QUOTE --
"Healthcare cost savings will be realized by delivering truly effective health solutions directly to people themselves"

Very true. Empowering the individual is powerful.

Congratulations to you, Dr Davis!

I just had my first heart scan done this week for $99 at a local hospital. I've been following a low-carb eating plan for several years. My score was 0 in three of my arteries and 18.38 in the left circumflex. Since this is my first scan, I don't know how it compares to before I began eating low-carb, but I'd like to think this is not a bad starting score and probably better than it would have been back when I was eating that "healthy" diet that is slowly killing so many. I will have another scan in a year, and see if I can tweak the diet a little to eliminate the small build-up I have. I am very motivated to avoid the prescription-drug, expensive procedure path that so many take as they age.

Wow Brilliant blog Dr. Davis i stumbled on it 3 days back and took time off from work and went through all your articles from april 2006 till now in 3 x 16 hour shifts. Stupendous stupendous work. By the way im a 25 year old attorney. I lost my father and grandfather to inexplicable health issues and your blog has lifted the veil on the cause - low fat high carb and high sugar diet, nutritional deficiencies especially k2 us being strict vegetarians. My mom is showing arthritic symptoms very young in her early 50s. For my parents (being high up in the government) there is no medical facility or procedure out of reach, but curative medicine is a huge drag when prevention is possible. Being bed ridden for years is hugely taxing on nuclear families whatever be the status or financial pull of a person. I Being the only child of my parents and having gone through all the trauma of attending law school caring for my father and moving houses simultaneously, your blog is endlessly empowering and valuable.

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Nice discussion very informative.

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FYI:
Radiology, November 2010
CT Scans and Cardiovascular Health

http://www.ivanhoe.com/channels/p_channelstory.cfm?&storyid=25336

Mike V

Thanks for sharing the informative post.

Super jazzed about gteting that know-how.

You know what, I'm very much inlcnied to agree.

Great Article.  As I'm sure you know by now, I've been kind of a lipidpanelaholic since having a MI 2 yrs ago.  The hardest information to find is that of how long it takes for lipids to respond to diet changes and how sensitive they can be to even the smallest amount of carbs.

Are you sure that sort of response is not due to gluten/gliadin/lectin/transfat? Four crackers doesn't sound to me like much of a carb load, but for a gluten-sensitive person like me, that could set off some inflammation.

Dr. Davis,
How does alcohol fit in to the above "equation"? Specifically wine.

Marc

I have been on a wheat-free and carb restricted diet for about 7 weeks, and being concerned that I might be Apo E4, and therefor need to also limit saturate fat as you explained in an earlier blog, I asked my doctor to order a small LDL test.  No independent lab here that I consulted knew what that was, nor obviously did my doctor, since he just ordered "small LDL".  The local hospital lab finally found the following, which is what I will have blood drawn for tomorrow:
Lipoprotein Fractionation Panel 1, Ion Mobility
Which includes:
Choesterol; HDL Cholesterol; Triglicerides; :Lipoprotein (a); Lipoprotein Fractionation Panel 2, Ion Mobility (LDL, Total; LDL, Medium and Small; LDL, VerySmall; HDL, Large; LDL Peak Diameter, LDL Phenotype)

I hope that this is what I need.  Probably it is overkill, but in this case apparently my Medicare Advantage plan will cover it since it has been more than 3 months, since I had a simple panel done.

Is there a simpler test for small LDL?  By the way the CPT codes are 80061, 83695, 83704

Sounds like cheat days may not be that good of an idea...

Yes, it does cast cheat days in a new light!

That's it, Sam.

It shouldn't be that hard. The information is actually fairly straightforward and provides crucial information.

Hi, Marc--

Alcohol does indeed slow or stop weight loss, especially if more than a serving or two are consumed. So it pays to minimize during a weight loss effort.

Probably not, Howard, since those components have not been associated with triggering of small LDL. The trans fat component can indeed trigger small LDL, but it seems to occur even with foods minus trans fats.

However, I am impressed that gluten/gliadin/lectin rolled off your tongue!

The problem is carb creep. I experienced this a few months ago when I received the results of my HbA1c test. I was still in the prediabetic range and it was higher than the HbA1c test I had a few years earlier. I didn't get it? I thought I was consuming less carbs then I was. When I actually looked at my diet there were carbs creeping in: dark chocolate and small "safe starches" (e.g, potatoes, yams). Another factor that may have impacted my blood sugar was the stress of travel/visiting family during that three month time period. My understanding is that elevated cortisol levels can raise blood sugar. In any case, my recent HbA1c is in normal range. I think this is because I eliminated even small amounts of dark chocolate and "safe starches" (see Jimmy Moore's comments about safe starches).

How low should we go in carbohydrates to avoid increasing small LDL?

I'm not sure that wheat has this acute effect on everybody. In fact, I know it doesn't happen with me. I keep a close eye on my lipids and my small LDL particles remain "relatively" low despite the fact that I consume wheat/sugar products. Then again,  my blood sugar does not significantly rise after carbohydrates, so maybe that's why. If I eat a massive plate of pasta, a glass of fruit juice, and dessert, my blood sugar may (keyword, "may") rise to 120, if that, but then it goes down to about 80 about 45 minutes after the meal. No joke. In other words, I'm thinking this effect may have to do with the degree of people's volatility to rising blood sugars. Just a guess.

Fyi, I'm the apo E/4 person who's LDL amount/particle number (226, 2,000) is extremely sensitive to saturated fats and thus I'm always lost in the conundrum of balancing fats with carbs. Difficult!

I know that if weight loss is involved, it can take a few months after weight stabilizes for lipids to normalize.  If minimal or no weight loss is involved, how long does it take?

With the example about 4 crackers would be as low as 10g carbs.  Curious of the overall effects of say 10g carbs of sweet potatoes....

Then it depends on which parameter you are talking about, Teresa.

Small LDL requires just days to respond, while triglycerides require weeks to months, while HDL requires months to years.

Hi, Davide--

No doubt: Individual tolerances to various foods, including carbohydrates, can differ. And the apo E4 person has a tougher time of it.

Unfortunately, Jethro, there's no quick and easy way to decide this, since individual sensitivity varies.

Although imperfect, you can use HbA1c, an index of glucose and not of small LDL, to gauge whether you've been triggering higher blood sugars that often parallel the triggering of small LDL particles. You could, of course, obtain lipoprotein testing 48 hours after ingesting a known amount of carbohydrates, e.g., 20 grams, but that is logistically difficult.

That all said, most people can get away with 15 grams carbohydrates per meal, while some can't tolerate more than 10, yet others do fine with 30+ grams.

Excellent point, STG! And I like the "carb creep"!

Did you see this, Dr. Davis?

http://medicalxpress.com/news/2011-10-common-link-autism-diabetes.html

And it takes years to unlearn all the inaccurate stuff learned in school, and to find and learn the good stuff that is out there.  Thanks.

How does one check to see if they are apo E4?

How does it affect lipid results?

Dr Davis:  What is the small LDL profile for native populations that consume tons of of carbs and no signs of heart disease; also, the Japanese consume lots of carbs- easily 3 cups of rice per day which is about 120 carbs from rice alone.  Low level of CAD; what are their levels of small LDL.  I know for myself ApoE 3/3 that carbs do affect the small LDL level i have and in any event in the absence of a statin i produce tons of LDL particles large or small depending upon carb levels.  I believe genetics plays a large role.
Thanks

No doubt, Steve.

However, I'm unaware of lipoprotein assessment done to answer these questions. That would be interesting, however.

Easy, Stephanie: Have an Apo E test run.

Yes, agreed, Teresa: New lessons to learn every day in this Information Age!

Thanks, Barbara. No, I hadn't seen this. But I'm not the least bit surprised!

I find it wonderfully satisfying that the puzzle pieces are falling in place, just like that 1000-piece jigsaw puzzle we struggled to put together, with the last few pieces fit just perfectly!

Dr. Davis,
Have you heard or read about Lumbrokinase helping to lower small "a" particles?
Just wondering.
Dee

Dr. Davis,

There seems to be a lot of mention of the E4 ApoE genotype.  What about those of us that are E2/E4?  Any different instructions for us?

Thanks.

With this very tough pattern, you are best following lipoproteins and glucose measures like HbA1c to gauge response to various dietary manipulations. The basic diet approach, however, is largely the same; it just may require some adjustments, e.g., fat intake.

Sorry, Dee, no info.

Where did you hear this?

Here is the quote.  Appently it just helps lower the LP[a]  and does not have any terrrble side effects.  I may try it, nothing else is working.  My little a is 43 and rising in spite of all I do.

"The one nutraceutical that has shown promising clinical results in actually lowering Lp(a) is a lumbrokinase product made by Canada RNA Biochemical called Boluoke. Like its chemical cousin nattokinase, lumbrokinase is an enzyme that helps break up fibrin—a fibrous protein that helps form blood clots—to avoid too much clotting and keep blood flowing optimally."

:

Dee

I have my results.  My PCP reported these to me "for my records" with no further comment.  Maybe he can't interpret them?
Total Cholesterol: 231 (My PCP surely would think this is high.)
I find it strange that they did not report LDL direct, though perhaps it is not done because of the breakdown below.  
Calculated LDL: 133 H MG/DL
HDL: 85 Mg/dl  This is higher than I have ever had measured.
Triglycerides: 64 Mg/Dl  Even Simvastatin only got it down to 84.  I conclude that I am not Apo E4.
The range after \ below  is the range they cite, I presume, as normal.
Lipoprotein : <10  NMOL/L \ <75  I presume this is a good result.
LDL, Total: 2268 H NMOL/L  \ 440-1600
LDL, medium and small: 651 NMOL/L \ 144-787
LDL, Very Small: 277 NMOL/L \ 75-419
HDL large: 9315 H NMOL/L  \ 469-5258
LDL Peak Diameter: 227.5 Angstrom  \216.-234.3
LDL Phenotype A  Pattern A     I believe this to be the preferred pattern, low small LD and Triglycerides.  Ref: Obesity (2009) 17 9, 1768–1775. doi:10.1038/oby.2009.146--Reversal of Small, Dense LDL Subclass Phenotype by Normalization of Adiposity
Patty W. Siri-Tarino1, Paul T. Williams2, Harriet S. Fernstrom1, Robin S. Rawlings1 and Ronald M. Krauss1

Does this calculate to large LDL = 2268-651 =1617 (Not including medium)?
When should I do this test again?
Comment?

Hi, Sam--

The "pattern A" comment is misleading. About 40% of your LDL particles are small, too much.

It means going back to the strategies to reduce small LDL, such as wheat elimination and limiting carbohydrate exposure. It is worth repeating about 2 months after weight has stabilized following a diet change.

I have been on a no-wheat, limited, very-low carb, diet now for 6 to 7 weeks already.  I cringe to think of what the numbers may have been before.  I initially lost about 12 pounds in less than 2 weeks to get to 148, I am 72-in tall, and have stabalized there by eating more high-fat non-carb stuff.  You say 40% small.  You must be using the medium and small (640) over total (2268) to get 40%.  Apparently medium and small includes the very small, which must be a fraction of small?  How long should it take for the very small to approach zero?  Isn't that the more important number?  I will be out of the country for 2 weeks.

Thanks

Yes, exactly, Sam: Combine medium and small.

Dietary and weight changes usually exert effects on small LDL within a few weeks, much faster than most other parameters.

Get a VAP test....this measures your small particle/large particle LDL.
labcorp code 804500

I am going to try to get a VAP test.  No doctors know of it....only folks on the web.  Why?  It seems like a very important test to measure your LDL properly.  Can someone elaborate on this further?

Easy, Pb: There are no drugs--read: "no financial incentive"--to treat the abnormalities generally uncovered by lipoprotein testing like VAP. Thus, no push to get it tested.

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.