Much of the $23 billion spent each and every year on statin drugs is really targeting the treatment of “high cholesterol”—but actually unhealthy distortions in lipoproteins—created by consuming grains.
Most people, unfortunately, continue to focus on fat consumption, especially saturated fat, as the cause for high cholesterol and have been led to believe that cutting saturated fat and statin drugs are the solution. So let me try and clear up this somewhat confusing issue and show you that 1) there is no real benefit to cutting saturated fat, 2) grains and sugars cause distortions that increase cardiovascular disease, and 3) statin drugs do not fully address the causes of cardiovascular disease, accounting for their relatively trivial benefits.
Here is a typical panel of someone who consumes grains:
Triglycerides 170 mg/dl
LDL cholesterol (calculated) 150 mg/dl
HDL cholesterol 40 mg/dl
Total cholesterol 224 mg/dl
In other words, HDL cholesterol is lowish, triglycerides high, LDL cholesterol and total cholesterol high. What does this mean? Let’s take each, one by one. It’s a bit complex, but stick with it and you will emerge smarter than 95% of doctors who “treat” high cholesterol.
Triglycerides are the byproduct of two digestive processes: 1) De novo lipogenesis or the liver’s conversion of the amylopectin of grains and other sugars into triglyceride-rich VLDL particles that enter the bloodstream, and 2) absorption of dietary fats (which are triglycerides themselves). De novo lipogenesis dominates triglyceride levels in the bloodstream, far outstripping consumption of fat as a determinant of triglyceride levels. This simple fact was only identified recently, as the rise in triglycerides that occurs after consuming fats and oils develops within 2-4 hours, but the much larger rise in triglycerides from carbohydrate-to-triglyceride conversion starts 6-8 hours later, a fact not uncovered in older studies that failed to track this far out in time. (And, in certain genetic types, such as apo E2, the rise from carbohydrates in grains and sugars can last for days to weeks.)
LDL cholesterol is calculated, not measured. The Friedewald calculation, developed in the early 1960s to provide an easy but crude means of estimating the quantity of cholesterol in the low-density lipoprotein fraction of the blood applied several basic assumptions: 1) that everyone consumes an average diet of average macronutrient composition, and 2) that the triglyceride content of all lipoproteins remained constant from person to person (which is not true, but is wildly variable), and 3) that all LDL particles are the same (also not true, as LDL particles vary in size, conformation, surface characteristics, etc.).
Grain consumption, thanks to the process of de novo lipogenesis, increases blood levels of triglycerides and VLDL particles. VLDL particles interact with LDL particles, enriching LDL particle triglyceride content and reducing cholesterol content. This leads to a process of LDL particle “remodeling” that creates small LDL particles–glycation-prone, oxidizable, adherent to inflammatory blood cells, and persistent in the bloodstream for 7 days, rather than the 24 hours of more benign large LDL particles. Grains thereby trigger the process creating persistent and damaging small LDL particles; fats trigger the process that does not.
When we cut out grains and sugars, the Friedewald calculation is therefore no longer valid, as the assumptions–-weak to begin with–-are disrupted. LDL cholesterol, this crude, surrogate effort to indirectly quantify LDL particles, is therefore completely useless—the calculation of LDL cholesterol is INVALID. This has not, unfortunately, dampened enthusiasm among my colleagues nor the drug industry for trying to treat this number with statin drugs to the tune of $23 billion per year.
Better ways to quantify LDL particles: NMR LDL particle number (which includes quantification of small and large LDL particles) or an apoprotein B. (Each LDL particle contains one apo B, which thereby provides a virtual count of LDL particles, but no breakdown into small vs. large.) Lipoprotein testing has been around for over 20 years, is inexpensive and available—but requires an informed doctor to interpret.
HDL cholesterol is, unlike LDL cholesterol, a measured and reliable value. Ironically, it is among the most ignored. Grain-consuming humans tend to have low HDL because the high triglyceride/VLDL particles interact in the bloodstream with HDL particles, enriching HDL particles in triglycerides and reducing cholesterol content. This leads to a reduction in HDL size and HDL quantity, thus low HDL cholesterol values. The lower the HDL, the higher the cardiovascular risk.
Total cholesterol is the sum of all three values: LDL cholesterol + HDL cholesterol + triglycerides/5. (More accurately, LDL cholesterol is the calculated value: LDL = total chol – HDL – trg/5.)
Given the mix of values, total cholesterol is therefore essentially useless. A large increase in HDL, for instance–-a GOOD thing–-will raise total cholesterol; a large reduction in HDL–-a BAD thing–-will reduce total cholesterol: the opposite of what you would think. Total cholesterol can indeed yield useful prognostic information when applied to a population, though the relationship is weak. But it is useless when applied to an individual.
If we reject the silly and simple-minded notions of cholesterol panels, and apply the greater insights provided by advanced lipoprotein analysis, several nutritional observations can be made:
–Saturated fat increases HDL, shifts HDL to larger, more protective, particles, and triggers formation of large LDL particles.
–The amylopectin carbohydrates of grains trigger higher triglycerides, thereby providing more VLDL particles to interact with HDL and LDL particles, the process that leads to triglyceride enrichment and smaller ineffective HDL and smaller atherogenic LDL (heart disease-causing).
–Given the unusual persistence time of small (7 days) vs large (1 day) LDL particles, grain consumption is FAR worse than fat consumption.
You can begin to appreciate how overly simplistic this notion of “reducing cholesterol” using statin drugs really is. You can also appreciate that the real situation is a bit more complicated and beyond the reach of most busy primary care physicians, while being outside the interests of most cardiologists, obsessed as they are with revenue-producing activities like heart catheterizations, stent and defibrillator implantation.
A typical response in the cholesterol panel of someone who has eliminated all wheat, grains, and sugars would look something like this:
Triglycerides 50 mg/dl
LDL cholesterol (calculated) — mg/dl
HDL cholesterol 70 mg/dl
Total cholesterol 200 mg/dl
I left the LDL cholesterol blank because it can do just about anything: go up, go down, remain unchanged—but it doesn’t matter, because it is inaccurate, unreliable, invalid. If you were to measure advanced lipoproteins, however, you would see a dramatic reduction or elimination of small LDL particles and reduction of the total count of LDL particles (since the small LDL component has been reduced or eliminated) with large LDL particles remaining.
Common distortions of cholesterol panels can be easily explained by the chain of events that emerge from a diet rich in “healthy whole grains.” The relatively trivial benefits of statin cholesterol drugs (about a 1% reduction in real risk, not the inflated “relative risks” quoted in ads and statistically-manipulated studies) should come as no surprise, since high cholesterol is not the cause for cardiovascular disease.
So, to satisfy my doctor, if I do a fat fast 24 hours before a cholesterol panel (I have already eliminated grains), my total LDL should be down and he will be happy?? I think we all need to be able to make the doctor happy for insurance purposes, but then when they ask how we got our numbers down credit low carb, high fat or ketogenic diets.
Teri L wrote: «…if I do a fat fast 24 hours…»
Can you describe what that is.
«…my total LDL should be down…»
What information are you relying on that suggests that will result? I’m inclined to suspect that most forms of fasting are going to mobilize fat stores, and confound lipid metrics in unpredictable ways.
And what is “total LDL”? There is the mostly useless TC (Total Cholesterol) and the even more useless LDL-C.
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I have been following the Wheat Belly lifestyle for three years, losing 70 pounds and my medications, including those for diabetes. I’m 60 years old and my expectations was that the cholesterol would be lowered like the A1C and triglycerides. I should mention that I am taking all the recommended supplements from the Wheat Belly site, including Omega 3 every day. So, I paid for an NMR lipid panel myself at a local lab and found that though my HDL was 57, my LDL-P was pretty high (2542) and LDL-C was 180. I waited three or four months and did the panel again. Almost the same result. HDL was 30.1, A1C was good, triglycerides 107, blood sugar was good but the total cholesterol 293 and LDL-P particles was high (2394) and LDL-C (215). Small LDL-P was 1197.
I am essentially on a very low carb, high fat, grain-free diet. I get a moderate amount of exercise three times a week. What am I doing wrong? Do I need medication again for the cholesterol? Do I need to see a doctor who understands this lifestyle, and where do I look for a doctor in my state?
Larry Lovering wrote: «…losing 70 pounds…»
Are you still losing weight? If so, it will distort lipid and blood sugar labs.
«…including Omega 3 every day.»
What product and dose?
«…my LDL-P was pretty high (2542)…»
Do you happen to know your ApoE genetic status? If you have had a 23andme test run, that status can be determined from SNPs rs429358 and rs7412 in the Raw Data.
Separately, have you had Lp(a) tested?
«…expectation was that the cholesterol would be lowered like the A1C and triglycerides.»
What was the number for A1c? Lab and doctor assessments of “normal” are not usually useful. What we look for is HbA1c 5.0% or lower.
«…HDL was 57…HDL was 30.1»
That’s clearly not moving in the desired direction.
«…triglycerides 107»
That’s above the WB target of 60 mg/dL or less. I presume it used to be quite a bit higher?
«…blood sugar was good…»
I assume this is Fasting BG. Number?
«…where do I look for a doctor in my state?»
What state?
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From the top:
1. I’ve been pretty steady on weight the past three months (after the tests): 175.
2. I use Nordic Naturals Pro Omega, 3 in the morning, 2 at night (total 3200 mg)
3. I’ve never had my DNA done.
4. I don’t believe I had the LP(a) done.
5. For A1C, July: 5.6, Oct: 5.6
6. My triglycerides were over 280 three years ago.
7. Fasting blood sugar, July: 87, Oct: 96
8. Connecticut.
Thanks, Bob!
Larry Lovering wrote: «I’ve been pretty steady on weight the past three months (after the tests): 175.»
I have no way of knowing if that’s your ideal weight, but at least if its stable, weight loss is not confounding the lab metrics.
«I’ve never had my DNA done.»
It might be worthwhile if the numbers can’t be moved around to your satisfaction. Or as lipid wonk Dr. Peter Attia put it: “ApoE is one of the few genes I think it’s worth knowing early in life.” I tend to think that there are a few more. If you can’t get insurance to cover a specific ApoE test, the 23andme investment can illuminate at least couple of other areas that might need diet tweaking. I haven’t yet figured out if the SNPs associated with Lp(a) correlate highly to actual measures of Lp(a).
«For A1C, July: 5.6, Oct: 5.6»
That’s elevated, and is consistent with the elevated TG reported earlier. This all could be as simple as your intake of available carbs (the “net carbs”) being higher than you suspect (if you are indeed shooting for WB targets on that). An investment in a glucose meter, and some postprandial readings would shed some light on this.
«My triglycerides were over 280 three years ago.»
You have made excellent progress.
«Fasting blood sugar, July: 87, Oct: 96»
WB target is under 90 FBG (fasting), and no change PPBG (postprandial: the bump, if any after the meal).
«Connecticut.»
Readers from the region may have some suggestions. I’ll poke around a bit as well.
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Boy, finding a doctor, that is the million dollar question!
Pat wrote: «Boy, finding a doctor, that is the million dollar question!»
I had some general advice on that on another thread recently:
https://drdavisinfinitehealth.com/2016/02/breaking-up-with-grain/comment-page-1/#comment-64251
Alas, it is apt to be the case for some time to come that the best doctor is the one you don’t need.
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I just saw this article in the UK Daily Mail:
http://www.dailymail.co.uk/health/article-3460321/How-Big-Pharma-greed-killing-tens-thousands-world-Patients-medicated-given-profitable-drugs-little-proven-benefits-leading-doctors-warn.html
——————————————————————————————
How Big Pharma greed is killing tens of thousands around the world: Patients are over-medicated and often given profitable drugs with ‘little proven benefits,’ leading doctors warn
* Queen’s former doctor, Sir Richard Thompson, has backed new campaign
* Experts calling for urgent public enquiry into drugs firms’ ‘murky’ practices
* They say too much medicine is doing more harm than good worldwide
* And claim many drugs such as statins are less effective than thought
The Queen’s former doctor has called for an urgent public enquiry into drugs firms’ ‘murky’ practices.
Sir Richard Thompson, former-president of the Royal College of Physicians and personal doctor to the Queen for 21 years, warned tonight that many medicines are less effective than thought.
The physician is one of a group of six eminent doctors who today warn about the influence of pharmaceutical companies on drugs prescribing.
The experts, led by NHS cardiologist Dr Aseem Malhotra, claim that too often patients are given useless – and sometimes harmful – drugs that they do not need.
They maintain drugs companies are developing medicines they can profit from, rather than those which are likely to be the most beneficial.
And they accuse the NHS of failing to stand up to the pharmaceutical giants.
…..
Writing for MailOnline, Dr Malhotra says commercial conflicts of interest are contributing to an ‘epidemic of misinformed doctors and misinformed patients in the UK and beyond’.
…..
Furthermore, he adds the NHS is ‘over-treating’ its patients, and claimed that the side effects of too much medicine is leading to countless deaths.
And he claims the full trial data on statins – cholesterol-lowering drugs prescribed to millions – has never been published, and also points to questions about the power of Tamiflu, a drug that has cost the NHS nearly £500 million.
The group has called on Parliament’s Public Accounts Committee to conduct an independent enquiry into the safety of medicines.
They claim public funding is often allocated to medical research because it is likely to be profitable, not because it will be beneficial for patients…..
————————————————————————–
It appears the US and UK are in a dead heat on this issue. It’s nice to see that prominent UK doctors are speaking out too. It’s too bad they aren’t speaking out about the effective alternative to these do-nothing drugs.
Hi Bob Niland,
I have been grain-free & low carb for several years and consume only WB-approved healthy fats. So what’s with these numbers? HDL & LDL have both been mostly trending up prior to and after going on WB. Trigl have dropped with elimination of grains (and I dropped 20 lbs and my IBS, BTW.) Below are my last 2 standard chol panels + a VAP test.
2-1-16. Total chol 368; d-HDL 103; Trigl 52; VLDL(calc) 10.4; LDL(calc) 254.6
Note: I had started the recommended dosage of Carlson’s fish oil about 6 weeks prior. I had also DC’d the flush-free niacin I’d been taking up until then.
6-22-15. Total chol 324; d-HDL 111; Trigl 36; VLDL(calc) 7.2; LDL(calc) 205.8
10-7-14 VAP test. LDL 181; HDL 115; VLDL 16; Trigl 67; Non-HDL 197; ApoB100(calc) 119; Lp(a) 13; IDL 10; LDL-R(Real)-C 159.
Real-LDL Size Pattern “A” (large, buoyant). Remnant lipoproteins 19.
FBS has been consistently around 86. Vit D runs around 60-80. Just noticed Feb.1 TSH was 4.3, *way* higher than its usual 1.2 or so. At some point CRP and homocysteine levels were done and an A1C and all were OK. (I don’t have a copy of those reports.)
I am not on any medications but my PCM would really like me on a statin. However, when he ran my numbers through an I-phone app with the latest guidelines, it turns out I don’t require treatment. (Don’t remember the name of the app.) I’m not over-weight and have no other known risk factors or health issues (although a few years ago I underwent a “routine” course of chemo following breast CA surgery.) So for the time being I’ve been given a reprieve. My PCM is the one who originally suggested niacin but I experienced the flushing of an immediate-release product and switched to flush-free … as I’m now aware, that might not have been a great move.
Haven’t quite figured out what’s going on here. I’m considering starting Slo-Niacin, but the web site states that it’s taken to maintain healthy levels of HDL, and mine’s already off the charts! According to an article by Dr. D. in Life Extension magazine (March 2007) Slo-Niacin is an *extended* release preparation, which is safe when used properly, as opposed to *slow* release products which can be quite risky. The article also states that niacin (as nicotinic acid) lowers LDL and Lp(a) and I’ve seen similar statements from other sources, as well.
Thanks for you consideration.
OOPS! TSH was 1.8 ….. had my finger on the wrong line. (Whew!)
Kate wrote: «So what’s with these numbers?»
Keeping in mind that I’m not an expert, I can suggest some avenues for further investigation. But first, some context: what’s the actual concern?
«I have been grain-free & low carb for several years and consume only WB-approved healthy fats.»
Have you done anything for gut flora? (daily prebiotic fiber, course of probiotics)
The 2016-02 TG and HDL look fine. The TC and LDL-C aren’t terribly meaningful, as the base article here points out.
It takes some time for fish oil to take full effect. Have you had Lp(a) retested since 2014? That VAP reading appears comfortably low, but it would be nice to confirm it (and if you get it via NMR, the reference range will be shifted much higher, so don’t get alarmed).
Niacin is no longer considered a primary therapy on Cureality. It is still a tool in the bottom of the box for Lp(a) when it doesn’t respond to other strategies.
The TSH of 1.8 (which I presume replaces the 4.3) is elevated by Wheat Belly standard, and indicates a need to get some actual thyroid tests (fT3, fT4, rT3, TA). TSH is a test of pituitary response.
The other VAP numbers are not in a form that I’m familiar with, except the IDL, for which the target is zero. If you can get another test, see if you can get an NMR.
«…CRP and homocysteine levels were done and an A1C and all were OK.»
Consensus “normal” is rarely Wheat Belly “healthy”, particularly HbA1c. Having these numbers would be useful.
«I underwent a “routine” course of chemo…»
That might have been fairly disruptive to your microbiome.
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Hi Bob,
Thanks for weighing in on my labs. After considering your question,“what’s the actual concern,” I had to admit that my thinking has, of late, been a bit skewed by what appears in my eyes to be outrageous LDL numbers, and then doing what the media and consensus medicine does, i.e., looking at a *number* in isolation and running with it. Looks like old thought patterns were coming back to haunt me.
I really appreciate your ability to cut through the rhetoric, analyze situations, and offer rational suggestions. I will follow up on the Lp(a), IDL, and the rest of the lipids, preferably with an NMR. I’ll also make a point of nailing down the inflammatory markers and addressing the thyroid with *real* tests. I’ve been using raw potato starch & inulin for prebiotic fiber. As I’m reviewing the WB recommendations, I’ll need to beef those up a bit, as well as the probiotics.
Thanks again for your help.
Kate wrote: «After considering your question,“what’s the actual concern,” I had to admit that my thinking has, of late, been a bit skewed…»
Well, it’s easy to get alarmed on events like “…my PCM would really like me on a statin.” They never tell you that they say that to pretty much everyone. There are MDs who think _everyone_ should be on a statin.
My more detailed lay opinion about statins is here, by the way:
https://www.cureality.com/forum/topics.aspx?ID=18537
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Bob, thanks so much for pointing me to your outstanding article. I’ve spent the evening going through it, as well as following the links you provided to some very impressive web sites ….. and following links from those links, too! At this particular moment I’m being captivated by the Statin Nation blog. ( http://www.statinnation.net/blog/) You’ve done all of your readers a terrific service (as you always do.) Thank you!
I was a firm believer in the diet-heart hypothesis until I read about Otzi, the 5000 year old mummified caveman that was discovered in 1991. Examination of his body showed that he was not obese or sedentary, and he obviously ate an organic diet. Despite all of this, there was clear evidence of him having atherosclerosis in his 40s which is when he died (as a result of being shot with an arrow, not heart attack btw).
I have a feeling that someday people will recognize the notion that diet and exercise affect heart disease risk being just as foolish as thinking diet/exercise can affect male pattern baldness. Genes are destiny. This whole idea that we are designed to live to 130 years old if we just ate the right things and exercised a little seems so silly to me. Nature wants us to live long enough to pass along our genes. After that, nature doesn’t care if we live or die.
Shakey McShakerson wrote: «…Otzi, the 5000 year old mummified caveman…»
As you point out, Ötzi had a fully expressed genetic tendency to heart disease.
He also had bad teeth:
https://drdavisinfinitehealth.com/2013/04/teeth-and-grains-dont-mix/
His Wiki page says: “These oral pathologies may have been brought about by his grain-heavy, high carbohydrate diet.”
He was an einkorn eater (that’s an authentic neolithic wheat). There are other Ötzi ailments still being elucidated, such as possible ulcers from the Helicobacter pylori.
«I have a feeling that someday people will recognize the notion that diet and exercise affect heart disease risk being just as foolish as thinking diet/exercise can affect male pattern baldness.»
Exercise effect is relatively minor compared to diet. Diet is huge. Low net carb is in particular critical for those dealt an unfavorable genetic hand, such as ApoE ε2s and ε4s, and those with Lp(a).
«This whole idea that we are designed to live to 130 years old if we just ate the right things and exercised a little seems so silly to me.»
You won’t find that conjecture made here. We don’t yet know what an optimized diet is going to do for lifespan, but my guess is that being healthy into our 90s, irrespective of what 23andme says, is within reach.
«Nature wants us to live long enough to pass along our genes. After that, nature doesn’t care if we live or die.»
I’m not so sure that’s true for a parental and tribal species. Elders can contribute a lot to the success of both their progeny and the tribe. Long-lived humans probably had a tribal advantage.
At any rate, we know that living to over 110 is possible, and we’re rapidly identifying factors that shorten that. Dying sooner may become optional. Watch out for arrows. Don’t eat the einkorn (or its progeny).
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I personally eat einkorn every once in a while (every one-two months I’ll have some). It doesn’t seem to have the same effects on me as modern wheat. Otherwise, I keep to a very low carb diet (though I do eat cheese). We are trying to keep the whole family wheat-free, but it’s tough with the kids. For instance, they freak out if they have eggs for breakfast too many days in a row. So, about once a month to once every 6-8 weeks, I’ll make sourdough einkorn bread and use the sourdough starter to make waffles and freeze them. So, every 4-8 weeks, we allow the family to have waffles and bread made from einkorn.
BobM wrote: «I personally eat einkorn every once in a while…»
As Ötzi reminds us: eat authentic neolithic grains; get authentic neolithic ailments.
One of the first things my family did on encountering Wheat Belly in 2011 was to misunderstand the message and buy a bag of einkorn flour. We never finished it. This must be some sort of rite of passage.
If you search this blog on einkorn, you’ll get a lot of hits, like:
https://drdavisinfinitehealth.com/2014/02/should-you-eat-kamut/
I’ve also written a short article on heirloom wheats (follow the breadcrumbs from my UserID link here).
«(every one-two months I’ll have some)»
For many people, that can suffice to sustain chronic and entirely optional problems.
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Shakey McShakerson wrote: «This whole idea that we are designed to live to 130 years old if we just ate the right things and exercised a little seems so silly to me. Nature wants us to live long enough to pass along our genes. After that, nature doesn’t care if we live or die.»
To see how the facts apply to us as individuals you have to step outside of your agricultural-abundance paradigm. True, humans today live short lives, but we also live short reproductive lives compared to pre-modern humans.
During times of overcrowding nature cares much less about our individual survival than even you indicate. In fact, nature would prefer that an extremely large portion of today’s human’s die before reproducing. In order to escape this fate we must understand nature’s mechanism for imposing this dastardly sentence upon ourselves and our loved ones.
The current overcrowded state of humanity can be blamed entirely on agricultural carbohydrates. The increasingly early deaths ascribable to metabolic diseases like diabetes, heart disease and cancer, can be blamed entirely on ……agricultural carbohydrates. In millions of individual cases medical science has been able to prolong the lives of humans afflicted with these diseases, but it has not been able to stem the adverse reproductive effects …..PCOS in women, early sterility in men, etc.
If I remember correctly the NOVA special on Otzi said that Otzi shared blood lines only with people who today live on the Mediterranean island of Sardinia. As NOVA correctly implied, for the last 10,000 years, since European agriculture began, Europe has undergone a near-constant overrun and replacement of its inhabitants by outsiders. People from Otzi’s bloodline inhabited most of Europe, and were replaced everywhere besides Sardinia.
Today the birth rates in many European countries is approaching 1 child per every 2 people. That rate results in halving a country’s population every 20 years. There’s a reason why people from primitive cultures are overflowing the borders of “advanced” western countries.
I am a diabetic on glypizide and metformen. This is day 10 of making this lifestyle commitment and my blood sugars are pretty wacky. After experiencing low numbers on day 8, I tried not taking any meds on day 9. My numbers stayed in the 120’s all day with HS at 137. Upon waking I was at 145 this morning. Is dropping my meds premature?
Laura wrote: «I am a diabetic on glypizide and metformin.»
But not on insulin; would I be correct if I guessed T2D?
As I comment further here, keep in mind that even if I were a doctor (which I’m not), any speculation on a specific case would require a lot more information, such as what exactly you are doing in diet, historical blood sugars, weight loss progress, and whether you are working with a physician who knows that you’re undertaking a diet that is going to result in reduced and eventually inherently stabilized BG.
«This is day 10 of making this lifestyle commitment and my blood sugars are pretty wacky. … Is dropping my meds premature?»
I don’t recall seeing any specific advice on a taper-off protocol, but I would expect that what most people do is continue the meds, dosing as suggested by what the glucometer reports, and being sure to avoid hypoglycemia (which is mentioned in the following article as a risk with glipizide):
https://drdavisinfinitehealth.com/2015/03/if-you-have-diabetes-no-low-blood-sugars/
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My identical twin brother consumes wheat and grains. I do not.
We each had our panels done by SpectraCell in October 2014.
As Dr. Davis suggests, my brother’s triglycerides (120) are higher than mine (75). Usually when I get tested locally my triglycerides are about 60. I’m not sure why SpectraCell’s number was higher, but it does illustrate that inconsistencies can occur between different labs.
My brother’s VLDL particle value was 103. Mine was 29. SpectraCell suggests a good value is under 85. As Dr. Davis explained, VLDL sort of goes hand in hand with triglycerides. So it makes sense that my values are lower than my brother’s.
As Dr. Davis would predict, my grain-eating brother’s HDL (32) is lower than mine (46). It would be nice to have a value of 70 as Dr. Davis illustrates, but I’ve never come close to that. My best HDL value was 60, which I achieved while taking niacin (nicotinic acid). But I don’t like taking niacin due to the flushing problem, higher GGT, higher urate level, higher HbA1c, and possible liver distress (I get itchy).
My brother’s Trig/HDL ratio is 3.75. Mine is 1.63. Some sources say you should aim for a value under 2. If so, I’m in a better position than my brother.
As Dr. Davis suggests, LDL might go up or down when going grain free. In my case it went up from about 140 to 160.
Despite being off grains, my LDL particle number (1306) and apoprotein B (130) are nothing to write home about. My brother’s values of 918 and 89 are better, and evidently that’s because he takes a low dose of Lipitor (5 mg/day).
The statin seems to be beneficial in that regard. But some other numbers tell a different story.
For example, my brother’s fasting insulin was 12.1 and mine was 6.7 uIU/ml. The lower the number, the better. SpectraCell wants it to be under 21, but other experts say it should be below 10, preferably 5, or maybe closer to zero.
Lp(a) is sometimes considered to be genetic, but my brother’s number was 25.9 and mine was 14.1 mg/dL. My value used to be higher but it has come down from the diet improvements I have made. SpectraCell aims for a value under 30, so we’re both OK but my value is better.
Same with hsCRP. A value under 1 mg/L is the target. My brother was at 2.15 and my number was 1.28. Another test result I got in May 2015 from a local lab was 0.7, which I was pleased with.
Our genetic status is ApoE3 and according to “23 and Me” we are no more likely to get heart disease than the average person.
My twin brother underwent quadruple heart bypass surgery in 2008 but he still eats his usual diet, which includes bread, pasta, desserts, juice, etc.
My brother weighs 178 lbs. with a 39 – 40″ waist. I weigh 148 lbs. with a 35 – 36″ waist.
I think I’ve been successful in avoiding my brother’s fate by adopting the recommendations of Dr. Davis.
My brother passed a treadmill test in 2007 and one year later he couldn’t walk a short distance without experiencing extreme angina, which is when he had to get bypass surgery.
I know I have some heart disease too based on my calcium score and a 64-slice CT angiogram. I usually last about 13 minutes on a Bruce treadmill stress test and then the cardiologist says I failed it and they can detect ischemia.
But maybe I’m keeping things in check because I certainly haven’t developed the debilitating blockages that my brother had in 2008.
I’m not sure how big a role particle size plays. Dr. Stephen Sinatra and Dr. Jonny Bowden say the large particles are like harmless cotton balls and the small dense particles are like BB’s.
But I believe I’ve read that the large particles are 27 nanometers and the small ones are 23 nanometers. A better analogy would be comparing them to a baseball versus a tennis ball.
The heart disease I have is from eating a sugar-laden high-carb diet for the first 50 years of my life.
You can make the sort of changes Dr. Davis recommends and you will likely lose weight and lower your risk of cardiovascular disease. I refuse to take a statin and do not require any drugs. I intend to keep it that way for the rest of my life, which I believe is possible using the Wheat Belly protocol.
Malcolm wrote: «Lp(a) is sometimes considered to be genetic, but my brother’s number was 25.9 and mine was 14.1 mg/dL. My value used to be higher but it has come down from the diet improvements I have made.»
What specifically are you doing for Lp(a)? I wrote a bit about the Cureality approach in a response earlier on this thread.
«Same with hsCRP. A value under 1 mg/L is the target. My brother was at 2.15 and my number was 1.28.»
I suspect that reducing inflammation is a complex topic that has not yet been fully exploited in terms of identifying and reducing trigger factors. For example, reducing Omega 6 Linoleic Acid exposure is part of the Wheat Belly approach, and turns out to be not that easy to do, as we get a lot of it second hand, undeclared.
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Bob:
The first approach that worked for me to lower Lp(a) was taking niacin. I took a 500 mg tablet 3X per day of fast acting vitamin B3 (nicotinic acid) – the type that tends to produce skin flushing. Here’s what happened:
Aug 2010 – Lp(a) 32 – Not taking niacin
Dec 2010 – After using niacin for the preceding 3 months – Lp(a) 18
Mar 2010 – Not taking niacin the past 3 months – Lp(a) 26
July 2011 – I was taking niacin again – Lp(a) 19
Mar 2012 – I was taking niacin and getting into Wheat Belly – Lp(a) 13
After March 2012 I stopped taking niacin and continued to monitor Lp(a). It has remained consistent.
July 2012 (16), Oct 2012 (16), Jan 2013 (16), Mar 2013 (15), Sept 2013 (15), Jan 2014 (15), Oct 2014 (14.1).
Therefore, I attribute this to the Wheat Belly approach that I have maintained since that time.
I don’t have as many readings from my twin brother. They are higher than mine.
In March 2012 his Lp(a) was 27, and in Oct 2014 it was 25.9.
Note: The date Mar 2010 in my chart should say Mar 2011. Sorry about that.
Malcolm wrote: «The first approach that worked for me to lower Lp(a) was taking niacin.»
Niacin seems to be the only thing that consensus medicine has to offer for Lp(a).
Are you doing anything on fish oil consumption, and if so, what product and daily intake? (whole fish consumption counts here as well)
And do you know what technique (VAP, NMR or electrophoresis) SpectraCell uses to assess Lp(a)? The Cureality target level varies substantially by test process.
Unlike many lipid labs, even where the numbers matter, they often measure something that’s a proxy for the real problem, and trying to move the numbers directly may be unwise. With Lp(a), however, the apolipoprotein(a) is itself an adverse agent, and measures to reduce it directly are worth considering.
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As someone who is finding adequate medical information almost impossible these days, can you elaborate further, Dr. Davis, on statin use when someone has high lipoprotein a and a 3/4 genotype. One doctor tells me I need more statins and another doctor tells me to stop statins all together. I am wheat, grain and sugar free and very confused by all of this.
Thank you.
Pat wrote: «…statin use when someone has high lipoprotein a and a 3/4 genotype.»
As I understand it, those are two separate challenges, and neither of them are addressed in Wheat Belly Total Health, being relatively rare. These don’t arise on the Wheat Belly Blog very often, but arise frequently on Dr. Davis’ Cureality {membership} site, which has a significant cardiovascular focus, being an evolution of his former TrackYourPlaque site.
Both conditions suggest that some informative testing is in order. Based on what I’ve seen on Cureality, this might include an advanced lipoprotein panel, CAC scan, hsCRP, meaningful thyroid (fT3, fT4, rT3, TA), serum Vitamin D and perhaps others. Any hypothyroid must be corrected (and consensus medicine’s assessment of “normal” isn’t optimal).
For both conditions, the basic starting advice is to follow the Cureality (Wheat Belly) diet in all respects. This is much more than just grain and sugar avoidance.
On Lp(a), there is specific advice in the Cureality Heart Health Track. High dose fish oil (above the basic 3 grams/day) is recommended, then DHEA supplementation, and finally niacin if the condition hasn’t otherwise responded (and it takes some time for the fish oil to have its effect).
On the ApoE ε3/ε4, apparently most people respond to the diet. Here’s Dr. Davis on that:
https://drdavisinfinitehealth.com/2014/10/say-statins/comment-page-1/#comment-57796
Are statins supposed to be of any use in Lp(a)? I’m seeing conflicting reports (and their side effects would have their normal full impact). There is, by the way, a medication for Lp(a) in development, and now in Phase 2b trials. It’s too early to say if it may be expected to have a favorable profile for therapeutic effect, side effects and improved all-cause mortality.
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Thank you Bob for taking the time to answer my comments and questions. I really appreciate all of your information.
Just getting advanced testing is a challenge in itself, but I will keep trying.
WoW! Thank you Dr. Davis for explaining this in terms that a non-medic like me can understand. What a great shame, if not scandal, that more medics cannot be similarly open minded like you and embrace the shift from conventional, albeit out of date, inaccurate and bogus wisdom, to the real truth about the effects that diet can have on health. Thank you once again!