Interesting that your warning about nattokinese is FOLLOWED immediately by an advertisement for.... nattokinase extracts!

Actually most nattokinase does not contain vitamin K2.  When nattokinase is extracted from natto, the K2 is separated and sold as another profitable byproduct.

Wait a minute though! Was there any indication that he needed a real blood thinner before his clot? Maybe he was just taking it like a daily aspirin to "thin the blood" not for therapeutic blood anticoagulation. His clot was unfortunate but probably could have occurred with a cardiologist sactioned baby aspirin.

Anon--

He was taking aspirin, as well.

However, aspirin does NOT prevent deep vein thromboses that lead to pulmonary emboli, regardless of dose. Aspirin is a platelet-inhibitor, not a true "blood thinner" that works by way of clotting proteins.

Was he using nattokinase as an excuse not to take his warfarin, or something like that? Otherwise it seems very unlikely that the nattokinase had anything to do with the clot. If anything, I'd worry about nattokinase causing bleeds, not clots.

Curious if you ever recommend pycnogenol in cases where there is a risk of DVT? I believe there is at least one study showing a reduced risk of DVT in those who took pycnogenol.

I'm not saying it's better than anti-coagulants, but it may be better than aspirin.

Real anti-coagulants?  Like the red clover extract coumadin?  Patients on coumadin even with careful control often suffer excessive bleeding or more clots and strokes.    
I guess the point is that clotting control is very difficult and that the number one drug is a natural medicine, herbal extract.

One time, I was at a local vitamin shop when I saw that the supplement I was thinking about buying contained nattokinase.  Having read your blog and knowing what you think of nattokinase, I put the product back on the shelf.  The proprietor of the shop asked me why I did not want that supplement, because in his opinon it was a very good product.  I said that I did not want to take anything with nattokinase in it, and he said, "What do you have against nattokinase?"  I didn't bother to explain myself to him, figuring that I would just be wasting my breath.

What is your opinion about doing higher dose mixed tocopherols, which do work on the clotting cascade. Or garlic and omegas which decrease platelet aggregation. What is your stand on normalizing your vitamin K content and then titrating your dosage of coumadin up to theraputic INR. As far as the nattokinase is concerned, do you like any of that style of enzyme? lumbokinase, serrapeptase. Although they don't have any effect on INR they should have an affect on FDPs

That title is misleading.  People have been known to have near death cardiac events while taking fish oil, vitamin D3, and high dose niacin too.

As well, on rare occasion, people have been known to have a recurrent DVT and/or PE while on warfarin therapy, even with an INR as high as 2.5.  Therefore, does that mean warfarin is an ineffective anticoagulant?  Of course not.

This whole blog is about how we as individuals need to take control of our own health.  That just because we're taking a therapeutic medication or supplement, it does not therefore absolve ourselves from further investing in a life style that is proven to lower risk factors that may cause catastrophic health events.  

I totally agree that some of the marketing claims made concerning nattokinase are inflated and frankly, unbelievable - particularly about its capabilities as a thrombolysis.  And I agree that if your doctor advices that you need heprin or warfarin therapy in order to prevent a catastrophic health event, you certainly need to heed that advice.

But, count me down as someone who has extensively studied this subject and is still open to the possibility that nattokinase may contain some attributes in the prevention of venus thrombosis from a novel approach that needs further clinical investigation.

Dr. Davis,

I wouldn't be so quick to blast nattokinase because of this isolated incident or lack of research.

Nattokinase is a "mild" blood thinner. Taking it once a day will not do more than relieve inflammation and slightly improve a person's circulation.

A person would have to take it every 4 times a day (800 IU) on an empty stomach for if he desires a therapeutic effect. I would be curious if this patient of yours even took 200 IU per day (because a lot of products don't even contain that much).

I have personally witnessed an improvement in circulation after taking nattokinase.

I would like to add one more thing...

I'm sure you have had experience with patients who took 400 IU of vitamin D in tablet form, and did not see any results after six months either. Was it because vitamin D is a worthless supplement, and should not be used?

Sorry, I was misspoke about the dosage. Nattokinase is measured in fibrinolysis units (FU), not IU, and the effective dose ranges anywhere from 2,000-8000 FU per day.

Also, here's actual scientific research (albeit small), not marketing hype, on nattokinase.

http://www.ncbi.nlm.nih.gov/pubmed/19358933

http://www.ncbi.nlm.nih.gov/pubmed/18971533

I've like the taste of natto from the moment I tried it. I am, however, a bit weird. ;)

Dr. Davis -- my question here is, could the nattokinase cause the blood clot (doesn't seem the be the case)?  Are you saying that it didn't matter that he was taking nattokinese because it doesn't reach the bloodstream to clear clots (so he would of had the clot anyway)

Secondly, if he was taking nattokinese that had vitamin K2 <--- is it possible that increases in K2 might cause abnormal blood cloting?

Vitamin K2 does not cause blood clotting any more than topping up your gas tank makes your car go faster.

Whether nattokinase has other effects is not my point. My concern is that people frequently ask if they should treat their DVT or pulmonary embolus with nattokinase. This is a death sentence. It should NOT be used for a such a purpose unless there were a large treatment trial proving equivalence or superiority to existing therapies.

Eric,

High dose mixed tocopherols use the same mechanisms as Wafarin/Coumadin.  They block the reabsorption of vitamin-K in the liver.  Vitamin-K is necessary for the liver to synthesize and release clotting proteins in the blood.  Warfarin/Coumadin is much, much more consistent than tocopherols in maintaining vitamin-K malabsorption and a safely prescribed INR range.  

Titrating a Warfarin/Coumadin dosage never made sense to me. It is not toxic other than causing vitamin-K deficiency. What difference does it make if the dosage is 20 mg or 20 mcg to maintain a therapeutic INR?  Your liver will need to be equally deficient in vitamin-K no matter how you caused the deficiency.

Garlic, ginger, ginkgo, curcumin, n-3, aspirin, N-acetylcysteine, Plavix, and yes tocopherols too all are anti-platelet agents.   They are effective at preventing arterial thrombosis, where anticoagulants have little effect. Conversely, anticoagulants are effective at preventing venous thrombosis, where anti-platelet agents (unfortunately) have little effect.

I'm giving my son nattokinase, one tablet daily and he also takes Vitamin K2. He has not been prescribed blood thinners, only aspirin which I stopped many months ago.
Are you warning of not replacing prescribed blood thinners with natural therapies?
If blood thinners have not been prescribed, is it of benefit to supplement with nattokinase?

Hi Dr. Davis

I was wondering if you could help me with something.

I've been monitoring my blood glucose recently with a basic monitor, and my readings would suggest that I am on the verge of impaired glucose tolerance, but not quite there yet.

I was reading about continuous glucose monitoring systems. I would love to have on if these to more thoroughly monitor my blood glucose, but every model out there requires a prescription to obtain one. I don't understand this, because they are not dangerous in any way.

Do you know of any way a non diabetic can purchase one of these?

Any information you can give me would be greatly appreciated. Thank you.

Rob

Dr. Davis, i am a 45 year old female who recently started taking Lovasa for high triglycerides , i am also on garlic tabs and one baby asprin per day . Is is safe to replace the garlic and asprin with one tab of Natto- K per day and is it safe to take with Lovasa? I am about 20 lbs overweight do not drink or smoke and swim and or walk 3 days per week. i am genetically predisposed to high triglycerides but never had a problem until i gained the weight. Until i get the weight off i am trying a more natural approach. Help!

[...] why you need to think for yourself and question studies. See, “Near-death experience with nattokinase | Track Your Plaque Blog, “Nattokinase supplement medical uses, safety, benefit, side effects,” and “Fight [...]

Acta Haematol. 2010;124(4):218-24. doi: 10.1159/000321518. Epub 2010 Nov 13.

In vivo evaluation method of the effect of nattokinase on carrageenan-induced tail thrombosis in a rat model.
Kamiya S, Hagimori M, Ogasawara M, Arakawa M.
Source
Nagasaki International University, Sasebo, Japan. kamiya@niu.ac.jp

Abstract
Thrombosis is characterized by congenital and acquired procatarxis. Nattokinase inhibits thrombus formation in vitro. However, in vivo evaluation of the therapeutic efficacy of nattokinase against thrombosis remains to be conducted. Subcutaneous nattokinase injections of 1 or 2 mg/ml were administered to the tails of rats. Subsequently, κ-carrageenan was intravenously administered to the tails at 12 h after nattokinase injections. The mean length of the infarcted regions in the tails of rats was significantly shorter in rats administered 2 mg/ml of nattokinase than those in control rats. Nattokinase exhibited significant prophylactic antithrombotic effects. Previously, the in vitro efficacy of nattokinase against thrombosis had been reported; now our study has revealed the in vivo efficacy of nattokinase against thrombosis.

PMID: 21071931

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

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