pregnant mares urine, or manufactured from soy, is not a requisite of the human body and IMO doesn't belong there. Give women a foreign hormone substance for years and wonder why the alarming results?  Hummm...

As for pregnenolone, I don't think so, at least not for me.  At this late date, I doubt that my body would be efficient in utilizing it, or sending it down the correct pathway.  Why not just use the real things?

madcook

DHEA can cause substantial hair loss in men, it did suddenly and acutely in me.

I'm no expert but it's my understanding that pregnenolone is the raw material for the production of DHEA, which is the raw material for the production of testosterone, estrogen, and progesterone.

It's also my understanding that it's always best to try and supplement "bioidentical" hormones that are closest to the natural target hormone.

If that's true and if pregnenolone is low and DHEA normal (say through supplementation) what's the point of taking pregnenolone at all?

I've been on bioidentical hormones (progesterone) for 18 months and have had incredible success. I'm under the care of a MD who specializes in bioidentical hormones. Bioidenticals are safe and effective if the supplementation is medically supervised.

At 47 yo, still cycling regularly but definitely perimenopausal the past few years.  New cycles start every 14-20 days (normal in every other way) if I don't use progesterone, but with progesterone, cycles are closer to normal length, every 21-28 days.  

I've been using bioidentical OTC progesterone cream for a little over two years with very good results and no side effects that I can detect.  Just this week I switched to a higher prog dose via compounded Rx, as symptoms were returning/increasing the past couple months (especially midcycle extreme breast tenderness and increased lumpiness- negative ultrasound and mammograms though thermogram was suspicious, plus last exam indicated return of uterine fibroid - all suggestive of high estrogen/low progesterone imbalance).  

A recent luteal phase test of estradiol showed it to be twice as high (549 pg/ml) as the upper end of the ref range, which explains the dramatically increased symptoms.  Guess those ovaries are screaming in protest during their decommissioning!  Progesterone levels were in the tank.  So was 8am cortisol level.  

BTW, I've always avoided any supplemental phytoestrogens such as soy, "menopause" herbs, etc.  Numerous lood tests over the past 15 years have indicated no lack of estradiol (esp in recent years), but in fact, chronically low progesterone, despite regular cycles.  

Along with years of undiagnosed hypothyroidism, I think low progesterone and a slightly shortened luteal phase were likely reasons why I had trouble conceiving 8-15 years ago (despite two infertility work-ups and "expert" review of my tests).  Wish I knew then what I know now (don't we all?)

This backlash against biodidentical hormones, orchestrated by Wyett and other Big Pharma patent holders is very disturbing.  Like any other drug, the skill, experience, and knowledge of the doctor is crucial in prescribing them for the best effective treatment.  

I've been cautious about self-treating with OTC hormones without some experienced guidance, including pregnenolone, because I wasn't sure it wouldn't convert to more estradiol instead of the progesterone and testosterone I needed.  But it took a long time to find an MD which the right experience.  Of course, she's not in my HMO-subscribed system so I have to pay out of pocket for office visits or compounded Rx, but it's worth it.  She writes the lab orders on a Rx form, which I take to the HMO lab, so insurance covers any of the lab tests they do.  Results are faxed to the ordering MD, even though she isn't in the system.

I guess I'm just an ignorant old Luddite, but I'm skeptical of all substances that don't come in natural foods. No prescription or OTC stuff for me if I can avoid it.

Anna,

Late 40's are a rough time of life, kind of like being a 13 year old girl in reverse.  Ovaries are cranky as they rev up and as they rev down.  Next they start behaving like loose lightbulbs. They turn off for a month or three then they turn right back on.  It is hard to relie on hormone levels in that phase because things just keep changing.
Late 40's usually screams progesterone deficiency.  First up to treat is usually vitex 500mg whole fruit daily.  Takes 3 months for full effect. Dirt cheap.  It works as a prolactin inhibiter and a progesterone booster.  Second is progest cream.  Third compounded progesterone or prometrium.  Route of prometrium varies with symptomatology.  Can't sleep?  Progesterone needs to be oral.  Still can't sleep?  Take it with food at bedtime to enhance absorbtion or up the dose.  Hung over in the morning?  Take it earlier.  Sleep not an issue but can't stand those early periods?  Use the progesterone vaginally at night.  Just shove it in as high as it will go.  The gelatin capsule dissolves and it goes straight to the uterus.

From my experience, bioidentical hormones really do work! After hearing so many people, like Susanne Somers and Oprah, talk about the
benefits of hormone replacement
therapy, I decided to give it a try. I looked around a lot, and I
finally chose VieNue
Bioidentical Testosterone Cream. All I have to say is, IT WORKS! My mood
is so much better. I feel healthier. I have a healthy love life again - I
used to always feel so "not into it." Now my husband and I are connecting
again like we did years ago. Definitely give VieNue Bioidentical Testosterone
Cream a try, you won't regret it. Here's the link vienue bioidentical testosterone cream

You need to do a lot of reserach before starting hormone therapy... You should always have your hormones tested first! Saliva test is the best way to test your hormones levels. Also you need to use a compounding pharmacy that you can trust and a good doctor. This website helped to show why to choice bioidentcal hormones and you can even find a doctor in your area: http://www.bodylogicmd.com/research/safety-of-bioidentical-hormones

I have been researching the bioidentical hormone therapy topic for a while and would like to see what people's opinions on the health benefits of bioidentical hormones like the reduction of breast cancer as explained in this article,

http://bodylogicmd.com/hormone-articles/review-of-hormones-and-breast-cancer-can-we-use-them-in-ways-that-could-reduce-the-risk

Can you address the cardiovascular risks associated with bioidentical supplementation as compared to typical pharmaceutical hrt?

Bioidentical hormones are products that are chemically identical to what's made in a woman's body.
Some are approved as medications; others are supplements. Learn more about it from professionals in the field.

Why not simply increase dietary cholesterol?

I have watched the video and it's sad that corporate pharmaceutical industries have to chemically alter a natural substance in order to get patent for synthetic medicine or synthetic hormones but I think synthetic hormone should not have been approved for human use in the first place. It must have helped many people but in the long run it did more harm than good.

Bioidentical hormones refer to hormones that are identical to the chemical structure of the hormones produced by a woman’s body therefore it is better and safer than synthetic hormones. Understanding your symptoms will also help you prepare for it and modification of lifestyle issues like healthy diet of organic foods to resist minor signs, light exercise to improve blood circulation level can help regulate the symptoms of hormone imbalance. Compounded bio-identical hormones are pills, creams, gels, suppositories, injectables, sublingual drops or lozenges that are prescribed by health care providers who tailor the dose to a woman’s individual symptoms and concerns.

Pregnenolone is the first biochemical step in the conversion of dietary cholesterol (yes-cholesterol!) to numerous other hormones. Pregnenolone is the source of the hormones that lie at the center of the bioidentical hormone controversy: estrogens, progesterone, and testosterone. We therefore already have our own over-the-counter, non-prescription form of bioidentical hormones.

I find it curious why people don't want to know or talk about their numbers ... blood sugar, blood pressure, blood fats.  My brain tells me it's a form of denial, but choosing not to see it won't make it go away.  I know it's not easy quitting smoking or starting an exercise program, but at least you're alive.
That's all, don't mean to sound bleak  

I'd love to see more studies looking at glycated hemoglobin and heart disease risk. Many of the changes Dr. Davis recommends, limiting fructose  & glucose, wheat elimination,  and even correction of vitamin D levels can reduce a person's glycated hemoglobin levels.

Nephropal has a recent blog on fructose
Fructose Intake and Kidney Stones
I was interested to see the impact of fructose on magnesium status.
I wasn't aware also that
High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation

Stanhope et al is a very interesting study. I'd love to see it repeated with a larger group of subjects as well as with different percentages of fructose consumption and in diets with different macronutrient composition. I'm assuming fructose sweetened drinks were used rather than actual fruit as they are directly comparable with glucose sweetened drinks?

So I guess I've got to give up all fruit now. What is the acceptable level of fructose per day?

"a diet rich in fructose"

OK avoiding ALL wheat seems to be a good idea.  But avoid all/virtually all fructose?  Do you really think that for a healthy active person i.e. someone exercising, that say 1 cup of berries and an apple or 2 per day is too much fructose?

Okay, you make a clear case against fructose and sucrose... and I thank you for making it clear to us, but...

Fructose is in almost everything, including some of the most antioxidant rich, nutrient dense fruits and vegetables.  I'm sure your not advocating we all stop eating fresh pomegranates, apples, berries, tomatoes, peppers, lettuce, cabbage, etc.

We await your guidance on what would be a safe upper daily limit for fructose consumption that would help us avoid its coronary risk factors while we may continue to enjoy the numerous benefits that reside in the same foods.

So it's clear that what is proposed eg in the popular in Europe Montignac diet - use fructose in place of sugar due to its low GI - may be a harmful bs. But if I keep my carbs under 100g, do you think it makes much difference if it's fruit, honey, veggies or just a handful of pure fructose powder?

After watching the u-tube video "Sugar the Bitter Truth" by Dr. Lustig, I concluded that fructose is more a direct cause of heart disease rather than just another risk factor like cholesterol. Fructose actually causes the arteries to become inflamed and inflammation is the beginning of heart disease, right?
Josephine
Hawaii

Can you comment on the role of fresh fruits like apples,oranges,berries,etc?Do they also raise the risk factors?

Sugar Is a Poison, Says UCSF Obesity Expert
This article highlights the main points of Lustig's 80 minute video
Sugar: The Bitter Truth

This is what Lustig has to say on fruit.
Fruit is fine but we should think twice before drinking juice or feeding it to our kids. The fiber in whole fruit contributes to a sense of fullness. It is rare to see a child eat more than one orange, but it is common for kids to consume much more sugar and calories as orange juice.

Eating fiber also results in less carbohydrate being absorbed in the gut, Lustig notes. In addition, he says, fiber consumption allows the brain to receive a satiety signal sooner than it would otherwise, so we stop eating sooner.

The video goes into the biochemistry of fructose metabolism in some detail. I urge you to stick with it although it is quite complex. It gets a bit clearer when you reach the summary slides at the end.

As an answer to your many inquiries in todays comments. You can never go wrong following the lead of our ancient ancestors.  Yes they ate some fruit, mostly berries that were seasonaly availlable only,  very small and not very sweeet by todays standards.  I eat a cup or less of only berries, combined with 2 tablespoons of high antioxident cacao nibs and a tablespoon of ground flax seeds for breakfasy wvwry morning.  This keeps my blood sugar below <100 mg/dl and my A1c levels below 5.  This is a work in progress, because, I am on a constant experimental path of reversing my metabolic syndrom diseases.  As an asside, there is a Dr. Bernstein who wrote several books relative to diabetes, who said that he hasn't had a piece of fruit in 30 years, all without ersity what so ever.  

The few doctors who's advice I follow without question are You Dr. Davis along with Dr. Kenneth Tourgeman M.D. "nephropal.blogspot.com"

For health reasons, I strictly try to mimic the eating patterns of our early ancestors where possible.  Yes they ate fruit, limited by seasonal requirements.  However, the fruit they ate was very small and not very sweet, not like today's farm engineered varieties. Therefore, I limit what fruit I eat to one cup or less daily.  I combine this with 2 tablespoons of the antioxidant rich super food cacao nibs (dark chocolate), and 1 tablespoon of ground flax seeds.  When in doubt I ask myself the question, "what would my caveman ancestors have eaten?"  I live by this health supporting guide.  I find the food delicious and very satisfying.  

Of course, I would not do any of this without the sage advice of a few brave doctors who care only about reversing or curing disease and do not give a whit about following some outdated and wrong dogma. More valiant doctors must step up.  

I have become healthy because of you Dr. Davis, through your fine blog, and the direct care and supervision of Dr. Kenneth Tourgeman  "nephropal.blogspot.com"

The best types of fruit and berries are those with the highest nutrition to fructose ratio, like blueberries and strawberries. If eating an apple, consider just eating the skin and a little farther in; no need to eat all the way to the core.

Billye and StephenB--

Excellent insights into how to keep fruit in the diet without suffering its adverse effects.

Anon--

Yes, Dr. Lustig does an absolutely bang-up job of describing the rationale behind the destructive effects of fructose. It is the best presentation on this topic--and from the principal investigator, no less.

It is a must-see. I watched it last night.

Slides used in a previous presentation by Dr Lustig.
these are mostly the same as those used in his recent You Tube video but may be helpful for people with poor internet connections who are not able to watch the video.

Dr. Lustig's lecture is incredible-- I just finished watching it.

I think he overstates the case for fiber, and is too accepting of glucose in the diet, however. I agree that glucose is much better than fructose, and isn't a huge problem for a healthy person, but given that most Americans are metabolically "crippled" and teetering on the edge of diabetes, heart disease, etc., it would seem wise to me not to go pushing glucose as a great thing.

My quibbles with Dr. Lustig are minor, however. Overall it's a fantastic presentation.

How would you explain the evolution of primate frugivores in relation to human health, and why a diet probably greater than 50% fructose is obviously benign for them?

(Yes, I know current fruit varieties have more fructose.)

My daughter (who is Canadian) is currently in the US doing some research at the National Archives. She mentioned to me that she finds the fruit juice she's had too sweet to drink (she's staying at a hotel, so fresh fruit is hard to come by and the breakfast is all wheat). This was not only some anonymous apple juice, but also a bottle of Tropicana (she didn't check the label to see if there was added fructose), so she has switched to water. She also commented on how ridiculously large the portions were in restaurants.

It's no wonder that Americans are getting larger and larger (Canadians are too, but not as quickly.)

Also note that many foods labeled "heart healthy" because of low-fat, low saturated fat, addition of sterol esters, or fiber, also contain fructose sources, especially high-fructose corn syrup.

Hilarious Billye!

"For health reasons, I strictly try to mimic the eating patterns of our early ancestors where possible. Yes they ate fruit, limited by seasonal requirements. However, the fruit they ate was very small and not very sweet, not like today's farm engineered varieties. Therefore, I limit what fruit I eat to one cup or less daily. I combine this with 2 tablespoons of the antioxidant rich super food cacao nibs (dark chocolate), and 1 tablespoon of ground flax seeds. "

And did our ancient ancestor blend powdered cacao nibs and flax with their berries? SO much for strictly following cavemen.

This is fact. Hepatic metabolism of fructose also differs greatly from that of glucose. Fructose-induced hyperlipidemia has also been hypothesized to be of intestinal origin. That can be risky.

Congratulations Amy!

And here I thought that plaque was in your arteries for life... and then tonight I find this blog.

Amy (and Neal) give all of us inspiration to truly modify our lifestyle.

I'm also especially gratified that a woman now holds our record. I'm uncertain why, but the ladies have been shy and the men remain the dominant and vocal participants in our program. Speak up, ladies!

Thanks for blogging on this extremely important topic. The news coverage of this story was REALLY garbled.

Here's a related question. Have you seen anything about the purity of the Vitamin D being sold in oil capsules. As enthusiastic as I am about it--I've had my levels measured and the supplementation has definitely raise them, I'm concerned about what contaminants might be in the pills since they all come from those Chinese factories full of adulterants.

Any data on this?

One possible explanation as to why someone would purchase a supplement rather than a prescription drug is that the person has no health insurance and cannot afford or find a doctor who will write the prescription required for the drug.

Of course, it is worth mentioning that lovastatin  originates naturally in RYR, and only became a drug courtesy of big pharma reinvention and patents?
MikeV

My cardiologist recommended I try Red Yeast Rice, as an alternative to Zocor, just to see if it can raise my HDL some and possibly push my LDL/Triglycerides down a little (they are already normal).

Several weeks ago there was an article in regard to a major Chinese study on RYR - http://www.theheart.org/article/875035.do

They used a specific type of RYR, Xuezhikang. The data from this study showed that RYR had better results than statins (In Western studies) in preventing a repeat heart attack. There was also a lower risk of mortality and cancer (which is rare to see in any statin study).

And it is theorized that the non-statin components of RYR is why there is such a benefit. Most RYR studies have shown than the lovastatin dosage can be really small, yet have an equivalent or greater effect than a normal dosing of a statin. Lower dosage = less side effects, which is why many people prefer trying RYR over statins.

As for the consumer labs report, are you allowed to post some of the brands that passed the test at least? Or several that didn't? I am currently trying RYR from Thorne, as they supposedly have good testing labs and also source their RYR from the US. But there is no actual way for me to know how good or bad their RYR is...

If mainstream method cholesterol lowering is poisonous via supplemental or pharmacuetical methods, it shows that essentially this is slow poison. Not meant to be!

As a physician and advocate for self-care and an integrative approach toward managing your health, I totally agree with your perspective.   Why take a nutritional supplement that contains similar family of compounds "HMG Co-A Reductase Inhibitors" when all that you get is additional risk due to quality assurance problems. A recent study published in the Mayo Clinic Proceedings actually showed that lifestyle change + RYR was as good as high dose Zocor in lowering LDL cholesterol, and ensured greater weight loss than Zocor.   Many people then assumed that RYR was the way to go because it’s ‘less toxic’—as I wrote in my blog, in my view, this is the wrong conclusion.  

http://www.revolutionhealth.com/blogs/bradlyjacobsmdmph/lifestyle-and-herb-as-14623

I just received my NMR lipoprofile results and I am not sure what to look for in the numbers.  Any help would be appreciated:

LDL-P           584
Small LDL-P     242
Chol Total      121
LDL-C           52 (FASTING)
HDL-C           51
Triglycerdes    91
LDL particle size 21.8
large HDL-P     10.8
large VHDL-P     0.7

I am a type 2 diabetic and not taking any medicine for it and lost 80 lbs over the years.

I was surprised that no one has mentioned anything in this blog about the total phytochemistry of Red Yeast Rice, where the deep red purple color of the extract may ahve something to do with its bioactivity, and how it was used in TCM (traditional Chinese medicine) many years before Lovastatin was sold as drug for blood stasis (this means in TCM thickened blood that clots easily). Red Yeast Rice is known to contain a phytochemical array of flavonoids, phytosterols, and other monacolins besides the K. The flavonoids are the compounds that give RYR the reddish-purple pigment color. A wide array of flavonoids from many sources are known to modulate both cholesterol and lipid metabolism, while having blood thinning effects and being able to decrease smooth muscle cell growth of the arterial vessels (see grapefruit flavonoids and cholesterol lowering studies). Phytosterols are known to have cholesterol lowering effects. Other monacolins are in RRY and FDA even has allowed or not objected to the use of another type of monacolin (J) from Red Yeast Rice to be considered for use as a dietary supplement according to a letter submitted to the agency. It could be that the synergy of all of these components could be working to lower cholesterol. A side note is that the edible Oyster mushroom contains monacolin K and is considered a lipid lowering botanical with safe, food use.

In effect, red yeast rice IS a statin drug, albeit a highly variable and weak one. Although readers of The Heart Scan Blog know that I am a big fan of nutritional supplements and self-empowerment in health, I am a bigger fan of truth. I despise B--- S---- of the sort that emits from some nutritional supplement manufacturers and drug companies

What do you consider to be ideal cholesterol readings? I am about to visit a new doctor, a D.O., and I am sure she is going to insist on blood tests for cholesterol plus stress testing, etc. My thyroid TSH was 2.70, but she is already showing reluctance to prescribe any thyroid meds. It is going to be a battle.

And it is not just about the wheat either.  It’s all carbs.  Fructose, oats, rice, pasta, potatoes and certain fruits, etc. all drive up HbA1c and small LDL.  Just for a reality check I bought a can of and made a bowl of “properly prepared” Scottish oatmeal yesterday according to Nourishing Traditions.  Those are the minimally processed chewy steel cut oats soaked with warm water and kefir overnight and served with butter and cream.  Yeah, they were good alright, but my fasting BG was 88 and one-hour PP was 158.  A fast 5-mile run and it was back down to 84.  The container is in the garbage can now.  This morning was two pasture raised eggs and bacon with ½ cup of blueberries and Greek yogurt.  Fasting BG 89 and one-hour PP was 88.  My HbA1c went from 5.8 to 5.1 in less than a year and hope to get below 5.0 soon.  The stubborn small LDL percentage dropped during same time period but still have a way to go in that regard.

I'm not completely sold on HbA1C < 6.0% being a useful metric for anything but populations.  The problem is that the current HbA1C tests do not control for erythrocyte age and I see wide variations among piers on simialr  grain free lowish carb healthy diets.

There has been much more research on this effect as it pertains to diabetics that have falsely low HbA1c:  http://www.ncbi.nlm.nih.gov/pubmed/9773739
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581997/

There is some evidence out there that it works the other way as well, and it makes intuitive sense that the lower inflammation and oxidation associated  with a healthy diet would increase erythrocyte longevity.

Of course observational studies about any topic (small LDL or HbA1c) are always to be taken with a grain of salt.

I wonder if you have ever experienced with any of you patients  what is going on with my husband?  He has very few small LDL particles, at least according to a VAP test - he is type A with lots of large, fluffy LDL.  But his HbA1c is 6.1.  His fasting glucose is 80, 1 hour post-prandial it's 1685, triglycerides are 60.  This is all on a grain-free, very low-carb Paleo diet.  Do you have any clue what is causing the HbA1c to be elevated?  Could it be anything besides carbs?  He gets lots of exercise and is very fit and lean.  

Some have suggested that too much protein can also cause elevated HbA1c, due to gluconeogenisis causing higher levels of glucose.  But why would the body make more glucose than it needs?  And why would that excess glucose not show up in his fasting and post-prandial glucose numbers?

Is there any other factor, besides blood glucose, that can contribute to elevated HbA1c?  No doctor yet has been able to answer this question for us.

Sorry for the typo, his 1 hour post-prandial glucose is 85.

The most common explanation, Rosanne, is that the HbA1c can stay high long after blood sugars have come under control.

It may be due to the extended longevity of RBCs that occurs in the setting of low-carbohydrate diets that allow a previously high HbA1c to stay high for an extended period.

There's also the possibility of a hemoglobin variant that allows this.

I would put more stock in the blood glucose values by fingerstick than the HbA1c.

Thank you for explaining this.  I just had my blood work done for the first time since quitting wheat and going low carb in April.  Since I've lost a lot of weight, and a lot on my waist, I am very curious to see what my numbers are.  This will help me compare the important stats.  What is an ideal HbA1c?

I can't go near oatmeal, steel cut or any other type.  Its just eggs and avocados for breakfast these days with a lot of Asparagus in the spring with my yolks.  Oatmeal has been banished for good.

Your article discuses how the combination of small LDL particles  and high blood sugar
results in plaque. Is the article cited below  by University of Washington at St. Louis useful here? The article points out the role of low Vitamin D in plaque formation with LDL  and high blood sugar. Or am I confusing two separate mechanisms in plaque formation.

http://news.wustl.edu/news/Pages/14489.aspx

Hi, Bob--

Yes, I believe it is two unrelated mechanisms. However, this is a fascinating finding to tell us why people do so well from a heart standpoint when we correct vitamin D deficiency.

Smart move, Pj!

Hi, Arlene--

We aim for 5.0% or less.

Thank you for explaining the topic. i learn more about Small LDL. great post.

Dr. D,  
Can this be related to the lysine- arginine balance in the body? Would taking arginine supplements affect the amount of lysine residue causing problems in any way?  Just thinking out loud ...

Thanks!

Jeanne

HI Doctor Davis,

I know its not the right place, but I could not find your email.

I read "wheat belly", it was revolutionary for me,  and I am persuaded it can bring much relieve to many ailments.

I also wrote several posts about this issue on my health blog (in Hebrew)  based on your book and your Blog.

Thank you for the great service you are offering in your work!

Amit.
Israel.

Hello Dr. Davis,
I'm new to your blog. Just finished reading Wheat Belly. Excellent book! I also listened to the podcast with Robb Wolf. That's how I heard about you. Not to get off topic (didn't know how else to contact you) and this is probably a silly question, but would like clarification if you could help. I've been purchasing the 85% Lindt chocolate bars until you mentioned that you eat the 90%. I read the label and it said that it is pressed with alkali. You mentioned to avoid this process as it removes the healthful flavonoids. By saying "pressed" is that a different process? The chocolate was very good, but I want to make sure I'm getting the healthful flavonoids, especially when we don't eat too many sweets. Thank you so much for your time.

Hi Dr.,
I am confused how to  reconcile  HbA1c details  from J Am Coll Nutrition 2005, Vol.24(1):22-29
"Dietary Carbohydrate and Glycated Protein in the Blood in Non-Diabetic Subjects"
http://www.jacn.org/content/24/1/22.full
(and their relevant references no. 10 -  19 & 34-39 )

This has been going on for 2 1/2 years and in fact, the longer he has been low-carb Paleo, the higher the HbA1c has gotten.  When he started, it was 5.5 and has slowly
crept up to the 6.1 reading.
Thanks for the mention of the hemoglobin variant, I guess that's must be it.  Can we stop worrying about the HbA1c since his glucose values are so good?

Dr. Davis:
What do you you think of Jenny Ruhl's advocacy of the 5% club at Blood Sugar 101? Your guidelines appear to be more aligned with Dr. Bernstein's and Dr. Ron Rosedale's? Do you think that all individuals ( including prediabetics, daibetics and glucose intolerant ) should strive for a HbA1c below 5%?

HI, STG--

That is precisely what I aim for, also: HbA1c of 5.0% or less. At that level, metabolic consequences of blood sugar essentially disappear. This is, of course, at variance with conventional guidelines.

That would be my vote. Ask your doctor, also, about fructosamine, another sugar markers.

Hi, Might--

Were you referring to their conclusion about polyunsaturates?

My bar says "processed" so, yes, the flavonoid content can be expected to be reduced in this bar. The best way to get a full dose of cocoa flavonoids is in undutched cocoa powder.

I still think you can enjoy your dark chocolate, but you just might not expect full benefit from this particular bar.

Thank you, Amit!

What is the wheat situation in Israel? Is it pushed there as much as it is here by official agencies and food companies?

Sorry, Jeanne, I don't believe the answer is known.

Hi Dr. D.,
Authors in this report say glycated protein & HbA1c do not interact  with blood glucose in same way (ref #17) and that it is glycated albumen rather than glycated hemoglobin that is very senstitve to blood glucose levels (ref # 18,19); especially since 60% HgA1c is genetic (ref #61).
AGE (advance glycation endproducts) they say is more indicated by fructosamine level from high blood glucose. Although diabetics with high fructosamine also have high HbA1c. whereas for a non-diabetic  high fructosamine does not relate to their HbA1c level (ref#16).
This impies that (since most obese individuals never will become diabetic &  longevity/cognitive function of the overweight is good) a lot of the risk factor of small LDL with HbA1c depends on genetics/ epigenetics.
My confusion is if your insistence on HbA1c for non-diabetics is misdirected or just due to it being a common first test people can do.

Wheat is the most common carbohydrate in Israel. It is eaten almost every meal. I think that the largest source of calories is wheat.

Regarding Diabetes there is no awareness that whole wheat is especially bad for such patients. Diabetes association (and many more) do recommend whole wheat. Although they are suggesting to avoid eating large quantity of bread at once.

Wheat is being pushed, though, I don't think that somebody here is pushing wheat deliberately, just coping recommendation from abroad, and using the most cheap and easy carbohydrate.

Amit.

I have been on my Wheat Bellies journey for 8  weeks now.  I am trying to follow your suggestions on heart health and I know that you have your plate full right now, but just a request.  Have you ever thought of doing healthy heart retreats?  I would love to have a chance to go away for a long weekend, have all my blood work done right, have it evaluated, talk to a doctor and then maybe have a few cooking classes.  Throw in a few yoga classes or walks for stress reduction and you have a whole picture!!  

I have high blood pressure that is 'controlled' to some degree with Tekturna (150mg) and Amlodipine (10mg). This morning it was 150/90, so it is often not very controlled. Since 9/1 and going wheat free, I have lost 23 pounds but still have 50 to lose.  My take away from your writings is that plaque is the  main cause of heart disease and that keeping a low blood glucose level is the best strategy, but there is not much about  high blood pressure in your work.  What role does it play and will being a wheat free low carber offer me relief from my high blood pressure?  Or will it stay high since I have a family history of high blood pressure and therefore will probably have to continue on my meds.  While I, of course, am doing everything in my power to lower my blood pressure, is it not really a number I should focus on when trying to control my heart health?

Hi Doc,
have you seen this? You are prominently featured here:
http://www.lef.org/news/LefDailyNews.htm?NewsID=11842&Section=Nutrition
Great summary!

Are you going to translate his books into Spanish some day?
I'm very interested in reading them. thanks

Hi, Marta--

There has been interest specifically in Wheat Belly for translations. Spanish is at the top of the list.

When that happens, I will announce here and elsewhere. Thanks for asking.

Thanks, Renfrew!

Life Extension has been an important supporter of my efforts and vice versa.

Hi, Nora--

Excellent suggestion on the heart health retreats. I've thought a lot about it and will likely do it in future. Just not quite sure about the details. One hurdle: Few people want to fly to Milwaukee, so we'd have to find an exotic or interesting, probably warm, place to do it.

Hypertension is indeed a big issue. It is also among the last things to respond to weight loss and diet, often lagging behind many months after weight loss. So it really pays to be patient while you are on this health journey. Given your family history, you still might be left with hypertension, but at least you will have minimized it.

Thanks, Amit.

By the way, all anyone has to do is check a fingerstick blood sugar 1-hour after consuming anything wheat to observe the astounding blood sugar consequences of wheat consumption.

Hmmm. I'm sorry if I'm being dense, Might, but I'm still not sure I follow.

I'm not actually advocating anything except to show how glycated small LDL is a really bad player. When viewed from multiple different directions, small LDL particles are looking worse and worse. In this instance, having any measure of glycation phenomena, whether fructosamine, glycated albumin, or glycated hemoglobin, suggests that small LDL particles are also being glycated and thereby gaining heightened atherogenic potential.

Dear Dr. Davis,

I am reading your book Wheat Belly and want to thank you so much for writing this book.

I've avoided gluten for years.  Arthritis and other annoying symptoms vanished...but I started gaining weight!   My blood sugar starting rising!   I couldn't understand it!  It was horrifying!  Well thanks to you, I realize that gluten free breads, candies, flours,  frozen pizzas, pastas and those gluten free "tv dinners" sold at Whole Foods did nothing to help my waist line or blood sugar.  I am now following the wonderfully easy plan in your book and am confident the weight will come off.

Thank you for such terrific recipes.  Will you be writing an accompanying Wheat Belly cookbook as well?  I certainly hope so.  Please do!   If not, can you recommend some cookbooks that comply with your eating instructions?

Thanks again for such a life changing book.  Sally

There are a few people in Israel trying to enlighten others about the dangers of wheat and other 'modern' carbs.  My sister is one of them, has been trying to think of ways to get some essays to the public.  But what Amit says is correct - a lot of wheat is eaten there, many people buy small breads  rolls daily - it's very fresh, delicious, so it will be a tough thing to stop. Many of the best restaurants in Israel serve Arabic food which always comes with freshly baked loaves of pita.  The 'national snack' is pita stuffed with falafel (fried balls of ground chickpeas, onions, garlic and spices), fresh & pickled vegetablesj, hummus and/or tehina sauce. This is available everywhere and always fresh.  Becasue the food is generally very good in Israel and also very fresh it's hard to avoid wheat, which I've noticed every time I visit.

Dr. Davis, the evidence speaks for itself that consumption of carbohydrates, increase small LDL, suggesting an LC diet of less than 50 grams to mitigate the damage.
But what about endurance athletes (runners, cyclists, triathletes etc.) that work out one and a half to three hours per day and consume copious amounts of carbohydrate to fuel their long workouts.
Is the exercise neutralizing the carbohydrates' harmful effects? If so, can you suggest a dosage for certain amount of exercise?

Hi Dr. Davis,
Non-diabetics just seem to have one feature going for them - their platelets don't respond the same as diabetics. I am inclined to think that albumin in our blood is more relevant than the hemoglobin being glycated . (This is not to criticize your preventative approach , since Type II diabetes can go on to develop &  I like what you are teaching us about small LDL.)

" One common qualitative change in plasma albumin is nonenzymatic glycosylation, which occurs during states of prolonged hyperglycemia....Platelet aggregation ...is enhanced in the presence of albumin that has been incubated in a medium containing levels of glucose that are higher than would be seen in normal patients but are consistent with those seen in diabetics....(Journal of Parenteral and Enteral Nutrition 18:516-520, 1994)

Once the glycation of albumin fosters more platelet aggregation in diabetics (& the insulin resistant person!) their platelets show more secretion and adhesion leading to the vascular plaque build up that the insidious small LDL can get into. Yet, for the non-diabetic the +/- 570 insulin receptors on each platelet normally respond differently to their insulin exposure.

Specifically (in non-diabetics) the insulin actually stymies the platelet from becoming "activated" and probably explains how it is that not everyone who eats carbohydrates suffers cardio-vascular insults. Of course there are non-diabetics with genetic variants that adversely affect their plaque dynamics (ex: defect in insulin receptor signalling, that receptor's Beta subunit, G-protein pathways).

( For the techno-nerds: proper insulin receptor response on platelet keeps  platelet cAMP level from dropping & so no endoplasmic reticulum calcium floods out into platelet cell cytosol, platelet granule doesn't secrete ATP, platelet alpha-granule doesn't secrete P-selectin & there isn't mitogen-activated signalling to make thromboxane A2 , etc.  Basically, in the diabetic/insulin resistant these processes go forward uninhibited by normal insulin signalling & their circulating platelets don't keep rolling along suspended in the bloodstream .)

Omega 3 Fish Oil BAD NEWS for Apoe 4/3!!!  

Ok Dr. Davis, I really need your advice on this one.   In following TYP, I have been taking 3200 mg day EPA/DHA fish oil 1.4:1 ratio.   Recent testing shows I have gotten my HS Omega 3 Index to 9.5,  and my Omega 6 to Omega 3 ratio to 2:9  so this pretty good.   Now for the bad news....ever since I started taking 3200 mg day fish oil...over a 2 month period my HDL went from 48 to 38, a whopping 20% reduction in the critically important good HDL that I need to remove plaque.  I exercise extensively, and I also take 10mg day crestor (crestor is one of the few statins that's supposed to raise HDL not lower it). Now,  I have heard from several sources that Fish Oil (more than 1000 mg day) supplements are actually BAD for Apoe4/3 people because it lowers HDL.  So now I am confused Dr. Davis.....do I follow your TYP advise and stay on 3200 mg day fish oil in order to keep a close to 10 HS Omega 3 Index....but suffer lower HDL and less plaque removal/reversal....or do I stop the Fish oil in order to raise my HDL  but suffer the risks of little to no fish oil??

Please advise...

An extremely confused Apoe 4/3

Hi Adam,
HDL drop can be due to accelerated small HDL's  breakdown/clearance & if that was mostly lingering small HDL then it didn't have much reverse cholesterol transport function left in it anyway. If total HDL drops but small HDL turnover is  now more optimal &/or if it is a greater % of the large HDL then there is better reverse cholesterol transport dynamic despite the total HDL drop.

ApoE has 299 distinct amino acid positions & the difference between the 3 types are due to which amino acid is in positions 112 & 158 ( respectively ApoE4 @112=arginine & @158 =arginine, ApoE3 @112=cysteine & @158=arginine, ApoE2 @112=cysteine & @158=cysteine). Because ApoE4 has arginine at position 112 this then orientates facing away from the standard grouping of 4 helix at that N-terminal to more closely cozy up to the alpha-helix of the C-terminal that in ApoE naturally overlays the N-terminal. Thus ApoE4 can uniquely feature a "salt bridge" to that C-terminal that affects how ApoE unfolds/functions when ApoE goes to work.
ApoE's manner of unfolding at it's N-terminal  is crucial to how it deals with lipids, phospholipids (ex: cell membranes)and  proteoglycans on a cell surface. Fish oil alters cell membrane phospholipid composition and then the proteoglycans there must suitably interact with that EPA enriched type of cell surface. Since each ApoE's C-terminal presents an interface that challenges  how that ApoE  works at any target cell the  peculiar ApoE4 "salt bridge" uniquely conditions the way interactions play out. (And each of the separate 3 classic types of ApoE  can get mutations, mostly at positions 136-150, to complicate degree of LDL receptor interaction, etc.)

Dear Doctor Davis,

I am wondering if you can clarify the "oxidized LDL Cholesterol" concept.  Including, of course the Small LDL as well.

I began wondering if the oxidation is primarily in the package, the LDL wrap, the signaling protein, or the internal body of cholesterol itself. Of course, all of the above is also a possibility.

The nature of the oxidation could be a good clue as to how it is especially detrimental to health, and so far, I haven't found much easily available on the mechanisms of the detrimental effects. While it is useful to know the harmful nature of oxidized small LDL, some insight into the mechanism of harmful effects would be welcome and minimize the nagging question of "Why" for me.

This might be of interest:

A large study called the STRRIDE trial looked at the effects of different intensities and volumes of exercise on LDL particle size in sedentary, overweight men and women over eight months [3].  Group A performed 176 minutes of low intensity exercise (walking) per week.  Group B performed 117 minutes per week at a moderate to high intensity (jogging, cycling, or using an elliptical machine).  Group C exercised about the same amount of weekly time as group A, but at the same intensity as group B.  

As one would likely guess, group C showed the biggest improvement in changing LDLs from small and dense to large and buoyant.  However, a more telling sign was that group B had a stronger effect than group A, despite exercising an hour less per week.  In other words, intensity is more important for improving LDL particle size than volume of exercise.

A follow-up of the subjects in this study showed some discouraging and encouraging effects on the particle size changes [4].  The discouraging news was that five days of inactivity following the study almost completely attenuated the particle size benefits from the trial.  However, before you start labeling exercise as futile, consider this: while five days of rest basically brought the exercise groups back to baseline LDL particle sizes, they were still much better off than the sedentary control group, who experienced significant digressions in particle size during the course of this study

Hi James Buch,
The enzyme hepatic lipase's (HL) lipolytic hydrolysis of the phospho-lipids on the LDL surface changes it so that LDL's load of cholesterol esters can get taken out; this reduces the molecule's volume and thus is then small LDL (smLDL). Men have more HL than women, until they go through  menopause, and this propensity toward smLDL ( that can get oxidized) may explain male's earlier tendency of coronary artery disease. Visceral/central obesity trends to upregulate HL & it seems visceral obesity affects men more than women (of course central obesity in both women & men will raise both  genders'  HL enzyme levels). What decreases HL levels are things like calorie restriction & aerobic exercise (sedentary life increases HL).

Doc harps on avoiding elevated triglycerides after meals that load triglycerides into VLDL  molecules because the enzyme cholesterol ester transfer proetein (CETP) shunts triglycerides from VLDL (& chylomicrons) over to the standard circulating "big bouyant" (large & fluffy) LDL and fosters transfer of cholesterol out of that LDL; the triglyceride takes up less space and thus get smLDL.
Central obesity usually correlates with elevated triglycerides and increased HL levels. However, if triglyceride genetics (or epigentics from Doc's diet ,etc.)  in the obese without that usual accompanying high triglycerides then that upregulated HL doesn't cause a lot of that individual's standard "big bouyant" LDL to become smLDL. HL also hydrolysizes triglycerides (and phospho-lipids) of chylomicrons, BetaVLDL, IDL, LDL & HDL. Both CETP & HL enzymes being elevated alone, or together, can provoke smLDL - genetic polymorphisms exist for both enzymes.

sm LDL has less antioxidants left yet it's surface has higher ratio of poly-unsaturated acids which make it's phospho-lipids more at risk of oxidation. And smLDL has less sialic acid left on it's surface which fosters more poly-anion proteoglycan binding that increases the smLDL molecule's transportability across the endothelial lining into the artery wall .
Doc harps on need for Magnesium because in real time magnesium is what interrupts the oxidation of smLDL from locking into an altered state & then salvaged plain old smLDL doesn't get to go on to be so damaging.

Continued for J. Buch,
Oxidized small LDL (oxLDL)  has fragments from it's oxidized PUFA (poly-unsaturated fatty acid) that are reactive aldehydes (ex: malon-di-aldehyde & 4-hydroxynoneal-lysine) which then fragment that smLDL's  lipoprotein ApoB.  That peroxidation of a PUFA acyl chain of  the smLDL phospholipid  leaves a type of carboxyl portion that the beta-2-glyco-protein I (Apo H) binds to using a "reactive" ketone as ligand link. Thus it is the position of the "reactive" ketone (keto-cholesteryl-9-carboxy-nonanoate) on the involved cholesterol molecule's spine that determines the % of glyco-protein bonding that occurs (genetics influences ketone placement on a human cholesterol molecule).

Magnesium (Mg++) in the very early stage of glycated protein (Doc warns against advanced glycation end products) hooking up with LDL reverses the glyco-protein link to the "reactive" ketone. But if deficient Mg allows time to consolidate that contact then only a physiologiclly abnormally high pH will let Mg re-break that bonding.

Immunological T cells respond (with age & gender differences)  to try to get oxLDL off the artery wall;  and, if there is too much to handle there is the risk of developing a so-called oxidized LDL-containing Immune Complex (oxLDL-IC). And this oxLDL-IC provokes cytokines that perpetuate the inflammation response. Over time and older age there is  less output of a malon-di-aldehyde oxLDL  immune response; which is possibly what leads to long established plaque having less lipid component and more involvement of collagen. It is relatively younger plaque that is unstable and more likely to rupture; the collagen draws in more Calcium and unfortunately provokes artery hardening problems.

Now the lipid part from this oxLDL-IC gets into an immunological monocyte cell's endosome  and the ApoB gets into that same monocytes lysosome - sub-compartments inside the cytosol (cell interior). Then the lipid part in the endosome triggers heat shock protein (HSP 70/70B) which wrenches things so that the lysosome can't get to work on the lipid and ApoB prevents the lysosome from doing proper interactions at the inside of that cell's membrane to expel  the burdens. Once oxLDL cholesterol esters bulk  up a macrophage (monocyte) due to increasingly futile lysosome  activity  it becomes the notorious "foam" cell. Eventually that macrophage cell dies and the whole load get's polymerized into plaque.

Hi Dr. Davis - with your indulgence:
Back to platelets( see above Nov. 7): vascular remodeling with age &/or ROS exposes a bit of phosphatidyl serine  that platelets can "snag" onto as platelets flow along. Key to accomplish platelet snagging is signaling by  the promoter P2gamma12 and normally insulin signaling down inhibits P2gamma12. But, notably for Type II diabetics (and assumedly proportional to an individual's insulin resistance) their insulin doesn't inhibit that snag signal. Type II diabetics also have P2gamma12 upregulated in their platelets. And if anyone is of P2gamma12  haplo-type H2 those individuals will have even more of the receptors for it and therefore an  increased risk of peripheral artery disease. Irregardless of haplo-type, the Type II diabetic's propensity for peripheral artery problems are compounded by  their basal level of excess P2gamma12 .

Adhesion to the artery then physically involves the platelet surface Glyco-protein Ib & vonWillebrand factor hitched to collagen provoking Integrin 2beta1 (GPVI) so the platelet/collagen sets in place. If the level of promoter P2gamma12 in that challenged site is fortuitously low then the rate of adhesion to the blood vessel is poor. So, predictably, for Type II diabetics the adhesion rate (like platelet secretion & aggregation) is higher than normal. GPVI insult also signals a release of ADP & this ADP (like collagen itself) independently induces aggregation of platelets; the plaque recruits to build itself up to be more fibrous. The plaque matrix serves as nesting for oxLDL & dying macrophage foam cells to polymerize with.

ROS remodeling agents of the vasculature come from mitochondrial activity and  it appears certain (overlooked) relevant gene pheno-types (and their respective polymorphisms) can be pro-plaque (or preventative) - speaking here in the sense of  a primal influence on plaque risk as well as  tendency of the actual amount of plaque. Sirtuin 5 (Sirt5), a mitochondrial Sirt (there are nuclear Sirt too) binds to Uncoupling Protein 5 (UCP5) and governs that (& other) UCP. Sirt (there are 6 types) remodels chromatin (DNA spooled around a histone ) via histone de-acetylase enzyme; while our UCP (there are 5 types) work in the inner mitochondrial membrane governing the proton electro-chemical gradient that is integral to the chain of oxidative phosphorylation (a way to generate ATP, among other functions).

Sirt action on DNA includes (among other dynamics) the cellular level encoding of how individual fatty acid metabolism fine tunes -  lipid fatty acids included.Sirt action on DNA includes (among other dynamics) the cellular level encoding of how individual fatty acid metabolism fine tunes -  lipid fatty acids included. Doc's diet/protocol may ( I suggest) sometimes  tweak out favorable health response(s) via induced epigenetics, because of remodeling that is induced in the chromation DNA unit packaging . Sirt's histone de-acetylase working depends on NAD- to drive Sirt and Doc's diet/protocol theoretically seems to be capable of altering NAD flow patterns from his weaning of cells'  mitochondria off of glucose.

UCP5  rules the inner mitochondrial membrane potential & the rate of oxygen use, which can become relevant to ROS levels. Both UCP5 and Sirt5 are upregulated in hypertension and Type II diabetics; the confluence of having geneticly more UCP5 along with Sirt5 are implicated in increased carotid artery plaque. (Of course nothing is linear in humans so haplo-type T- carrier UCP5 polymorphism rs5977238 benefit with less plaque risk and reduced plaque numbers.) Note: I am skipping over other Sirt & UCP; but will add that lots of pheno-typic UCP1 spins out extra amounts of reactive super oxide to drive down nitric oxide and implicated in accelerated aging of the vasculature.

Might/Doc - Does this mean that if you DONT have proper insulin receptor response that all of the things listed in the last paragraph become untrue? (meaning bad?)

Would this mean that you are implying a low carb diet would be the best solution due to the insulin issues?

I ask because I cannot raise my HDL for the life of me. It is completely stalled at 40. And my LDL is primarily small dense kind. I have only really had this problem since going "LC Paleo" and adding a ton of sat fat to my diet but then I added back in starches and other carbs and became more moderate carb, while still continuing to eat bacon/eggs/cheese/cream/butter/beef/coconut oil/ghee/nuts etc.

Now I've got people telling me to go back to LC, and exactly the reverse, people telling me that I need to cut out the fats including dairy and go low sat fat.

Mito....:
I have viewed your comments at the Hyperlipid and always appreciate your detailed biochemical/physiological explanations per topic. Your grasp of details and mechanisms is amazing! What is your background? Are you a biochemist by trade?

A retreat is an excellent idea!  It would be a great time of learning and discussions. I vote for Gulf Shores Alabama

HI STG,
My hope here is that I never hijack Dr. Davis'  blog ( I never personally posted on Hyperlipid blog).  I trust  Doc's readers know he is not responsible for any errors I make. Being semi-retired from consulting on agro-industrial projects in developing countries I feed my mind by keeping up with health science & commenting here about correlations to Doc's work.

Hi J. Kronk,
Saw your 11 Nov. query &  feel diet advice here is for Doc to offer (not me). Doc discusses ApoE pheno-types he restricts dietary fat for. You "tagged" me where I  was elaborating on platelets' interaction with insulin & how insulin resistance is a game changer (not sure what confusing).

If one is insulin resistant then the signaling to build-up (anabolism) from insulin is selectively diminished and consequently break-down (catabolism) signals get  into play. Proteo-lysis is protein cleaving and HDL's protein component can be more rapidly subject to proteo-lysis; which I presume (?) is why/how some people degrade their HDL so quickly. Genetic quirks (& gender) also hit HDL levels notably;  yet  if quick enough turnover the "stale" HDL  might be being replaced by more functional HDL. According to the "HATS" study HDL alone is not a predictor of coronary artery disease mortality.

Niacin usually decreases rate of catabolism of HDL,  it helps secrete more ApoA1 to make into HDL & decreases amount of  smLDL. Niacin isn't perfect since it alters the extent to which HL (hepatic lipase enzyme) can work on a  HDL molecule to morph  it into the kind of HDL that has the maximum reverse cholesterol transport capability. HL is what hydrolyses the triglycerides in HDL - so, basicly if HDL loaded with trigs it has sparser room for scavenging cholesterol.


One's genetic response to increased levels of circulating palmitate free fatty acid can interfere with insulin signalling in the liver. Whether clinically insulin resistant or due to a genetic quirk (you?),  palmitate can phosphorylate liver insulin receptors in a manner unlike "normal" individuals do in the Akt process (insulin normally should get Akt going to stop liver gluco-neo-genesis - since insulin has glucose to drive into cells ). Essentially "excess" palmitate, in this example, is causing only a partial phosphorylation of Akt & is how researchers can use very high fat diets to induce experimental diabetes .

I don't hear you being insulin resistant, so address genetics of Protein Phosphatase 2A (PP2A), which  has components involved in it's regulation and is subject to different structure. How PP2A parts interact with distinct parts of the Akt molecule can  impair some interactions,  yet leave other parts of Akt responsive ( to do what Akt  is normally designed to do). Palmitate can raise PP2A levels in the liver by 30%; so basically the more PP2A  around and/or the molecule's genetic tweaks the weaker a key part of  the liver's Akt response is going to be.

Since palmitate  being in the liver does not stop insulin there from fostering more trigs there are still post-prandial trigs going into the VLDL . In other words the liver insulin resistance and rogue genetics can leave the part of Akt that governs lipo-genesis still responsive to insulin. Doc warns us about trig enriched VLDL & chylomicrons promptly driving  smLDL that doesn't degrade & small particle numbers measure high; he is more adamant about post-prandial trigs but genetic high overnight trigs can occur.

I don't think coconut oil acts the same way high animal fat sometimes does on Akt . We internally make palmitate when acetyl-CoA acted on by enzyme acetyl CoA carboxylase  to make malonyl-CoA that fatty acid synthase converts to palmitate. I think most of coconut oil's fatty acids are metabolized before getting into that pathway so maybe coconut oil is worth parsing when genetics or insulin resistance drives up smLDL.

Mito..
Excuse my error about you posting on the Hyperlipid. I guess I have read your posts elsewhere. In any case, your posts are very educational and explain precisely the biochemistry  Thanks for sharing your knowledge!

Hi Dr. Davis,
I’m 47 yrs old. I’ve had migraines since I was a teen and I developed Athsma this past January (hate it). During the process of discovery the drs found I have a 50% blockage in one of the 5, non critical, arteries running along the back of my heart. Scared me, to say the least. I’ve always eaten quite healthfully (for what I knew), am thin @ 6′ 1″/155lbs (was 175lbs in Jan.). Had total cholesterol of 200/LDL of 146/HDL of 50. Drs wanted me to do Lipitor. Researched and said, “No, thanks.” Started exercising 5-6 days/wk (lifting + walk/run), taking red yeast rice, fish oils, fish, no meat, no dairy, no eggs, lots of veggies/fruit, etc., but still eat beans, oats (every AM), occasional wraps. After 6 wks my blood work (VAP) was as follows: LDL=86, HDL=43, VLDL=17, TOT. CHOL=146, Trigycerides=66, Non-HDL (LDL+VLDL)=103.

Seemed GREAT to me! The dr wasn’t impressed. Said my ‘particle size’ was small: LDL1(a)=8.1, LDL2(a)=0, LDL3(b)=39.5, LDL4(b)=24.9. Density Pattern=B.

I’ve continued but don’t know how to elevate my HDL and reduce the particle size/change the pattern to the more favorable ‘A’. Getting down about this. Working hard but, seems like I can’t find answers that work, anywhere! What might you would work in my situation? Also, Is niacin ANDRed Yeast Rice a bad idea?
I’ll hang up and listen. Thank you,
Mark

PS - I left this post on another page, as well.