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.

What's your opinion of the study showing that vitamin D levels above the low end of the normal range were associated with elevated CRP levels?

Correct Spelling:  Myocardial Infarction

Er, Joke, sweetie..

HH

What an extremely informative article.

In 2000 I had cardiac bypass after multiple failed stents. In 2003 I thought I was dying. I was short of breath and had pitting edema and many other health problems. My doctor told me I was probably reblocking and suggested a cardiac cath.

I did not know about a connection between wheat and the heart but I did find a connection between my peripheral neuropathy and gluten. Up to the time I stopped gluten, I was carefully following the AHA dietary guidelines for a healthy heart. I even followed the Ornish diet for about a year. All I did was get sicker and sicker.  Dropping my favorite food(wheat) and all gluten was what made the big difference in my health. My PN is no longer painful or progressing. I also had complete resolution many other symptoms including the pitting edema and  shortness of breath. It has been over 8 years and my heart is still doing great.

Of course there are other factors to consider which Dr. Davis addresses on his websites. Vitamin D, blood sugar, thyroid to name a few. I am a work in progress.

Dr. Davis
I am not trying to say you are wrong, Quite the opposite, I think you are on the right track with your program.  But, have you had enough people in your program long enough to make a statistically significant sample?  I am sure there are more people in the world who don't follow your program than do.  That alone would make it more likely for the non-followers to have a heart attack.

MI (myocardial infarction), usually a sequel of ischemia,  is often preceded by episode(s) of angina. In many resilient people the angina event offers the heart a chance to deploy inherent plasticity in what is called "pre-conditioning". Many  who have angina episodes 1-3 days before suffering a full on MI  seemingly paradoxically recover with less serious subsequent arrhythmia ,and for the next 1-5 years have lower susceptibility for in hospital dying (statistically).

"Pre-conditioning" is a likely explanation for Doc's preventative MI protocol for many middle-age & up adults. Ischemia (felt as angina)causes a heart cell mitochondrial response, and also surface of that cell response. This involves channels & potassium with the same name in those respective membranes, but depending on which part is involved the level of reaction differs. And of course, there are isoform variations of this potassium ion channel that responds to ATP molecules (K-ATP).

Mitochondrial K-ATP (mtKatp) is only discussed here. Ischemia results in some heart muscle cell not being able to sustain ATP output. In healthy heart cells it is  normal levels of ATP that keep the channel mtKatp closed. Healthy mitochondria don't ideally let in too much K because it makes them osmoticly swell inside, among other side effects.

Potassium flooding into a mitochondria from a channel mtKatp opening up does several  significant things. One is keeping detrimental calcium (Ca++) from getting into the cardiac cell which is being forced to deal with a ischemic event. Otherwise Ca++  instigates unwanted pore openings in that mitochondria's membrane; letting the inside/outside balance of that mitochondria & the cytosol interact detrimentally.

In other words a significant up-stream "pre-conditioning" benefit is from mtKatp channel opening in response to when that heart muscle cell is unfortunately suddenly challenged by ischemia. Doc tries to prevent high blood sugar (hyper-glycemia) like in metabolic syndrome & t ype II diabetes because hyper-glycemia itself opens mtKatp channels; but this is at the wrong time.

Meaning the hyper-glycemic individual, despite having mtKatp channels quite open, has lost a large part of their potential heart cell plasticity (ie: recovery despite ischemia) because they can't turn on their  crucial natural "conditioned" response to ischemia . They lose an important preventative mode; since, for them,  the protective "pre-conditioning" dynamic can't flip "on" into action because it wasn't  kept primed in the "off" position. When young this doesn't usually matter because time hasn't set them up for ischemia yet.

Dear Dr. Davis,
Many people have confusion about who to believe on this issue like myself.  I have followed the low carb, no wheat diet for over a year.  HDL went up to 58 from 42.  I am a big fan of yours and convert to this lifestyle. The confusion happens like this:  I shared your book and forum with our family doctor, and told him about the results I had.  He seemed interested.  I saw him a few weeks later at a social event and his responses were this.
1. LDL size is insignificant.  If he sees a patient with elevated cholesterol with pattern A LDL, he will still put them on a statin to stop Plaque progression, he sees it as insurance.
2.   He says they are proven to stop plaque progression.
3.  A person gets enough vitamin d from diet and walking to their mailbox everyday.
4.  The only thing that matters to him is reducing total LDL to 50 or below for at risk patients.
5.  If you have heart disease, than there is no need for a heart scan, because we already know you have heart disease.

I think many people read your forum, get excited to hear about your approach, and then go talk to their primary care physician and get shot down on it.  It can be confusing and discouraging to say the least.

Conan,
That's the standard lingo fed down the medical pipeline. I've heard all of those as well. Plus this one; "there is nothing we can do to lower LP(a), so there is no since in testing for it".

I've wanted to ask you to write about dairy and the heart since my heart attack, and now that you're done with Wheat Belly.   I talked with people years ago about your blog and about gluten-free (to no avail), and now they're telling ME about your book like it's a new discovery (how soon they forget!).  Funny.  

I was dx celiac 2-06 at the almost age of 46.  I'm obese and initially gained 22 lbs going gluten free because I turned to Yoplait yogurt when I didn't know what to eat (+ learning to substitute SAD diet with gf SAD diet).  I learned about insulin via Jenny's Bloodsugar101 blog, and I've whittled away at changing my diet ever since.  So many bloggers have changed my life, and I'm so grateful because I'm getting some QUALITY of life I never knew before.  

I was almost Paleo with a lot of cheating, and I continued having dairy until last year when I had a heart attack at age 49 after running my first 5K (trying to get healthy and lose weight).  

I won't go into the history of why, but I was not taking my usual omega3 supplement.  I was supplementing with 5-HTP (100mg) along with other neuro support based on urine testing from ND/MD because I was still a bit depressed (how would I know?  I've only known depression, and I thought most of my depression abated going gf).   While most of my symptoms abated going gluten-free, I was and am still trying to overcome fibromyalgia.   Fibro: lack of energy.  Muscle fatigue.  Actually, for years I had a-fib on and off.  Sometimes it was my thyroid (I have Hashimoto's, and it was in range at the time of the MI, though they didn't do a panel of labs), most of the time it wasn't.  

The year before my MI I went to cardiologist and I told him when I ate dairy (I'd gone from Yoplait full of rBGH at- the-time & sugar, to organic Greek full-fat plain) I had palpitations.  "Is it the calcium?" I asked.  "No, but here's an Rx for statins, hmm, though they'll exacerbate your fibro... How about some beta-blockers?"  I said I'd look into it (throwing the script into the trash).   I wore the Holter monitor and took EKGs, etc.  End of appt and relationship.  I continued to try to research online the best I could.

The day before my first 5k, I was in a weird place emotionally - anxious.  I ate and couldn't fill myself.  I had 3,200 calories where I usually eat between 1,500-1,800.  I considered it "carb loading" before the race even though I never researched what that really meant (too busy researching everything else).  Here's my food log for the day before the MI:

Bfast: Stonyfield cream on top plain full fat yogurt w/strawberries, blueberries, banana, flax meal, Member's Mark gf Spinach Asiago sausage.
Lunch: Stonyfield gf English muffin, 3.25oz gf deli turkey, 8g butter.
Dinner:  2 Amy's gf cheese enchilada dinners, 2 mangoes
Snacks:  46g (unpopped) organic popcorn & 1 stick butter, 1 banana, 20g sunflower seeds, decaf coffee w/15g heavy whip cream.  I was about a month into going caffeine-free.
Processed carbs:  148g, Fruit/other carbs: 154g Total:  302g
Fat:  184g
Protein: 101g
Fiber: 39g

My cholesterol at the time of MI:  
TC: 206  
Tri’s: 74  
HDL: 49  
LDL: 142
A1C: 5.5 which translates to an avg bg 111
BG: 118 (I'd been doing morning fasting tests, and it was hovering around 100, and I knew that wasn't good - hence the 5k.  I'd been walking for years though I was struggling to be consistent w/energy to exercise, something not uncommon w/fibro sufferers.)  
BP: 150/82
hsCRP: 3 (down from 6 which was down from 11 or 12 ~a year before)
Heterozygous for Factor V Lieden discovered when I had a Boston Heart Lab cholesterol study ~a year before.  
It was May, overcast, and not overly hot outside, more like the mid-60s - ideal even.

Thyroid lab early May:  TSH .7
Vitamin D:  tba. I have to look it up, but I have a history of tracking it and supplementing; it has been above 40 for years at least.  It's currently 65.

I had one cup of water before the race.  After the race I ate a banana and 4 c water (+ water provided via Dixie cups along the route which were a pittance).  I was red faced and hot.  I drove home to take a long, HOT magnesium bath, and went to bed due to fatigue.  I don't remember if I drank more water, or much more than that.  I was actually having the heart attack that night, but at the time I didn't realize it.  I awakened around 5 a.m. from a long, unfit sleep, even though EXHAUSTED.  I tried to eat a sweet potato for bfast but had anxiety - I had a bite or so, but kept putting the fork to my mouth and down to the plate.  I had a hard time catching my breath.  My left arm felt like a blood pressure cuff was stuck on inflate.  I called doctor neighbor who didn't answer, then called out-of-state husband who told me to take an aspirin.  I hadn't thought of it.  Oh dear - I had to find a gf aspirin, which I luckily had some expired gf baby aspirin, and took one.  In 20 minutes it was lessening my arm pain.  

I got to the ER, and THEN had to navigate the health care system as to what gluten was.  They thought I was crazy to worry if they're high dose aspirin or sublingual nitro had gluten - this, from two nurses with "IBS" ... the cardiologist has a regimen of drugs to give prior to the heart cath and I had them looking into the gluten ... the hospital DID have a gf menu (wonders!), but got the order wrong a few times and had to redo the meals.  I'm so glad I had my wits about me.  I lost two pounds in the hospital eating strictly Paleo. ;0)

A few months prior to this, I'd seen a hematologist to figure out my mysterious leg pains.  Most of my fibro pain went away with gf diet change, trying to balance my hormones, TRYING to get more sleep, exercise, etc.  But I couldn't shake the pain in my largest muscles.  I'd read about rhabdomyolysis and asked him to do a CK test as a base for when I wasn't in pain.  Sure enough, it was normal.   Whenever I'd try to jog hard I'd get horrible pain in my legs which took about 5-6 days to recover.  There were a few times I exercised so hard they seized up, esp the day after and it was all I could do to get to the bathroom - sitting was an ordeal!   It wasn't normal for as long as I'd been exercising, to have this pain.  I know people who run and never have pain, so it bothered me I had this and couldn't push harder.  

Sure enough after the 5k my quads were killing me.  The ER checked my CK, CK-MB, and troponin.  All were elevated.  When I brought up my theory about fibro and CK to the cardiologist he said everyone's CK goes up after exercise.   What am I to think?  Am I naive?  My heart cath was clear.  I was given marching orders to followup with my GP.  He told me to take a baby aspirin daily, but I'm trying to heal a leaky gut and don't do that.  I have taken fish oil again non-stop though.  

I read about dysautonomia, rhabdo/dehydration, hypoglycemia, and electrolyte imbalance.  I can't help but think my lack of energy had something to do with my heart attack.   I contacted a neurologist who said he didn't believe in fibro, and then tested/probed my muscles (they were responsive).  

Then I heard a podcast between Dr. Rosedale by Jimmy Moore.  Dr. Rosedale said (my words) that saturated fat covers your cell and energy can't get in (you need a balance of fats for cell membrane integrity).  Well, I'd been unbalanced.  I took a special, new blood test* and found my body reacts to dairy fat like gluten (which is hard on the adrenals therefore pushing cortisol? - my thoughts).  

I quit dairy completely and my daily, constant nagging quad/ham leg pain went away, I sleep better, my palpitations went away, my depression got, yet again, better, AND I lost 25 lbs EASILY (which is not something to which I'm accustomed).  

FWIW, I am very lactose TOLERANT.   When you hear about giving up dairy in the celiac community, it's often because a person is lactose intolerant not because of other food intolerance symptoms.   I was stubborn in giving up dairy because I was dependent on the negative drug-like effect it had on me.  I STILL crave it now and then, too.  You don't realize it until you give it up completely: not 90%, not 99%, but 100%.

I am just now trying a boot camp and have better exercise tolerance; my pain is still more exaggerated but I recover in time to exercise again in two days.  

Thanks for letting me share my story, and I appreciate all that you contribute to the awareness of heart health.  I've been a reader since 2006.

I don't think wheat is that bad. If you have been eating a lot of white flour products then you can become gluten sensitive. But, if you use sprouted wheat bread and find out about wheat grass juice, you can have awesome health. I think it is the GMO wheat to watch out for the most.

oops, forgot:
* Cyrex Labs Array 4 for Cross-Reactive Foods, info here:  http://bit.ly/thedrxreactivitypdf or www.thedr.com (Gluten World tab).

I responded to "milk butyrophilin" which is a milk fat protein.  Upon Googling around, I find it's associated with Multiple Sclerosis (http://bit.ly/ze5xOI).  I have enough autoimmune diseases, and will continue on my happy Paleo path.

Sorry, one more thing:  I am a slow caffeine metabolizer which apparently makes me more prone to heart attack:  http://bit.ly/zbc8L0 (even though I'd been off caffeine for a month or so, I thought it was interesting).

Gluten is gluten, whether it is in white flour or whole wheat or several other grains like barley.  Ask anyone who is gluten sensitive or a full blown celiac - and I know several,  any gluten will make them very sick.  It is a protein that their body cannot digest.  And it doesn't matter whether it is from GMO wheat or not.

Hi Dotslady,
For seratonin's (5HT) 16 different receptors to work they have to take routes that are paths which result in an increase in Calcium (Ca++) in that cell interior (cytoplasm).  Seratonin is an amine molecule. In humans there are 9 different trans-glut-aminase enzymes that when turned on by Ca++ binding  can also process the amine seratonin.

"Seraton-ylation" is the result of action by trans-glut-aminase enzymes causing seratonin metabolites that then interact with other cellular processes. Thus "seraton-ylation" of fibronectin results in more smooth muscle cells being produced & in another relevant instance induces platelets to put out proteins that foster coagulation.

2007 Japan  researcher  Miyazaki, et.al. (J Cardiovasc Pharmacol 2007 Apr;49(4):221-227) blocked seratonin & relieved symptoms of peripheral artery disease (PAD). Leg pains you suffer may be  PAD endothelial dysfunction from too much Ca++ influx into muscle cell's cytosol. And your 5HTP (precusor of seratonin) supplementation could be contra.-indicated.

Dairy has tryptophan & the calcium needed to process it into seratonin; yet your doctor told you dairy's calcium content was not the problem. Your depression bio-chemistry suggests altered seratonin metabolism. One's genetic variants of seratonin routing pathways are a jumble of factors, including particulars of calcium (ie: calcium channels in that cell's membrane & the site of stored Ca++ already inside that cell ); all modulated by seratonin reception peculiarities.

Your blood pressure of 150/82  may be due to "seraton-ylation" of fibronectin proliferating too many arterial cells (hyper-plasia) leading to stiffer blood vessel making for more tension (hyper-tension) as lcse ideal  contraction/rebound.(for geeks: 5HT2a receptor & transglutaminase induce serotonylation of a GTPase RhoA affecting proteasome's down of GTPase in a way that upregulates Akt thereby engendering proliferation of arterial smooth muscle cells resulting in diminished contraction capacity). Breathing problem you described is also precisely researched as  part of the "seraton-nylation" sequel involving trans-glutaminase using seratonin as an amine, not a hormone.

Normally people with elevated seratonin in circulation have a natural protective response whereby the number of seratonin receptors perched waiting in the cell membrane is reduced. But your vascular smooth muscle cells actually seem over receptive to seratonin & you've been innocently topping up with 100mg 5HTP daily (how long?) .

I think you will find a hailstorm of opposition to that notion, jhail.

I would invite you to read my book, Wheat Belly, that exposes modern wheat for the fraud it is.

Wow, Dots.

A revealing story. I'm glad you found your answer . . . despite your doctors.

Yes, dairy is a big problem for select people. I pick on wheat because it is a HUGE problem. But, for some, dairy can be a substantial second.

Yes, it is, Conan.

I can tell you that your doctor is reading the commentary and editorials in the medical journals and what we call "throwaways," the low-grade magazines that physicians are sent that are really thin disguises for advertising. It means he is not reading the primary literature, nor gaining an experience, nor is he thinking. He is simply regurgitating the superficial thinking of those who write these pieces. These pieces tend to be CYA with a slant towards drugs.

We are making progress, but it is painfully slow!

Informally, Teresa, there are approximately 1000 patients in the office who follow the diet, about 300 who do not. (The rest have non-coronary syndromes that are not relevant.) This was not a comparison to a population outside the office.

Hi, Anne-

Yes, but you have come a long way, much on your own intelligence, strength of character, and persistence!

No.

I meant myocardial "infraction."

It was a joke.

Even if you're lactose intolerant, milk in the US and Europe contains mainly A1 casein, while milk in Africa and Asia contains A2 casein. If anyone can't live without dairy, they should try to make sure they get it from an A2 cow such as a Guernsey.
More info: http://www.betacasein.org/?p=heart-disease

@ Might,
I noticed that people differ by how much they need to eat milk products. I don't  particularly care about anything made out of milk with the exception of butter and heavy cream for my coffee, even cheese (I eat it anyway because I keep buying it for other family members, but I would always choose some deli meat over a cheese) Does it mean their preference may depend on which path their serotonin takes? Some people actually crave such tasteless things like cottage cheese and plain yogurt.  It feels like there is some physiological difference besides taste preference..

Al- epic as usual. thanks so much for your posts. I don't have the background to truly comprehend much of what you say but I do love reading it. And it does help in an over-all general knowledge kind of way.
Doc- Thanks again for taking the time. It's tragic that too many of us (myself included) don't find out about this stuff until AFTER we've been stented OR WORSE. I only got here by innocently trying to find out about possible side effects for the 80mg/day of lipitor  they put me on no questions asked or answered. I'm still pissed about the quality of care I get from any cardiology related people I've seen. Yet I'm still afraid to  not take my meds.

In reply to the above comments - I'm aware that people who are gluten sensitive should stay away from all gluten products. However, for the rest of us, it's best to try to choose whole grain products. I have a friend who was a food science major, who told me that people become gluten sensitive from having eaten too many white flour products in their life. But, I know people who are gluten sensitive who can have sprouted grain breads and sprouted grain drinks. Everyone should avoid the GMO products though.

Hi GalinaL,
Others here have pointed out eating dairy give us a caseo-morph (ie: opiate like molecule) & this engenders an opiate brain response; so probably one's  real time response of contentment from eating dairy.  Then too dairy's tryptophan/calcium combo producing a bit of extra seratonin in popular legend is supposed to be how warm milk relaxes some into sleep.
"Seraton-ylation" is less about seratonin in a nerve synapse.  It is  how different  tissue cells' internal processing is modified after interaction with the unique amine characteristics of seratonin  (as opposed to any neuro-endocrine functions of seratonin). Your idea of dairy lovers sounds more like a conditioned response anticipating caseo-morphs; much like Doc says modern wheat can condition some people's neuro-physiology to crave wheat.

Hi jp,
Depression is unfortunately common after MI (myocardial infarction); which you may know from fellow patients or first hand. Long term ( not short duration use) of anti-depressant drug SSRI (selective seratonin re-uptake inhibitors) is associated with less MI fatatlity. First this was assumed to be due to SSRIs side effect of  reducing platelets (ie: thinner blood circulating) but 2011 published research disproved that mechanistic linear explanation.

The "Baltimore ECA Follow-up Study" (1981-1994) noted a higher incidence of heart disease for the depressed and those notably sad beyond +/- 2 weeks straight. Curiously, the depression link was more of a significant  factor for younger women followed up on. And most statistical reports concur that those with continual depression after an MI show an increased rate of fatality.

Seems there is an interplay between one's  "seraton-ylation" ( seratonin amine metabolism) quirks in the heart muscle cells (or other tissues) and the useable seratonin neuro-endocrine metabolism in the brain cells. I have a simplified explanation for this paradox (SSRI= good; yet seraton-ylation = risky) ; but nuances aren't detailed here & I may (!) be mistaken.

In true depression seratonin isn't performing normally in nerve synapses (ie: seratonin plucked back from the synapse action site too fast, precisely what re-uptake inhibitors slow down) so there is no need to contribute so many seratonin molecules to building up a reserve pool of seratonin for nerves to have ready to put into action (ie: pool always full enough since seratonin just pulled back in right away; or seratonin rarely even leaves pool to action site). This under-functioning leaves the depressed individual without the normal programming prioritizing seratonin  for nerves. In a sense their seratonin  may be more readily programmed to be used in non-nerve situations (ex: seraton-ylation leading to excess calcium in heart cell) in that individual.

The prolonged use of drug SSRI (ie: keeps seratonin lingering in the nerve synapse) indirectly favors seratonin getting put into the back-up nerve seratonin pool. The nerve cells in due time  register  they can/need to top up with seratonin. This is a variation of  "use it , or lose it" - and the individual re-programs to "fill" the nerve seratonin pool  with an accompanying down-shift of  some of the less important "seraton-ylation" farther away from the brain.

Unfortunately, not everyone's genetics will be able to re-organzize to prioritize nerve dynamic. Some might be stuck favoring  "seraton-ylation" in vascular smooth muscle cells, no matter how long the SSRI make the nerve seratonin pools ideal to orientate seratonin programs around.

Thank you.

Mighty-Al,
this is the 1st time i heard that angina as "pre-conditioning" of MI hence improving the survival/recovery rate!
your other comment equally awesome
thanks!

Hi PHK,
Pre-conditioning phenomena can be from other triggers other than occlusion of heart (ischemia). In ischemia the heart cell(s) affected tries to cope in quick time by instigating  the 1st stage(s) of pre-conditioning. This last for up to 3 hours. (The dynamics other than mitochondria Potassium, mtKatp, are quite convoluted.)

Then there is a delayed 2nd stage while that cell tries to switch over to put out the altered proteins that will act to limit any damage (minimize extent of infarct). This requires enough time for  that cell nucleus to get working on new program of suitable proteins ; the cell nucleus can preventatively shut down for hours without that cell dying.

Ideally after 12 hours the last stage of  pre-conditioning kicks  into gear and that gives cardio-protection for up to 3-4 days. This span of  protection corresponds to statistic of hospitalized myocardial infarction (MI) patients who had episode of angina 1-3 prior showing better prognosis.
Once the 2nd (late) of pre-conditioning in effect a lot of the benefit is from greater mitochondrial anti-oxidant levels up and running. This MnSOD keeps nitric oxide (NO) from being depleted by interactions with the reactive oxygen (ROS) on the loose as the heart cell tries to get back to using oxygen inside that cell normally.

ACE inhibitor drugs & dietary providers of that same inhibition (ex: mycelial/fungal fermented soy bean ACE inhibiting hydrolized by-products like miso and japanese "touchi"- black soy bean  enbedded in aspergillus  oryzae +/- 1 year) afford protection from infarct damage via molecular action just like 2nd stage pre-conditioning does. They do this by acting on the bradykinin molecules a challenged heart puts out; and then downstream there is more MnSOD available to take on the ROS load in order to not waste NO in reactions with those ROS.  

Exercise benefit to the heart is partly because it increases mitochondrial MnSOD; creating a predisposition for late stage pre-conditioning. One of the paradox of exercise is that it induces more inflammation molecules. The cytokines TNF-alpha & IL-1B acting in synergy (not stand alone drivers) induce cascades downstream that make muscles put out more MnSOD.

"Warm-up Angina" is a long recognized phenomena which is akin to an exercise ischemia. The push from one's resting heart wave and subsequent time recuperating  are suggested to be a version of  early stage pre-conditioning. This conditions one so that there is more time before same amount of exercise would drive you to hit an ischemia challenge; and also one would have to get hit by a greater degree of oxygen drop to trigger any ischemia challenge. The plasticity of the heart gets trained.

Another cause of post MI depression was pointed out to me by a friend who was familiar with the drugs prescribed after an MI.  One of the most common is a beta blocker which is designed to lower blood pressure and slow down the heart (I believe I got that right), so that the heart can heal.  One of the side effects (which nobody mentioned when prescribing the drugs) is that they make you feel physically lethargic due to the decrease in heart rate which can then lead to a perception of being depressed (rather than the type of serotonin related depression AL was talking about) because you don't feel like doing your usual level of activity, you may not even feel like getting off the couch - and you may not even realize why!  The lack of information about what to expect and the side effects of all the various drugs used was astounding.

Permit me to revisit Dotslady's myocardial infarction (MI, heart attack):
marathon over & by 5 a.m. she  suspects an MI. Thus, after  usual interlude of 12 hours any 1st phase of pre-conditioning did not manifest enough (any?) 2nd phase pre-conditioning to prevent her hospitalization for MI.
She had labored breathing after 12 hours instead. Pulmonary artery smooth muscle has the enzyme trans-glut-aminase II in between it's elastin & collagen "cables" layers.
The pulmonary artery cells' seraton-ylation (via trans-glut-aminase II) make for a version of  contraction (calcium influx & possibly cyto-skeletal filament actin alters). The increased resistance forced her pulmonary artery to struggle (labor) just to keep up with the base line need for oxygenated blood by the brain & vital organs.
Nitric oxide (NO) is capable of influencing the trans-glut-aminase enzyme and even keeps less amount of that enzyme being  deployed. But without the 2nd phase of pre-condtioning's MnSOD too much NO is busy being wasted interacting with ROS. And considering how Prozac (fluoxetine, traditionally used as a brain SSRI seratonin tweaker) inhibits trans-glut-aminase II enzyme we can see how an appropriate doseage of it (ie: enough fluoxetine drug to infuse relevant tissue cells other than the brain) helps in panic/anxiety to relieve breathing. Prozac blunts the ability of seraton-ylation to go forward in the pulmonary artery by an additional independant avenue than how it is otherwise acting in the brain.
Looks like Dotslady's dys-functional seratonin (ex: depression) hard wiring apparently did let some pulmonary artery seraton-ylation go forward after 12 hours. And then elsewhere seraton-ylation seems to have progressively gotten worse in some cardiac artery smooth muscle cells adding to the occlusion afflicting (attack) her heart muscle myocyte cells.
She is even a young, doctor guided & low-carb exerciser. Which suggests to me that seratonin quirks in some individuals can unfortunately over-ride the ability to get into play the 2nd phase of pre-conditioning.

Dr. Davis gave succinct MI advice (above) : "...supplement iodine and correct any thyroid dysfunction...." Just in case anyone misses that connection to my layman comments  I'll specify the relevance.
Low thyroid has (for decades) been clinically  associated with depression & Doc  is very concerned with adult onset hypo-thyroid. Examples of Prozac (fluoxetine) were given because drugs illustrate the seratonin factor.
My references to SSRI anti-depressant drugs  do not negate Doc's protocol for preventing MI.  Part of his clinical success may be how protocol limits adverse seraton-ylation.

Might,
awesome! thanks!
pam

Hi Might o'chroni AL:  
I appreciate your response, and I understood a lot of it.  I will reread it to understand more as time goes on.  FYI: the date of the heart attack was May 16, 2010.  

I had to look up my notes on how long I took the 5-HTP.  I took a formulary supplement: Travacor by Neuroscience (http://bit.ly/zhayn2), which I understand from my MD/ND had 100mg of 5-HTP for about 5 months.  

When I took my first dose it alleviated my leg pains(yay!), but I had side effect of a piercing headache in the back of my cerebellum area for a few hours while awakening, and in the morning.  However, after that few hours of pain, I was jubilant because I felt a sense of contentment I'd never felt before.  MD/ND told me to cease the supplement for a week, then titrate the dose to prevent the headaches.  I learned serotonin is also in your cerebellum, and even your eyes.  When I titrated the dose I never got back the lack of leg pain, nor the sense of contentment.

Anyway, I continued taking them, and by the time I had the heart attack, I was up to 2 pills.  By May 10, I'd added L-tryptophan (Jarrow, 500mg) for about 3 weeks with no effect, so I stopped that, and then added 50mg 5-HTP.  I noted I slept somewhat better.  That was for about 6 days before the heart attack.  I made no note of it, but I may have even tried taking 2-50mg 5-HTP for a few nights trying to sleep better.  

All the while, all I had to do was give up dairy.  At your suggestion, I've looked into PAD, but can't imagine it as I associate it with calf pain.  I will bring it up with my doctor nonetheless.  Thank you again for your response.  

Dr. Davis:

I agree.

If that were true, would babies have celiac disease?  Or is that because their parents ate too much gluten?  

Having an HLA-DQ gene predisposes a person to autoimmune disease.  Even then there are people without the genes we KNOW about for celiac in particular, HLA-DQ2 and HLA-DQ8, who don't tolerate gluten.  Up to 80% of the population has at least one HLA gene according to Dr. Fine of www.enterolab.com.   Approx. 30% of people of European descent have celiac genes in particular.  Autoimmune disease is triggered by stress (psychological or physical, chronic or sudden), virus, surgery, or pregnancy (which are all stresses to the body).  It's also triggered by eating gluten - whole grain or otherwise.  I wonder if you have the gene, or have stress in your life.

Hi Dotslady,
Your 5HTP supplement link shows it includes taurine. Taurine is pretty basic - yet your genetics seem to challenge a few basics.
Since  published in 1997 "Taurine Depletion, a novel mechanism for cardioprotection from ischemia" (see AJP-Heart, Oct. 1997; vol.273, No,4:H1956-H1961) has  influenced  research (2001 example is http://jpet.aspetjournals.org/content/298/3/1167.full).
Anyway, you took 5-HTP supplement with added in taurine. Taurine can accumulate in a heart cell  myocyte provoking unwanted conditions.
Beta-alanine molecule (which can not build up residually in a cell) is the crucially protective end-product from the Meditteranean Diet's high % of poly-amines per calorie of food volume ingested. Ignobly named, spermine, spermidine & putrescene are key poly-amines that we mammals can process into  Beta-alanine, which is what  counter-acts excess taurine in cells & thus protects heart muscle (ie: why Med Diet is heart healthy despite the dietician "No-No" items eaten) .

I got it!

Dr Davis:

I've been supplementing with Vitamin D3 for the last couple of years since a test revealed a level of 31 ng/dL. I'm now at 48 ng/dL. However I saw this recent finding that is of concern to me:

American Journal of Cardiology
Volume 109, Issue 2 , Pages 226-230, 15 January 2012
Relation Between Serum 25-Hydroxyvitamin D and C-Reactive Protein in Asymptomatic Adults (From the Continuous National Health and Nutrition Examination Survey 2001 to 2006)

"In conclusion, from this cohort of asymptomatic adults, independent of traditional cardiovascular risk factors, we observed a statistically significant inverse relation between 25(OH)D at levels <21 ng/ml and CRP. We found that 25(OH)D at a level ≥21 ng/ml is associated with an increase in serum CRP. It is possible that the role of vitamin D supplementation to reduce inflammation is beneficial only among those with a lower serum 25(OH)D."

http://www.ajconline.org/article/S0002-9149%2811%2902748-2/abstract

Runner2012,

The references for that article might give you some more helpful information. I thought these were good for adding more perspective to the study and its conclusions;

Michos ED, Streeten EA, Ryan KA, Rampersaud E, Peyser PA, Bielak LF, et al. Serum 25-hydroxyvitamin D levels are not associated with subclinical vascular disease or C-reactive protein in the old order Amish . Calcif Tissue Int . 2009;84:195–202;

Pittas AG , Harris SS , Stark PC , Dawson-Hughes B . The effects of calcium and vitamin D supplementation on blood glucose and markers of inflammation in nondiabetic adults . Diabetes Care . 2007;30:980–986;

Jorde R , Sneve M , Torjesen PA , Figenschau Y , Gøransson LG , Omdal R . No effect of supplementation with cholecalciferol on cytokines and markers of inflammation in overweight and obese subjects . Cytokines . 2010;50:175–180.

This was a flawed study with only so much potential to extract conclusions. The design of the study makes it hypothesis-generating, at best.

Your doctor isn''t current. You are better informed than he is.
I''d find a new doctor.

Dear Dr. Williams,

An update:  I figured out my fibro pain source:  I'm amine intolerant (histamine and likely tyramine - I'm working on an elimination diet).  I was on to something about the dairy, but it's more about fermented dairy, i.e. yogurt.  If you look at the diet journal I shared from the day before my heart attack, it was full of histamine:  yogurt, strawberries, blueberries, banana, sausage, deli turkey, frozen meals w/cheese and spicy tomato/enchilada sauce, mangoes (I know now if I have two that it's one too many), sunflower seeds.  Histamine levels fluctuate w/dose ingested and what the body can clear/process.  There's no testing in the USA that I know of for the enzymes responsible for clearing histamine (DAO and NMNT), hence the next best Rx: elimination diet.  My recent serum histamine and tryptase level was in normal lab range, but as I know from gluten intolerance this is not reason to not try diet.  I have joggled three days in a row 6.5 miles and without pain!   I asked my cardiologist at my annual checkup if histamine could have caused my heart attack.  He said he hadn't heard of it.  I know there are histamine receptors on the heart.  Yes, I've tried anti-histamines (don't work), and I've used with SOME affect a product called Histame.  Like with celiac disease I didn't have the "usual" GI symptoms.  My symptom would have been migraines .. in my LEGS (not my head); and I have two distinct pains - 1) hamstring aching and sometimes the striated muscles feel like taught piano strings, and 2) aching like a pushed and pulsating bruise above my left knee.  The more histamine I ingest the pain grows to the right leg (the hamstring pain always seems to start in the right hams).  Fermented foods cause the bruise-type ache above the knees; palpitations, and ankle edema (exacerbated by stress - always starts in the left leg and the more histamine I ingest it moves then also to the right ankle).  Too strenuous exercise is a stress btw.  Emotional stress also causes left ankle edema.  Could exercise stress, food allergy stress, emotional stress cause my heart attack?  I think so for me anyway.  I would REALLY appreciate your cardiologist thoughts about this as it affects 1-5% of the population (like celiac/gluten intolerance), and they don't know.  Since we have mast cells all over our body, everyone's symptoms are different.   Typical symptoms for histamine intolerance involve the GI or migraine/headaches, but until I read something about palpitations I never considered it.   DAO enzyme is made within a healthy intestinal mucosa.  I remember having these symptoms the year my Hashimoto's was dx in 1996 and attributing it to hypothyroidism.   I recently had a repeat Cyrex Labs Array 2 Leaky Gut test to assess my healing.  My first test I was still leaky, and this year it's mostly within normal limits.   I'm healing with gluten/grain/dairy/egg white/corn/legume/mostly nightshade  free diet (I have recently reintroduced potatoes, unfortunately that also includes chips!).  I'm experimenting w/elimination diet.   The crux of this?  Gluten damaged my gut and my health steadily went downhill.  I'm on the mend and excited for the first time since my celiac dx in 2006.  Thanks - have been reading your book - it's a great book!

edit to correct:  the second histamine enzyme acronym is HNMT not HMNT as written above.  It stands for Histamine N-methyltransferase (I've also read it as HMT).  DAO is diamine oxidase.  http://bit.ly/daohistamine

[...] Myocardial infraction | Track Your Plaque BlogJan 15, 2012 … 44 Responses to Myocardial infraction … I meant myocardial “infraction.” …. I’ve wanted to ask you to write about dairy and the heart since my … [...]

I always understood that men should get a PSA test prior to starting DHEA. Is that not the case in your experience?

Peace

Joe E O

Well, if I'd been your patient, you would have seen gynomastia in me at 25mg/day after about a month.

It sure did help my energy and mood, though -- wouldn't I love to be able to take it!  

Breasts aren't a good look for me, though.

"No wonder: Any hormone taken in extraordinary, supraphysiologic doses will exert wacky effects. Imagine taking testosterone or estrogen at 50 times the usual dose."

Thats why some people are hesitant to take Vitamin D in larger than "usual" doses.

I take 10,000 IU/day of D3...hope I don't grow a mustache!

Are there any interactions between DHEA and any medicines, specifically beta-Blockers?

I take 5mg of DHEA because testing showed slightly low levels. I can't say I have noticed any difference with this small dose.

I read on the the internet the the largest study ever done on DHEA came up with 2 very interesting findings. This was a double blind study mind you. Finding number 1 supplementing with DHEA did indeed raise blood levels of DHEA in the body. Finding number 2 the ones that received the DHEA and increased their blood levels reported no more of the supposed "positives" than the placebo group. No "better mood, no more energy . . . Authors conclusion: while supplementing with DHEA can raise blood levels its of no use. For those of you out there thinking thtas ridiculus remember we've had examples of this before. Rememeber the big homcystene controversy from a few years back? The higher the homocystene levels the greater the risk of heart attack. We knew that by using Folic Acid among other things we could reduce Homocystene levels and we did. However it din't do anything to lessen the chance for a heart attack. Just manipulating blood levels of substances doesn't mean your doing any good in some cases. Dhea and Homocystene are 2 very good examples. But hey placebo effect can be very real. We just ruin everybodies fun with are silly double blind studies.

Anonymous, do you have a citation for the double-blind study that showed no benefit?  "I read on the internet" is a bit broad.

I'm sorry I didn't cite the citation I was making a brief comment to a message on a blog not my senior thesis. A simple check of DHEA and google takes about 30 seconds to come up with the information. Sorry next time I cite a study I will do the proper citation.

The earlier anonymous posting seems to be true, if you google DHEA there doesn't seem to be alot of supporting evidence for many of the claims made about DHEA, and he's right it took about 30 seconds to see that.

TYP: try Google Scholar...

I recently took a four-month course of DHEA at 3x/d 25mg (75mg total per day) since it's showing some promise in women over forty who have been dubbed "poor responders" without much explanation in previous IVF cycles.  

It's used to induce a physiological state of PCOS - trapping antral follicles in the ovaries so when ovarian stimulation begins, the number of follicles that mature increases.

Anyway, for me it did trap antral follicles, but that did not lead to an increase in mature follicular development in the IVF cycle...I remained a "poor responder" to the injectable gonadotropins.

The side effects were minor for the most part, but the most disturbing was the redistribution of body fat...I went from, without a change on the scale in weight, a classic pear/hourglass to an absolute apple in less than two months, then continued to accumulate abdominal fat for the remaining two months.  This is a known side-effect in women and any woman considering supplemental DHEA needs to consider the risk to benefit for waist-hip ratio and waist circumferance.  

Other side effects were a loss of hair on my head, slight peach-fizz hair along my face on my hair line and an increase in appetite...although as I said above, I didn't gain weight on the scale, but did wind up with abdominal fat and a loss of LBM as evidenced by my declining muscle tone in my legs and arms.

Just something to consider if one is thinking about supplementing - perhaps getting tested for levels before supplementing blindly is a better idea than going ahead and not knowing if you're even deficient?

Great observations! Thanks.

Dear Anonymous,

What is your 25(OH)D level?

The reason I ask is because vitamin D has been given to infertile men (low sperm count). And I bet it works for some women as well.  (In animal studies, both vitamin A and D are used to 'reverse' infertility).

Did you know that silent celiac disease can cause infertility (which was news to me!)? (I had an article that discusses silent celiac disease recently).

Regards, G

What is your 25(OH)D level?

The reason I ask is because vitamin D has been given to infertile men (low sperm count). And I bet it works for some women as well. (In animal studies, both vitamin A and D are used to 'reverse' infertility).

My levels were within normal when we tested it in October and since it was winter, I was supplementing daily with 2000IU fish oil derived D3....so the vitamin D was covered.

Did you know that silent celiac disease can cause infertility (which was news to me!)? (I had an article that discusses silent celiac disease recently).

Yes!  I recently stumbled on data about celiac and asymptomatic celiac associated with infertility.  At this point, I've totally eliminated all grain based foods and we're seeing what happens.  Thus far we things are looking up - when we did a scan recently to track my ovulation, it looks like this cycle may bear two mature follicles sans any drugs...at my age maturing and releasing more than one egg happens...and we're taking it as possibly a side-effect of the removal of all grains from my diet. Thanks for the heads up though, if I hadn't already stumbled on it as a possibility - it would have been very useful information for me!

I have heard about prostate enlargement by using DHEA.

I recently requested my hormone levels be tested after being prescribed Prozac (don't want it!!) for pain in my back - trigger points - and my DHEA Sulfate level came back at 21.  I'm 39. My progesterone was 3.2.  Would a 20% progesterone cream with additional 15% DHEA 15% Pregnenolone three weeks per month help me???  Thank you for any information!

The doses we use for the above benefits, including Lp(a) reduction, range from 25-100 mg per day; most people do fine with 50 mg. We also adjust doses to starting blood levels. In this dose range, I have never seen any of the above side-effects.

1 year ago I went to the doctor due to a general feeling of malaise.  I saw a doctor who was on a rural medicine 6 week tour and his medical student.  The med student would not quit trying to figure out what was wrong with me.  A cardiologist was there on his once a month visit and reccommended this scan.  

The scan showed my arteries to have several areas of concern.  I was 53 and am a retired firefighter.  The scan report said my ateries belonged to someone 15 years older.  This caused the med student to call me at home that night to have me come in for another blood test.

So had the blood test the next morning.  Med student called and had me come back in.  Air life to a hosptital where the visiting cardioligist was waiting.  I had a silent heart attack that night.  The scan probably saved my life.