To Pedro  (posted here since Server blocked),
Journal Biological Chemistry 2003,278:54-63  "A Type 1 Diabetes-related Protein from Wheat" that refers to globulin (a storage molecule of wheat) being antigenic for autoimmune problems was where I saw wheat genome estimated in 2002 to be 16.5 gigabase. I read that article when tried to track down Doc's reason to declare wheat implicated in Type 1 diabetes. Full article at www. jbc.org/content/278/1/54.full

A 2010 reference to wheat genome is in journal Cytogenic and Genome Research, Vol. 129, No. 1-3, 2010 abstract's 1st sentence refers to wheat genome as 1C-17Gbp. English abstract at http://content.karger.com/
produktedb/produkte.asp?doi=313072

As I understand it 1 giga-base   =  109 base pairs, and mega-base =  106 base pairs; it's not a formula like that used to compare computer bytes of giga-bytes and mega-bytes.

You might have research use for the Harvard Gene Index Project's Computational Biology & Functional Genomics Laboratory; if use link below look at top of page and see a category for "Gene Indices", click there to then choose from subjects "Plants", "Animal" or several other indices.
http://compbio.dfci.harvard.edu/tgi

To Pedro  (Server blocked elsewhere),
Journal Biological Chemistry 2003,278:54-63  "A Type 1 Diabetes-related Protein from Wheat" that refers to globulin (a storage molecule of wheat) being antigenic for autoimmune problems was where I saw wheat genome estimated in 2002 to be 16.5 gigabase. I read that article when tried to track down Doc's reason to declare wheat implicated in Type 1 diabetes. Full article at www. jbc.org/content/278/1/54.full

Dr.Davis,

Just listened to the podcast, that's fantastic !

I have been diagnosed with TD2 last Sept, and since then being on the very low carb. Everything went well except my total cholesterol went out of control, and in January it was 400.

What I don't understand is my Lp(a) is close to 0 ( less than 5.0 mg/dL as it was reported).

Here is my latest direct measurements from SPECTRACELL LAB in Huston.

VLDL Particels: 122 nmol/L (needs to be < 85)
Total LDL Particles : 1271 nmol/L (needs to be < 900)
Non-HDL Particles: 1394 nmol/L (needs to be < 1000)
RLP(Remnant Lipoprotein) 205 nmol/L (needs to be < 150)
Small Dense LDL III: 552 nmol/L (needs to be < 300, marked as very high risk right now)
Small Dense LDL IV: 96 nmol/L (needs to be  7000)
Large Buoyant HDL 2b: 2045 nmol/L (needs to be > 1500)

Apo B-100: 127 mg/dL (needs to be < 80)
Lp(a) : less than 5 mg/dL (needs to be < 30)
C-Reactive Protein-hs : 0.2 mg/L (needs to be < 1)
Insulin: less than 4.0 uIU/mL (needs to be < 35)
Homocycteine: 12.3 umol/L (needs to be < 11)

Total Cholesterol: 259 mg/dL
LDL: 159 mg/dL
HDL: 59 mg/dL
Triglycerides: 118 mg/dL
Non-HDL-Chol : 200 mg/dL


I already removed the cheese and eggs from the diet, I suspect I am APOE 4.

Any comments on my pattern ?

thanks!

otterotter

To DCMarc  (server blocked where belongs),
Benfotiamine, a synthetic thiamine used in diabetic neuropathy, increases enzyme trans-keto-lase inside a cell. The use in diabetics and neuro-degeneration may (?) require professional consideration in cancer cases. Trans-keto-lase spurs cells to go into aerobic glycolysis (aerobic here refers to cell performing glycolysis despite oxygen being around for performing normal mitochondrial oxidative phosphorylation) for processing cells glucose; this aerobic glycolysis is the  famous Warburg effect and experimentally administering trans-keto-lase augments cancer cell proliferation (likewise experimentally spiking up thiamin increases trans-keto-lase).

Trans-keto-lase works for diabetics & in neuro-degeneration because  it pushes cell's glucose (via transcription once cAMP binds to it)  into the hexose mono-phosphate shunt ( of D-glucose-6p to D-glucono-lactone 6P to D-glycr-aldhehyde-3-phosphate) called the Pentose  Pathway (where hexose forms into pentose). This  process generates NADPH which boosts anti-oxidant glutathione ( & thioredoxin) production inside the cell. Also NADPH brings on the  activation of  the cell's endoplasmic reticulum's Unfolded Protein Response which helps the endoplasmic reticulum (ER) tolerate dangerous endoplasmic reticulum stress (ER stress is significant in diabetes and neuro-degeneration).

ER stress, with protein folding complications, sees NADP+ accumulate and so augmenting trans-keto-lase pushes quicker output of NADPH to keep pace; this  triggers the Unfolded Protein Response to induce Cu,ZnSOD expression that then alleviates the ER stress (ie: helps ER tolerate demanding conditions).  This helps in that it  keeps the stressed ER  ( a state that coincides with more local super-oxide O--),  from seeding the dangerous (and largely un-neutralizable) hydroxyl radicals (hydroxyl radicals come about when super-oxide related hydrogen peroxide  provokes Fenton  & Haber/Weiss reactions reducing Cu++ or Fe+++ ). This is similarly how trans-keto-lase also benefits cancer cells ( rampant cancer cell growth demands protein folding that formally stresses the ER); the prevention against reactive oxygen species means cancer cells don't suffer apoptosis (cell death).

Diabetics use of Befotiamine ( a dynamic fat soluble thiamine trans-keto-lase booster) will  help them similarly with their ER stress . In  their case the shift to using their regularly high glucose in the Pentose Pathway will mean quicker degradation of that glucose than if cells used mitochondrial oxidative phosphorylation. This also means the glycation (Doc warns against this from high glucose)  and thus tissue cells levels of advanced glycation end products (AGE) will be less; blunting the amount of AGE messing with monocytes and less endothelial dysfunction  amount to less inflammation, less diabetic oxidative stress and likewise less alteration of the vascular tissue such as atherosclerosis.

Experimentally induced diabetes is often done by feeding a very high  fat diet. Much of the fat in a very high fat diet  acts to drive down the level of trans-keto-lase due to a transcription adaptationum within 8 weeks in rodents. For humans thiamine (B1) is often recommended to diabetics; cauliflower is a nice thiamine source to make into trans-keto-lase.

To  B. Smith (Server won't post where belongs ),
Glutamine, an amino acid, is used by cancer cells to keep apoptosis (cell death) from happening in several ways. One way is how glutamine keeps the cell nucleus from condensing and stops the capsase 3 & capsase 8 cascades from starting apoptosis. The other way is how there is an increase in the  anti-oxidant glutathione synthesis when glutamine elevates NADPH (see comment above for ER stress).

Tumor Necrosis Factor alpha (TNF) works to destroy a cancer cell by running down that cell's mitochondrial glutathione level; this needs to be replenished with glutathione from that cell's cytosol. Once there is a 35% plunge in mitochondrial glutathione that  alters the mitochondrial membrane so that it stops bringing in glutathione to the mitochondria and starts leaking out cytochrome c into that cell's cytosol (which can jump start an apoptosis program). Cancer cells' rapid growth strains the normal oxidative stress limits of a cell, so cancer cells draw in lots of glutamine to boost the level of ready glutathione inside that cell; then the cytosol can continually shore up the mitochondrial glutathione levels to prevent one of the apoptosis scenarios from starting .

A cancer cell at some point has to "transform" to progress and needs lots of DNA at that stage; glutamine is needed for synthesis of cellular RNA & DNA. The bio-synthesis of nucleotides utilizes glutamine; and having lots of de-oxy-ribo-nucleotides around favors DNA replication at that cancer's key "transformation" stage (ie: S-phase). The use of glutamine by a cancer cell for converting into energy to run on, like some normal cells do, is not why cancer cells take up so much glutamine.

@ Might-o'chondri-AL
Dear Might, do you mind to tell what do you think about that cancer research result?
l http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3117136/?tool=pubmed

My cardiologist said, "look, I don't know about nutrition.  If you want to talk about nutrion, go talk to a nutritionist"

Hi GalinaL,
Cancer undergoes several oncongenic processes wherein the so-called epithelilial pheno-type cell (epithelial cells are +/-85% of cancer substrate cells) gets it's cell nucleus histones acetylated, which creates what is called "stemness"  (the ability of that cell to renew itself with potency, like our stem cells). This leads to a phase called epithelial-mesenchymal transition (where the morphing cell can go either way, either back to benign epithelial pheno-type or onward to dangerous mesenchymal pheno-type). It is when the enzyme histone acetyl-transferase no longer keeps that epithelial histone acetylated ( a sort of  limbo) that the epithelial cell's genetic expression gets knocked down permitting the further shift into full mesenchymal pheno-type .

What is important to realize about cancer cell's taking over a cell's nuclear DNA is that when the pheno-type goes from epithelial to mesenchymal the cancer cell's mesenchymal pheno-type somehow still retains the ability to perform the stem cell "stemness" of indefinite replication. Your cited authors point out that keotones boost tumor growth (+/-2.5 times) and lactate boosts tumor metastasis (+/- 10 times); and  also that their metabolic use raises a cell's Acetyl-CoA and this increases the acetylation of histones causing more gene expressio. And so authors report limiting ketones and lactate in cancer seem to be the "achilles heel" to cut off in order to stop cancer's "stemness" (ie: inherent potential); their extrapolation from this is interesting as a theory..

There are other processes beyond histone modification which show oncongenesis is not lineal. When the cancer cell is still just an epithelial pheno-type cell unit micro RNA (miRNA) of the miRNA-200 family group is un-methylated; and thus holds the epithelial pheno-type steady, because un-methylated miRNA isn't reactive enough for messenger RNA (mRNA) transcription. A 2nd stage is seen once hyper-methylation  occurs, while at the same time less miRNA is put out; this morphs the cancer cell into the mesenchymal pheno-type and at that stage metastasis is possible. While an advanced 3rd stage comes about when miRNA resurges somewhat; this is what makes extensive metastasis of cancer cells that have migrated start happening. (Lineal thinking about cancer is a trap, since it is methylation that lets cancer cells get going but later de-methylation that let's them thrive and patient outcome worsen).

Warburg effect is suggested, by cited study, to be almost a lineal concept; which they propose to re-define as desireable if it simply limits lactate and ketone production in a cell. This theory has it's own trap because in the Warburg effect +/-60% of the carbon from glucose undergoing aerobic glycolysis in cancer cells is actually being used by cancer cells as a carbon scaffolding for "de novo" fatty acid synthesis to feed into fatty acid oxidation. In other words the elevated amount of cancer cell's aerobic glycolysis (Warburg effect) is really fostering fatty acid oxidation; and fatty acid oxidation increases cancer resistance.

The cancer cells uncouple the mitochondria oxidative phosphorylation of glucose so that the a lot of the processing of glucose doesn't go all the way to normal completion of ATP production; instead cancer cells use the initial steps that perform oxidation of glucose to cleave off the carbon atoms from that glucose to use. In other words it is the mitochondrial uncoupling protein up-regulated by that cancer cell's genetic  transcription which, down the line, forces that cell to continue to escalate Warburg's aerobic glycolysis in order to keep up with energy demands as carbon skeletons get used up.

Metaformin's use in cancer treatment was suggested by study's authors to support their "reverse Warburg" theory : that it is by forcing Warburg's aerobic glycolysis to occur, due to Metaformin,  which accounts for cancer control seen. This seems too lineal an interpretation of the events; especially with regard to preceding paragraph's explanation of how Warburg relates to unpredictable carbon molecule usage. Metaformin reliably does inhibit the mitochondrial complex 1; and this will stymie glucose (and also glutamate, which cancer cells prodigiously take in ) from going on to produce ATP. I would suggest that this also stops the oxidizing of glucose molecules and thus sparse carbon skeletons are available to make into fatty acids for burning.

In addition Metaformin inhibiting mitochondrial complex 1 will also reduce fatty acid oxidation; this is because  NADH oxidation at that complex needs to happen in fatty acid oxidation. NAD+ is a crucial rate limiter in  fatty acid oxidation , but unless NADH can subsequently be re-oxidized as a molecule in the mitochondrial complex 1 it can't keep on driving fatty acid oxidation by lending out NAD+.  Metaformin use in cancer is even more complicated, because if the cancer has p53 then when glucose supply is low it manages to actually use more fatty acids to run on and then use auto-phagy house cleaning to avoid apoptosis death. Whereas, if a cancer does not have much p53 then Metaformin seems to be more effective in treating cancer.

Yup, and the nutritionist hawks the usual "cut your fat, eat more whole grains" line.

It's a comedy of misinformation with advice from agencies paid for by your tax dollars.

Hi, otter--

Obviously, I can provide only limited advice in a blog post.

But I agree: Apo E4 is a prime consideration. However, keep in mind that small LDL remains the most atherogenic (plaque-causing) of all your patterns and still deserves the primary focus. Also, if this blood sample was drawn with ongoing weight loss, this alone can provide substantial distortions.

Wow! I don't know who else would dissect that article like you did! I really, really appreciate you decision to replay on my question. Looks like  Metaformin could be healthful in more than one way in treating cancer.

Thank you for your efforts on topics like this! It's just not right that supposed experts are pushing this wheat and cereal garbage. Thankfully my wife has tapped in to some really good almond and coconut flour recipes recently, I don't miss wheat at all!

Glyco-sylation occurs inside a cell's endoplasmic reticulum lumen when certain  carbohydrates  (in the form of N-linked oligo-saccharides) meld with a newly folded protein that gets translated into  a glyco-protein.  There are different rates of activation and de-activation  between glyco-sylated and un-glycosylated proteins; this affects how that protein migrates as it tries to perform it's job and how  glycation can induce degenerative states.  Tissue cells with endoplasmic reticulum stress can exasperate certain disease progression because such "stress" there promotes more glycosylation.

I couldn't agree more with the advice to test every 15 minutes as a means of discovering your own "sugar curve." When I tried this, I found that my own peak falls pretty consistently at 75 minutes after beginning a meal. Testing at 2 hours completely overlooks my highest blood glucose levels.

It's a particularly good technique for those folks whose A1c levels are higher than their fingersticks would predict...it's almost surely because they're doing their sticks way past their glucose peak.

When test strips cost up to a buck apiece, it may feel hard to justify using six or eight of them on a single meal--but what you learn may save tens of thousands in medical bills!

Another great article - thank you! I'm curious about your thoughts on controlled 1 hour blood sugars (mine are rarely over 110) but baseline levels that aren't much lower. Typically in the 95-105 range. I will get something in the 80s occasionally, but 100 is more common. I never really spike - even a high carb meal will only get me to 130s or so and that never really happens as I don't eat much sugar/starch at all.

Another quick question: You've mentioned a couple times recently about this way of eating being particularly good for VISCERAL fat. That is exactly what I've found. Tremendous benefits and I feel great. I have leveled out for a while (months) in fat loss, however, with a good amount of subcutaneous fat still present. Is there another protocol for getting after this type of fat? I'm already no wheat, low carb, paleo.

Thanks again for your excellent articles! Always learning something new.......

Do you have citations to support your statement that glycation occurs at BGs of 100 or more?  This is one of the more-commonly discussed issues on diabetes discussion boards--but folks are wont to ask for backup.

Regarding glycation specifically...

1. Do you agree that fructose ("frucation") causes more AGE than glucose?
2. What to you make of Ray Peat's assertion that poly-fats are much more glycalating than glucose?

"The so-called "advanced glycation end products," that have been blamed on glucose excess, are mostly derived from the peroxidation of the "essential fatty acids." The name, “glycation,” indicates the addition of sugar groups to proteins, such as occurs in diabetes and old age, but when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do." (Fu, et al., 1996)." - Ray Peat

Thanks for the great article!
I've just begun tracking blood sugars closely, changed my diet to one very low in carbs and no grains, and am determined to find ways to keep at it. I've started a blog just track my progress and keep me honest: http://transformation-transformative.blogspot.com/
I'll also try the 15 minute testing to see where my personal peak in blood sugar occurs.
Again, many thanks!

Hi Dr. Davis:  What is the relationship between fasting BG taken at the Dr's office and A!C?  My fasting BG level is 73.5 but my A1C is 5.4.  I would have expected the A1C to more correspond to the fasting measurement; in the case of my wife it does.  Is it related more to the red blood cells lingering around longer or lipoprotein particles which increases the chance of glycation?  Recently had a larger than normal amount of carbs in a meal- rice and blueberries and BG spiked to 119, not to bad, but will experiment with carb portion to keep under 100 as BG may be a contributing factor to my CAD.  I am also a hyperabsorber of fat despite being an ApoE 3/3.

As an aside, i have sent around a link of one of your interviews regarding Wheat Belly and many eyes have been opened as well as many looking to buy the book.  Might not be a bad idea to have a link to any of your interviews on Wheat Belly posted to this site.
Thanks for the enlightening good work!

Well said, Annabel!

Hi, Shottle--
This will be the topic of an upcoming discussion. The documentation of this effect is quite extensive. It is no longer a matter of "if" but "how much."

Hi, Jeff--
This is one of oranges and apples comparisons.
Fructose does indeed induce flagrant glycation. Glucose induces glycation, though less vigorously.

However, there is a separate but very poorly named process called exogenous glycation which has less to do with glycation than with oxidation of fats.

This will be the topic of future discussions.

My first thought is that, if weight loss is ongoing, there is a temporary situation of insulin resistance that generally dissipates with weight stabilization.

It's also possible that your pancreas has inadequate baseline production of insulin. I'm hoping it's the first possibility.

Hi, Steve-

You will find that, if you did frequent fingersticks around the clock, the highish A1c reflects the higher blood glucose values that occur after meals.

Thanks for the feedback on the Wheat Belly project. I will indeed crosslink some of the more relevant discussions.

Advanced glycation end products (AGE) involve some of haemoglobin's hydro-carbon Beta side chain valine residue linking up to non-polar "glucose" aldehyde compounds and certain non-"glucose" aldehydes. Various pathological kinds of AGEs can occur from distinct events; in one situation it is macrophage activity producing enzymatic myelo-peroxidase, which can activate hypochlorite favoring a serine amino acid wing to form up to make the AGE called glyco-aldehyde.

Probably the AGE called methyl-glyoxal is the one most relevant to diabetes prevention; since Type 1 diabetics blood serum levels of methyl-glyoxal is +/- 6 times higher than normal. This AGE can be formed when the byproduct triose-phosphate (triose = subset of carbs) is generated from the glycolytic pathway called  Embden-Meyerhof; this  byproduct risks being made into methyl-glyoxal.

Maybe the most well known AGEs are the non-enzymatic Amadori products formed via hydrolysis; one is called glyoxal coming from glucose oxidation. And the other Amadori type AGE is 3-deoxy-glucosone (3DG), which requires fructo-selysine and the fructos-amine 3 kinase cascade to shuffle together 3DG.

Diabetes reveals the problem with AGEs; this is because diabetics risk incurring kidney nephro-pathy, One of the pathological results is oxidative kidney stress, which limits sodium (Na) excretion thereby fostering  hyper-tension . When AGEs like 3DG, glyoxal & methyl-glyoxal  (among others, like pentosidine ) circulate into the kidneys their carbonyl compounds  are hard to clear by the kidneys; the side effect is to engender  uric uremia problems and meanwhile levels of carbonyls build up in what is called "carbonyl stress".
Japan research of the plant compound chamaemeloside found that in humans it lowered levels of the AGEs 3DG & pentosidne better than any other natural remedy; optimal response was reduction of down to 1/5 th of subject's starting levels.  Chamaemeloside is the active compound in chamomile (Anthemis noblis); the extraction formula was 1 Kg of chamomile flowers steeped covered in 20 Lt. water for 3 hours at 80* celcius ( a lab temperature probably not critical for home remedy preparation).

Volek and Phinney in their new book about carbohydrate restriction think that as you increase  fat from 30% to 60% of your diet, insulin resistance increases, then it drops when you go above 60%.  It seems that among the most experienced researchers of carbohydrate restriction, there's little consensus about the optimal amount of fat or carbs.  Ron Krausse, for instance, thinks 35% to 45% is optimal.

Peter:
When these researchers talk about carb levels are they considering vegetables to be carbs, or just fruits, grains, potatoes?

You must mean, "can exacerbate certain disease progression...." meaning: to increase the severity, violence, or bitterness of; aggravate

This is wonderful information BUT I wonder if it might be unfortunate if folks who routinely have post-prandials of 120 to 140 take your 100 level as a sign of "failure"...things are seldom so cut and dried, black and white. I don't know if I'm hitting 100 or less  after every meal, but my A1C has dropped from 7.5 to 5.8 since last November restricting carbs. And I've lost 30 pounds. I will begin to be more dogmatic about one-hour glucose checks but my rough sense is that I'm not at 100 or less a majority of the time. But I might be wrong about that. Do you see what I'm getting at? Glucose control is an ongoing process that includes lots of self education since most GP's are not keen AT ALL on restricting carbs, including mine. When I read your post, my initial feeling was, "Cripes, 100 after EVERY meal? Don't think I can do that...."

From another commentator here, in an  earlier thread of Dr. Davis' here is how to use HbA1c to determine your average blood glucose level (note: this is not a morning "fasting" level) .
1st: multiply your HbA1c by 28.7
2nd: subtract 46.7 from 1st amount
3rd: take last number as your average waking hours mg/dL blood glucose over last  few months  
ex:  HbA1c of 5.4 x 28.7 = 159.98 minus 46.7 = 108.28 mg/dL of average blood glucose level

They don't count non-starchy vegetable as carbs.

Thanks for the heads up!

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Dr. Davis,
I have found that if I take my carb level too low (below 50g per day) that my fasting blood glucose levels actually go up rather than down.  If my carb intake is closer to 70-80, my fasting glucose is lower.

Have you had this experience with some of your patients?  Can you shed any light onto what might be happening?

Thanks!
Stephanie

Non-starchy vegetables do have carbs and I do have to count them. A half cup of broccoli can have about 6 carbs and since I limit my carbs to no more than 15g/meal, that broccoli on my plate is significant.

I found getting a scale that reads carbs too was an important tool for me. I found I was ofter overestimating how much of a low carb veggie I could eat. If my blood sugar starts to rise, I go back to measuring and that seems to get me back on track.

Anne

I think thats normal, its commonly encountered on paleo forums/blogs. It has something to do with physiological insulin resistance, Petro @ Hyperlipid talked about. Look here:

http://high-fat-nutrition.blogspot.com/2007/10/physiological-insulin-resistance.html

I wouldn't suggest that everybody blindly follow CHO < 50g / day. As always, its about the context. People usually forget that. We mostly extrapolate from results of people who already have metabolic problems.

Anyway, I am currently perfectly healthy apart from some minor dermatology problems (eczema).
When I have prolonged periods of reduced CHO input (around 50g / day), I eventually start having some mucus problems. Dry eyes particularly, but also joint pain. I am not 100% sure if its about low carb diet, but it looks like it. Now I target 75g < CHO < 100g per day by adding small potato and a bit more chocolate to my diet.

I think overemphasizing carb reduction is not good thing for most people. Carbs should go down by pretty big amount for most people, but not to extreme. In anyway, its better to measure then to guess. My sugar is never above 110 after meal and fasting is always around 95.

I decided to take this advice and have been tracking my 60 mins postprandial blood glucose for the past two days to see if all the years I've been low carbing have been making any difference. Especially working my way through different foods to see how they affect me and I've ranged from 64 mg/dl to 97 mg/dl so I'm pretty hapy.

However this evening 60 minutes after my dinner of panfried steak with a creamy cajun sauce I got a reading of just 55 mg/dl. A lot of websites say this is too low. I'm 32, healthy male, 5,9", weigh 160 lbs, not diabetic and I don't feel sick so I'm not sure what to make of this low reading. The only thing I did was finish a hard CrossFit workout about 30 mins before I had dinner... so a total of 90 minutes before the blood glucose test.

Any advice on what this "low" reading means? I'm hoping it's normal and means I'm burning fat!

I'm not surprised at all. I've "met" people on forums that are on this, and they rave about how much better it is than non-prescription fish oil.

Reminds me of years ago, when patients were given (in my area) "Anacin" in the hospital, then would ONLY take it for pain....other brands, or heaven forbid generic just didn't work as well!

Amazing, huh?

On the other hand, like you say, at least now they're giving it to patients.

Now how about Mg? CoQ10? Are they starting to show up too?

Not sure if you find this interesting or not, but after stumbling on your blog not knowing anything about Pectus Excavatum, I went googlin' and got a bit depressed, as it's not as benign a malformation as I was led to believe.

But I found this site http://www.ctds.info/pectus_excavatum.html which suggests that Vit D deficiency/rickets causes the malformation in many cases, and also that celiac disease might cause rickets in some due to malabsorbtion of vitamins/minerals etc.  I thought it was interesting as you've been posting about wheat and vitamin D and heart health, while perhaps they are also necessary for chest wall health.  I take heparin and low dose aspirin while pregnant to prevent fetal demise due to antiphospholipid antibody syndome (aware of that? causes blood clots), but I'm wondering if it somehow inhibited Vit D absorbtion in me when pregnant, couldn't have been a normal deficiency I was gardening in the sun during the entire pregnancy and I don't use sun block. I assume some of your patients are on blood thinners as I was? I know it effects calcium.

As for fish oils, Udo's blends are supposed to be incredible, several moms I know use it on themselves for exhaustion and over all health, and many moms swear that fish oils have helped their toddlers with speech delays.

Let me know if you'd rather I didn't yammer at your blog, I've linked to it from my little blog because I find your blog fascinating.

Happy 2007

As for hospitals, well, there's a reason homebirthers and women into birth politics are as passionately anti-hospital as they are, many bad medical practises continue in the litigation crazed society of the USA medical system, from what I read. Forward thinking countries like Germany and Sweden incorporate natural remedies and holistic medicine right in with the mainstream medical system...great role models for us north americans, but impossible in a litigation-mad culture. But, the pharmaceutical companies are to blame too, though that discussion requires tin oil hats.

Coenzyme Q10, no. Magnesium, yes. In fact, magnesium is pretty routinely checked and replaced via intravenous supplementation to avoid diarrhea. However, magnesium levels are checked because of heart rhythm disorders, not for general health.

I know of no interaction between blood thinners and vitamin D. However, you're absolutely right on the increased likelihood of vitamin D deficiency in the presence of bowel diseases like celiac.

I use RxList.com to check any and all medications I am prescribed (or friends/family are prescribed).

This about Omacor on their site:
The empirical formula of DHA ethyl ester is C24H36O2, and the molecular weight of DHA ethyl ester is 356.55. Omacor®  capsules also contain the following inactive ingredients: 4 mg α-tocopherol (in a carrier of partially hydrogenated vegetable oils including soybean oil), and gelatin, glycerol, and purified water (components of the capsule shell).

I mentioned in another comment that I am intolerant to soy, so I avoid it whenever possible.....but to put hydrogenated oils in a preparation touted as "pure"????

I realise it's a very small amount....but from what I've read on trans-fats, the only amount of transfat that is good for us is NONE!!!

Of course, the AHA also promotes foods that contain transfats in their "No Fad Diet" (see Regina Wilshire's blog post here: http://weightoftheevidence.blogspot.com/2005/07/aha-includes-trans-fats-in-heart.html)