For Vegans

I promise this page isn’t scary or mean!

Despite rumors to the contrary, I’m actually not on a rabid, foaming-at-the-mouth, steak-fueled mission to unveganize the world. My own diet is mostly plants, and I benefit in no way—financially or otherwise—if you decide to put an egg in your mouth instead of a lump of texturized vegetable protein. My sole goal with this blog is to squash out bad science and give folks access to accurate information about diet. What you decide to do with the stuff I say here is completely up to you.

As a former decade-long vegetarian (and vegan for the last few years of that), I understand and respect that food choices are sometimes based on more than our own health. Maybe you’re ethically opposed to killing animals for any reason, are concerned about the treatment of livestock on farms, or simply developed a crippling case of carnophobia after getting locked in a meat freezer when you were five (worst game of hide-and-seek ever). If this is you, I’m not here to talk you out of your choices or values—and even if we disagree on the specifics, I encourage you to live your life in whatever way you find most fulfilling.

Even though I don’t believe strict vegan diets are optimal from a health perspective, I do think there are ways to make the best out of a meatless, eggless, and dairyless situation. I’d like to offer some of those ideas on this page so that anybody personally committed to veganism can maximize their chance of staying healthy, and hopefully avoid the most common pitfalls us annoying ex-vegans blather on about. (Please note that this isn’t an endorsement for current omnivores to convert to veganism, and there’s no guarantee you’ll truly thrive even if you follow all the suggestions below—but I do think these guidelines will give vegans the best chance possible for warding off health problems.)

In no particular order of importance, here’s a summary of the list, followed by a more detailed version of each point:

  1. Eat real food—no fake meats, processed soy products, vegan junk food, etc.
  2. Avoid high omega-6 vegetable oils and take a vegan DHA supplement.
  3. Supplement with vitamin K2.
  4. Supplement with a vegan form of vitamin D3.
  5. Enhance your beta carotene absorption and conversion.
  6. Properly prepare any grains, legumes, or nuts you eat.
  7. Maximize iron absorption using vitamin-C-rich foods.
  8. Keep your thyroid in good shape.
  9. Take vitamin B12.
  10. Try going gluten-free.
  11. Eat some fermented foods.
  12. Supplement with taurine.
  13. Consider adding oysters or other non-sentient bivalves to your diet.

The long version:

1. Eat real foodI wholly believe the plant-based-diet doctors like Caldwell EsselstynJohn McDougall, and Joel Fuhrman are on the right track when they recommend eating things that actually still resemble food—leafy greens, fruit, tubers, squash, legumes, root vegetables, seaweeds, some nuts and seeds if they sit well with you, and so forth. Although I think many folks would do well with a higher fat intake than some of those doctors recommend (with some caveats we’ll talk about next), the concept of eating real food is a winner. This means ditching the fake soy meats, high-fructose corn syrup, artificial sweeteners, convenience snacks, TV dinners, and pretty much every single thing on this page. It may have been an exciting moment when you learned that Kellogg’s Unfrosted Pop-Tarts are vegan… but pop-tarts they remain. Occasionally indulging in something junkier won’t kill you, but don’t expect to stay healthy if everything on your plate was made by Morningstar Farms or Tofutti.

Just say no.

2. Avoid high-omega-6 vegetable oils like soybean oil, corn oil, cottonseed oil, sunflower oil, peanut oil, or margarines made from these oils. Instead, use heat-stable fats like coconut oil or red palm oil for cooking, and use macadamia nut oil or olive oil for cold dishes like salads. (Depending on where your city falls on the boondocks-to-urbia scale, the linked oils may be easier to order online than track down locally, but you can sometimes find them at specialty markets or request them through Whole Foods.)

Note: slashing your intake of omega-6 fats will reduce your omega-3 requirements, but I also recommend taking an algae-based vegan DHA supplement (like DEVA’s) and getting some ALA from ground chia seeds, hemp seeds, or flax seeds (always raw and not heat-treated, because their fats are extremely unstable). This is particularly important if you’re pregnant or breast-feeding.

"Soybean oil": writing it in Italian doesn't make the badness go away.

3. Secure a source of vitamin K2, pronto—especially if you want to stave off dental nightmares (like my own 14-cavity adventure). Woefully unknown to the public and mainstream health experts alike, vitamin K2 is critical for a healthy heart and skeletal system. Among other things, it helps shuttle calcium out of your arteries (where it contributes to plaque formation) and into your bones and teeth, where it rightfully belongs. There’s a new book out called “Vitamin K-2 and the Calcium Paradox” discussing this nutrient depth, but you can also find plenty of information on K2 online, like here and here.

Unlike vitamin K1, which is abundant in some vegan foods like dark leafy greens, vitamin K2 is only found in certain bacteria and animal products such as dairy, organ meats, and eggs. The chief vegan source is natto—a (not-so-appetizing) fermented soybean product that contains K2-producing bacteria. If you avoid soy, eat a raw food diet that disallows natto, or simply don’t want to shovel slimy ammonia-scented globs into your mouth, look for a vitamin K2 supplement containing menaquinone-4 or menaquinone-7 (usually abbreviated to MK-4 or MK-7). I personally use this brand for myself, both due to quality and cost, and can vouch for the incredible dental benefits it bestows.

4. Take enough vitamin D3 to get your blood level up to the 35 ng/ml markUnless you’re a Hawaiian lifeguard (or otherwise lucky enough to lounge outside all day in the sun), there’s a decent chance you’re deficient, especially if you live at a far northern latitude. Vitamin D is crucial for a wide variety of functions—everything from helping you absorb calcium to protecting against certain cancers—and it works in synergy with vitamins K and A to keep your teeth and bones strong. Unfortunately, since supplemental vitamin D3 is usually derived from wool, nearly all vegan versions contain vitamin D2, which is less potent and not always effective for preventing or fixing deficiency.

Source of Life Garden Vitamin D3 and Vitashine Vegan Vitamin D3 are currently the only vegan vitamin D3 supplements in existence. I highly recommend using either of those over the D2 versions more commonly available. I personally take about 5,000 IUs a day, but you may need to adjust your intake depending on your body size, how much sun you get, and whether you’re trying to aggressively treat a deficiency versus maintaining healthy vitamin D levels. (Also be aware that a small number of people react negatively to vitamin D supplementation, so be on the lookout for any adverse symptoms.)

5. Get the most out of your beta carotene. Vitamin A is crucial for healthy bone tissue, vision, proper hormone function, making fully-intact babies, and other things generally regarded as good. But plants don’t contain “true” vitamin A—only certain provitamins, particularly beta carotene, that your body converts into vitamin A. Unfortunately, the conversion process is wildly inefficient: most folks absorb only a tiny fraction of the beta carotene they consume, and only a fraction of that ever becomes vitamin A—leaving some vegans deficient even if they rival Bugs Bunny in carrot consumption. Although some people are just genetically doomed to be poor converters and will probably struggle as vegans no matter what they do, there are a few ways to maximize your absorption and conversion of vitamin A precursors:

  • Eat beta-carotene-rich foods along with some fat—such as oily dressing or avocado slices on a salad—to greatly increase the amount you absorb.
  • Identify and treat any food allergies, celiac disease, parasite infections, H. pylori infection, or low stomach acid, which can disturb your gut ecology and hinder absorption.
  • Make sure you’re getting sufficient iron and zinc from your diet, since these minerals are critical in converting beta carotene to vitamin A. If you’re deficient in them, your vitamin A status will probably be impaired.
  • Lightly cook some of your beta-carotene sources to break down fiber and improve absorption.

6. Properly prepare any grains, legumes, or nuts you eat. These foods contain phytates that block the absorption of minerals like calcium and iron, along with enzyme inhibitors and tannins that can cause digestive distress. If you choose to include grains, legumes, or nuts in your diet, you can neutralize some of the anti-nutrients and increase mineral availability by giving your food some tender lovin’ prep. For whole grains, do the following:

  1. Put the grains in a bowl filled with enough warm water to cover.
  2. Add apple cider vinegar or lemon juice at a ratio of 1 tablespoon for each cup of grain.
  3. Let it all soak for at least 7 hours at room temperature.
  4. Drain the soak water and cook the grains as you usually would.

For most legumes except dried lentils and split peas, follow the same steps as with grains—but soak larger beans for at least 24 hours (changing the soak water if they start to ferment) and double the amount of vinegar or lemon juice if you’re dealing with really small beans (2 tablespoons per cup of beans). Lentils and split peas should be soaked for 7 hours, but without any vinegar or lemon juice added. Raw nuts, too, should be soaked in warm water for 7 hours without an acidic medium, but you can sprinkle the soak water with sea salt (and then air-dry them once they’re done).

This may sound labor intensive, but it really doesn’t take all that much actual work—and your digestive system will thank you!

7. Eat high-vitamin-C foods along with iron-rich foods to enhance iron absorption, especially if you’re a pre-menopausal woman or otherwise struggle with anemia. Non-heme iron, the form found in plant foods, is less bioavailable than heme iron in animal products—but its absorption increases quite a bit in the presence of vitamin C. Try combining high-iron foods like chard, spinach, beet greens, lentils, beans, and quinoa with vitamin-C-rich foods like tomatoes, bell peppers, lemon juice, strawberries, oranges, papaya, kiwis, pineapple, grapefruit, or whatever else strikes your fancy. If you’re into green smoothies, those are prime opportunities to blend up something fruity and vitamin-C-packed with an iron-rich leafy green. Also avoid drinking tea or coffee with high-iron meals, since these beverages contain substances that reduce iron absorption.

8. Be kind to your thyroidHealth-conscious vegans may unintentionally wind up with two strikes against their thyroids: lack of iodine (either from cutting back on salt or switching from iodized salt to natural sea salt), and a menu packed with goitrogenic vegetables. Impaired thyroid function can result in fatigue, cold hands and feet, hair loss, poor concentration, trouble losing weight, and short-term memory rivaling your grandma’s—all of which you’ve probably heard a disgruntled soon-to-be-ex-vegan complain of at some time or another.

The best vegan source of iodine is seaweed, but some varieties contain much more than others. Here’s a table with the iodine content (among other nutrients) of several common sea vegetables.

Goitrogenic foods—which interfere with thyroid function—include cruciferous veggies like broccoli, cauliflower, Brussel sprouts, kale, kohlrabi, mustard, turnips, rutabaga, and cabbage, as well as soy products and millet. Strawberries, peaches, and spinach are also somewhat goitrogenic. You don’t have to give up these foods completely (crucifers in particular have some great anti-cancer compounds), but definitely scale back on them if they’re currently a large part of your diet, especially if you already have hypothyroid symptoms.

Not so innocent.

9. Take vitamin B12—about 10 mcgs a day, or 2000 mcgs once per weekI’d like to think this would be pretty obvious by now, but there are some lingering vegan authorities who seem to underplay the B-12 issue or even deny it altogether. Even “The China Study” makes B12 seem like small potatoes, when T. Colin Campbell writes: “If you do not eat any animal products for three years or more, or are pregnant or breastfeeding, you should consider taking a small B12 supplement on occasion.” This is sort of scary, since virtually every study conducted on the subject shows that vegans experience much higher rates of B12 deficiency than omnivores or vegetarians and have elevated homocysteine as a result (which increases blood clotting and raises your risk of heart disease). In fact, low B12 and high homocysteine probably contributed to the early demise of prominent vegans like H. Jay Dinshah and T. C. Fry (PDF).

Especially if you’re avoiding processed vegan foods (which are often fortified with vitamin B12), you’ll need to find a supplement and take it consistently, since there are really no reliable dietary sources of B12 for vegans. (Algae like spirulina, often rumored to contain B12, only has B12 analogues that won’t actually improve your B12 status.)

10. Try going gluten-free at least as a 30-day experiment, especially if you have possible “gluten sensitivity” symptoms like bloating, abdominal pain, joint pain, headaches, or migraines that aren’t improving from tweaking your diet in other ways.

11. Ferment some stuffRaw, unpasteurized fermented foods contain lovely bacteria that can help restore your gut flora, improve your digestion, and ultimately increase the nutrition you absorb from what you eat. It shouldn’t take more than 30 seconds on Google to find recipes for sauerkraut, kimchi, “real” pickles, fermented salsa, and other delectable vegan-friendly fermented fare, and most health food stores carry some of these things pre-made. “Wild Fermentation” by Sandor Katz is a great resource if you want to get your hands dirty in the lactobacillus-y goodness.

12. Consider supplementing with taurine, especially if you’re pregnant, nursing, or extremely active. Taurine is an amino acid found only in animal foods, and it plays an important role in brain development, maintaining healthy blood pressure, controlling blood glucose, reducing oxidative stress, and preventing damage to your retinas. Although your body can synthesize taurine from a combination of other amino acids, many folks—including children and pregnant or breast-feeding women—can’t produce enough of it to satisfy their needs without a direct dietary source, and at least one study has shown that vegan men have much lower levels of plasma taurine than nonvegetarians. NOW makes a vegan taurine powder, and there may be other brands out there if you do some sleuthing.

13. Look into “bivalveganism,” a combination of plant foods and non-sentient shellfish. It’s unfortunate this one ended up as unlucky #13, because I honestly think it could be a solution for a lot of struggling vegans. Bivalves—such as oysters and clams and mussels—are incredibly rich in nutrients that are absent or hard to get from plant foods. Oysters in particular are a great source of iron, B12, zinc, selenium, copper, and vitamin D, and have a small amount of true vitamin A as well. Bivalves don’t have a central nervous system and are generally not considered sentient by traditional criteria, so vegans who avoid other animal products may be more ethically comfortable consuming a few oysters per week. (If you want to hear about the potential role of bivalves in vegan diets from someone else’s mouth, here’s a very relevant article by Christopher Cox.)

That’s it for the Big Important Things. But for the sake of making this page insufferably long, here’s another pile of odds ‘n ends:

Keep in mind that it’s not what you eat—it’s what you absorb (or convert). Some diet-scrupulous vegans use programs like Cron-o-Meter to track their nutrient intake and ensure they’re hitting the RDA for vitamins, minerals, and amino acids. Unfortunately, these programs don’t distinguish between vitamin K1 or K2, don’t have RDAs set for nonessential amino acids like taurine, usually record beta carotene as “vitamin A” and don’t adjust for its abysmally low absorption rate (meaning that what looks like 100% of the RDA on paper might only be 1% of the RDA in your body), can’t tell you how much iron/zinc/magnesium/calcium you’re losing to phytates, can’t tell you how much non-heme iron you’re really absorbing—on and on. In other words, nutrient trackers can only show you what you’re putting in your mouth, not what your body can actually grab onto. (Worse yet, the USDA’s nutrient values may be wildly different than what’s on your own dinner plate, since the nutritional content of plant foods varies depending on growing conditions, soil quality, season, geography, and a host of other factors.)

Blood tests can’t tell you if you’re “deficient” in calcium. I don’t know if this belief is as common among regular vegans as it is among raw vegans, but some folks seem to think that a normal calcium value on their blood test is proof that they’re getting enough from their diet. This couldn’t be further from the truth. Calcium in your blood and calcium in your bones are two very different things, and in times of shortage, your body will happily yank calcium from your skeleton so you’ve got enough in your blood to stay alive. (Calcium is an electrolyte that helps keep your heart from spazzing out, and your body generally prioritizes “not dying” over losing bone density.)

When seeking health advice from pro-vegan resources, choose your sources wisely. This applies to pretty much any authority that dispenses advice about a diet they’re emotionally or financially invested in, and veganism is no exception. Steer clear of websites and forums that tend to “whitewash” bad experiences people have with veganism or that ban members who report health problems (not to name names). If someone says you can get all the B12 you need from licking your wrist, not washing your vegetables, or making sacrificial kale offerings to the Coenzyme Gods, run, far and fast. And as somebody who used to put full faith in everything I read on Vegsource.com, I’d also recommend doing your own research before trusting what you read on vegan sites about human digestive anatomy, meat studies in the news, and the miraculousness of seitan.

That said, my absolute favorite vegan expert is Jack Norris. Norris is a vegan RD who’s astoundingly honest about the shortcomings of a vegan diet, offers science-based solutions to health problems, and—unlike some others in his position—doesn’t sweep veganism’s potential pitfalls under the rug. Among all the plant-based health authorities out there, he is hands-down the most likely to give you the truth. Peruse his blog to get a balanced perspective of vegan issues without having bacon shoved in your face.

And if you’re sincerely interested in seeing the “other side” of vegan topics:

  • Tom Billings’ BeyondVeg is a fantastic resource for any truth-seekers in the health world, covering a range of topics relevant to vegans and raw vegans (including comparative anatomy of primates and humans, evolutionary history as it relates to the human diet, common raw vegan myths, and much more).
  • Meat: A Benign Extravagance” by Simon Fairlie is a must-read if your reasons for going vegan are at least partially environmental. There’s no doubt that our modern factory-farming practices suck, but this book shows—in meticulous, fantastically-researched detail—that reality is a lot more nuanced than we’re led to believe. Many vegan foods like strawberries, coffee, wine, chocolate, and asparagus are even more environmentally destructive than factory-farmed meat, and Fairlie shows that some of the damning statistics we hear about animal agriculture are grossly inflated. Based on Fairlie’s research, the most sustainable system is not a vegan one, but involves putting livestock on land unsuitable for plant crops, using animals like chickens and pigs to utilize food waste, and returning to decentralized agriculture.
  • If you’re interested in understanding why former vegans have un-veganized and questioned the ethical basis of veganism, check out the ex-vegan interviews on Rhys Southan’s blog, Let Them Eat Meat. Also worth reading is this detailed personal account of high-profile, former-vegan Tasha’s return to omnivorism. I’ve provided some of my own thoughts in an interview with the National Animal Interest Alliance.
And last but not least…

Don’t beat yourself up if you’re doing everything “right” and still not feeling awesome. Just like all those great-grandmas out there who lived to be 96 smoking a pack a day and choosing Guinness as their main food group, there are some folks who really do survive without animal products for a very long time. I have my doubts about how it’ll play out across generations, but on an individual basis, thriving vegans do exist (such as the phenomenal 60-year-old Lou Corona who’s been a raw vegan for 39 years (and who’s huge on fermented foods—hint hint)). But unlike the resilient great-grandmas who are viewed as lucky anomalies, the resilient vegans tend to get held up as universal examples of “Hey, if this person can do it, so can everybody.”

If you take nothing else away from this page, at least listen to this: humans are much, much more genetically diverse than most of us realize, and one person’s success as a vegan doesn’t guarantee your own. You may be truly physically incapable of absorbing or converting certain nutrients in their plant form. Your health history, your gut ecology, your medical conditions, and even what your mom ate while you were gestating all influence your current nutritional needs. Veganism is a modern experiment—a dietary situation humans have never before faced—and its full repercussions are still unknown. Trouble thriving is not a personal failure. As much as veganism roots itself in compassion, please consider that you, as a living breathing human, also deserve your own kindness.

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559 comments

  1. “It’s about cholesterol, stupid” (William Clifford Roberts, American Journal of Cardiology, editor-in-chief).

    Cholesterol cannot be too low, the lower the better

    “In view of the 10 to 1 gradient between concentrations of LDL in plasma and interstitial fluid, a level of LDL-cholesterol in plasma of 25 mg/dl would be sufficient to nourish body cells with cholesterol. This is roughly one-fifth of the level usually seen in Western societies. Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels. Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies”.

    –Nobel winners, Brown & Goldstein

    Furthermore, individuals born with extremely rare conditions that cause life-long LDL levels of <15 mg/dl display normal growth and actually experience increased longevity

    More Minger nonsense refuted here:

    http://healthylongevity.blogspot.com/2012/08/forks-over-knives-and-healthy-longevity_17.html

  2. Well the Krauss quote was from march 2012, way after the study you referenced.

    So you believe that if LDL levels increase, regardless of particle size and other biomarkers, you are heading straight for heart disease ?

  3. Heres the thing i don’t get Richard,

    LDL is only problematic when it is oxidized, small-dense LDL particles are a lot more susceptable to oxidation and small-dense LDL particles pretty much always show up with low HDL and high triglycerides. I don’t see the mechanism by how eating saturated fat causes low HDL, high triglycerides and small-dense LDL. I haven’t seen enough evidence to convince me that saturated fat causes dyslipidemia. Don’t you think refined carbohydrates and vegetable oils (consumption has increased substantially in the last 100 years) are far more likely culprits?

  4. PUFA vegetable oils have been shown to lower LDL in humans, does that mean that consuming more vegetable oil will protect us against heart disease.

    This is an interestng quote from Stephan Guyenet

    “Saturated fat does not influence LDL in humans in the long term. This is contrary to the mainstream consensus, but is an inevitable conclusion if you carefully consider the evidence from controlled trials and observational studies”

    It’s interestng that you have came to the complete opposite conclusion, someone must be cherry picking data.

  5. @Tom,

    I know you love your denialists. However, pay attention that what I am saying is shared by every single health institution in the world along with every single non-industry sponsored lipid researcher. The consensus on these matters among experts is similar to that the consensus in regards to evolution among biologists.

    LDL has direct causal role in the pathogenesis of atherosclerosis. However, a direct causal role does not imply that all with high x will get y. Most smokers do not end up with lung, however many of them do. Watch primitivenutrition’s segments “Anything but LDL” and “Futility of Cholesterol denialism”.

    As I’ve already indicated Stephen Guynet is one of the most ardent denialists on the web and is completely off the track. He has his expertise in obesity research and that’s the only issue where he do not harbour any pseudoscientific nonsense ideas. He thinks his own TC cholesterol 250 is fine, because his HDL is high. LOL. Guynet thinks that dietary cholesterol does not raise serum cholesterol even despite hundreds of metabolic-ward feeding experiments that show it does. He bases his notion on cohorts of extremely high risk American patients, among high risk patients consuming atherogenic diets dietary cholesterol does not raise serum cholesterol, when the starting point is healthy completely different pattern emerges.

    http://www.blogger.com/comment.g?blogID=1629175743855013102&postID=1401573240583600968

    Denise Minger think Esselstyn should have focused more on raising his patients HDL and lowering their triglycerides. Do you realiaze what a mess these people are?

    1) Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function
    http://www.ncbi.nlm.nih.gov/pubmed/16904539

    2) NY times (may 16th)
    Doubt Cast on the ‘Good’ in ‘Good Cholesterol’

    “I’d say the HDL hypothesis is on the ropes right now,” said Dr. James A. de Lemos, a professor at the University of Texas Southwestern Medical Center..”

    “The current study tells us that when it comes to HDL we should seriously consider going back to the drawing board, in this case meaning back to the laboratory,” said Dr. Lauer, who also was not connected to the research. “We need to encourage basic laboratory scientists to figure out where HDL fits in the puzzle — just what exactly is it a marker for.”

    http://www.nytimes.com/2012/05/17/health/research/hdl-good-cholesterol-found-not-to-cut-heart-risk.html?_r=2&hp

    3) ‘Good’ HDL Cholesterol Can Also Be ‘Bad’ (2012)

    “the HDL amplified inflammatory reactions several times over and could explain the latent chronic inflammation that is associated with high cardiovascular risk,”

    “Lowering the LDL level is therefore still even more important than raising the HDL level.”

    http://www.sciencedaily.com/releases/2012/01/120113210207.htm

    4) Some HDL, or “Good” Cholesterol, May Not Protect Against Heart Disease (2012)

    http://www.hsph.harvard.edu/news/press-releases/2012-releases/hdl-cholesterol-heart-disease.html

    5) HDL Not Always the Good Cholesterol We Think Says University of Chicago Study (2008)

    http://seniorjournal.com/NEWS/Health/2008/20081201-HDLNotAlwaysTheGood.htm

    Email this paper to Guynet. Another good one from Sir Richard Peto

    Meta-analysis of 395 metabolic ward experiments concluded that in typical British diets replacing 60% of saturated fats by other fats and avoiding 60% of dietary cholesterol would reduce blood total cholesterol by about 0.8 mmol/l (that is, by 10-15%), with four fifths of this reduction being in low density lipoprotein cholesterol

    Clarke R, Frost C, Collins R, Appleby P, Peto R. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ. 1997 Jan 11;314(7074):112-

  6. Lipid scholar paid by the Dairy Counsil, Egg Board, Pork Board, Cattlemen’s Beef Association and Atkins foundation see polyunsaturated fats healthier choice as a opposed to SFA and warns against the dangers of red meat

    2012 ADA Diabetes Dispactch

    “similar study using red meat as a primary source of protein found that high intake of beef and saturated fat had an effect that was not observed with either of these dietary components alone: all types of LDL particles, including small particles, increased significantly. On the basis of this finding, the National Institutes of Health recently funded a study comparing the effects of high- and low-saturated fat on diets containing red meat, white meat, and nonmeat as the major sources of protein”.

    “The bottom line,” Dr. Krauss said, “is that you can go high on fats and if you go low on carbs, especially sugars and white starch, and limit red meats, you don’t have to worry too much about saturated fat, although foods rich in polyunsaturated fat are a healthier choice. For most people, saturated fat is not the top priority in managing atherogenic dyslipidemia.”

    http://www.nxtbook.com/tristar/ada/day3_2012/index.php#/8

    Minger, Guynet, etc think SFA and red meat is if not good, at least harmless. Go figure. These denialists are even behind the industry scientists.

    ooh…btw the red meat – cancer link is also very strong in places such as Uruguy where all beef is grass fed and antibiotics banned.

  7. 1) Measuring apolipoproteins does not help risk prediction (June 19, 2012)

    “The study, published in the June 20, 2012 issue of the Journal of the American Medical Association, found that measuring a combination of apolipoprotein B (apoB) and apoA1, lipoprotein (a) (Lp[a]), or lipoprotein-associated phospholipase A2 (Lp-PLA2) gave worse predictions of risk than current lipid measures—total and HDL cholesterol. In addition, the study showed that measuring these alternative biomarkers added little information when added to conventional risk factors”.

    “Grundy adds that recommendations for statin use in primary prevention may need to be revisited now anyway, highlighted by the recent meta-analysis from the Oxford group that showed benefits of statins in much lower-risk individuals than those for whom treatment is currently advised. And he suggests that risk assessment may in the future move away from measuring many biomarkers and instead focus on subclinical atherosclerosis with imaging methods or simple risk projection based on age, sex, LDL levels, and perhaps another major risk factor”.

    http://www.theheart.org/article/1417589.do?utm_medium=email&utm_source=20120622_topStories_dreamail&utm_campaign=newsletter

    2) More evidence for lowering LDL to below 70

    “LaRosa, who wrote an editorial [3] accompanying Lee’s study, expanded on his views to heartwire: “I used to be skeptical about the idea of trying to achieve very low cholesterol levels, but now I am more accommodating. As cholesterol levels are coming down, we are seeing much lower rates of bypass surgery and elective angioplasty. I think elective angioplasty will eventually disappear altogether.”

    “Chimpanzees eat very little fat. They have LDL levels in the range of 40 to 70, and they don’t get atherosclerosis. He noted that levels of LDL below 70 are on a par with those of nonhuman primates who don’t develop atherosclerosis, adding that, like these primates, humans were designed to be vegetarians. “Our dental anatomy suggests that we are not meant to be meat eaters. Animals that eat meat have sharp tearing teeth, while we have flatter teeth more similar to vegetarian animals. I believe humans are not anatomically or metabolically designed to be meat eaters, and because we do consume animal fat that’s why we get atherosclerosis. Chimpanzees don’t eat meat; they eat very little fat. They have LDL levels in the range of 40 to 70, and they don’t get atherosclerosis. Maybe we wouldn’t get atherosclerosis either if we had levels this low.”

    http://www.theheart.org/article/1290061.do

  8. Minger thinks warnings against dietary cholesterol are something from the 1980’s. Not quite so. Oxidized Omega6 does not oxidize LDL, but dietary cholesterol does. So much for the free-range eggs.

    The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis (2005)
    http://www.ncbi.nlm.nih.gov/pubmed/16270280

    Consumption of eggs with meals increases the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation
    http://www.ncbi.nlm.nih.gov/pubmed/9001684

    When Minger says she is not a creationist, it’s like someone is saying I don’t believe in god, but Intelligent design is an astute theoretical framework.

  9. Richard

    “This hypothesis is supported by our feeding experiments in animals. When rabbits were fed oxidized fatty acids or oxidized cholesterol, the fatty streak lesions in the aorta were increased by 100%. Moreover, dietary oxidized cholesterol significantly increased aortic lesions in apo-E and LDL receptor-deficient mice. A typical Western diet is rich in oxidized fats and therefore could contribute to the increased arterial atherosclerosis in our population.”

    Don’t you see a massive problem with that statement ?

  10. Now, I don’t, and I can hardly think that you can either.

    If you want to believe untrained bloggers with TC cholesterol 250mg/dl instead of listening the IOM about the dangers of dietary cholesterol, then have it!

    Rainy-day reading for creationists:

    Even small amounts of dietary cholesterol were shown to increase atherosclerosis without evidence of a threshold beyond which a lower intake did not provide additional benefit

    Intimal Thickening in Normochoiesterolemic Rhesus Monkeys Fed Low Supplements of Dietary Cholesterol
    http://circres.ahajournals.org/content/34/4/447.full.pdf+html

    Atherosclerosis. Regression in nonhuman primates.
    http://circres.ahajournals.org/content/46/3/311.citation

    Arterial lesions and blood lipids in rhesus monkeys fed human diets.
    http://www.ncbi.nlm.nih.gov/pubmed/6832336

    Claiming that these experimental animal models are not relevant for humans would be like saying that the Darwinian foundation of our biomedical research is invalid. Do we any evidence in non-religous literature to make such a postulation, no we do not have!.

    A study on humans showed that dietary cholesterol was associated with increased carotid intima-media thickness, a marker of atherosclerotic independent of other risk factors

    Influence of lifestyle modification on atherosclerotic progression determined by ultrasonographic change in the common carotid intima-media thickness.
    http://www.ncbi.nlm.nih.gov/pubmed/9094885

  11. I provided a small glimpse to some of the best kept secrects of cholesterol denialists. No need to thank me. Use your freedom of choice.

    I am having a bit of break. I’ll be back soon.

    Everything you’ve learnt about diet online is flawed. Rescuing good science from pseudoscience,

    Richard

  12. If you feed a rabbit cholesterol, what do you expect to happen ? Rabbits do not consume cholesterol, they are herbivores.

    Look at the masai, they consume MASSIVE amounts of cholesterol and have a low serum cholesterol. Humans have mechanisms to deal with dietary cholesterol and the liver can manufacture 10-20 times more cholesterol per day than you could ever get through diet.

  13. Primitive nutritions excellent “anything but LDL” and “The futility of cholesterol denialism” -segments from his primitivenutritions -serie are recommended for lay people.

    Primitive Nutrition 45: Anything but LDL, Part III

    The best kept secret of Chris Masterjohn and Stephen Guynet. Our detailed understanding of the cause-and effect relationship of dietary cholesterol to plaque build-up in the artery walls.

    NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals.
    http://www.ncbi.nlm.nih.gov/pubmed/20428172

    Molecular processes that handle — and mishandle — dietary lipids
    http://www.jci.org/articles/view/35206

  14. I’ve just read Anthony Colpo’s post about primitve nutrition and yourself. I’m sorry but Colpo completely exposed you and your sources. Just like primitive nutrition, you just present cherry-picked, biased, irrelevent studies that fail to address the big picture.

    Having read thorugh all of your posts in this blog, it amazes me how many ad hominem attacks and logical fallacies you use. The way you refer to Densie as a “creationist” is offensive and downright stupid.

    I’m not going to post in here again as your shear presence raises my cortisol levels. I just want to thank Densie for taking the time to help vegans who are constantly being lied to by people like you.

    The only person in here presenting pseudo-science is you.

  15. LOL

    Incase you put your email here, I can forward you our whole discussion and you judge yourself tell who is cherry-picking. PlantPositive replied to Colpo in a lenght of 10 videos, Colpo responded to him in regards to one video, and in which he had terrible lie in it, something that is about to be revealed soon.

    Look for the denialists tactiques, when I pointed out to Colpo the epidemiologic data, people who maintain consistently TC cholesterol under 150mg are immune to heart disease, Colpo used an example of a dead person to show this premise as false, as if TC cholesterol levels at the age of lifespan would matter anymore, as if serum lipids would not lower about 10% already immeadiately after death, as if they was not co-founded by cancers, lipid lowering drugs, diabetes, blood pressure medication, heroin, rapid weight loss induced by detoriating health, chemotraphy, etc.

    When I addressed the lack of chronic disease among population who maintain very low cholesterol levels, Colpo started talking about total mortality as if having access to toilet, vaccines, and hospital to a give birth to the child would not be co-founded by these factors.

    Wacth out primitivenutritions response serie. Colpo did not even know that he was dealing with wikipedia’s parody page, he confused the term confusionist to confucian and apologist to apology. And no, he has not exposed anything except his own sillyness. His amateur status and lack of basic education is apparent.

    1. I think any educated person would come to the conclusion that primitive nutrition is the one cherry picking and has a blatant agenda. I’llcontinue to learn off people like Mathieu Lalonde, Denise Minger, Stephan Guyenet, Chris Masterjohn, Chris Kresser, Anthony Colpo, Robb Wolf etc. It’s funny how most of them guys were vegan at some point in their life and stopped due to poor health or lack of scientific evidence.

  16. @Tom

    don’t be ridiculous. What primitivenutrition showed to you was the role of multiple lines of evidence in shaping our health policy. The denilaists including Minger cover only epidemiology and diet trials with imaginary weaknesses they are able crunch out of them. That’s about 1/5 of lipid theory, and as Daniel Steinberg showed that the diet trial data is powerfull but not “airtight”. However, the denialists don’t talk you about the powerfull genetic data or the animal models that has accumulated over the years. No talk about bile-acids, surgery data, etc. They are stuck in their RCT -la la la land. LDL has a direct causal role in pathophysiology of atherosclerosis. This is the view that is shared by every major health institution in the world. If you to heartwire.org (theheart.org) you’ll notice that 100% the cardiologists and lipid specialists in the US are on board with LDL lowering “the lower, the better”. There’s no debate, the creationists have lost. What they have left is fooling stupid lay people.

    When Stephen Guynet with his TC cholesterol of 250 tells you dietary cholesterol and SFA does not have role in your serum lipids, you cannot but laugh. Just to give some perspective (Coronary heart disease was virtually non-existent in Central Africa):

    1) “As to the risk factors in predominantly rural African populations in southern Africa, the principal dietary sources of energy were in the past and still are to an extent cereals (maize and kaffir corn or sorghum) and their products, wild spinaches, and a variety of legumes (cowpeas, sugar beans, Jugo beans), along with relatively low intakes of most vegetables and fruits and infrequent consumption of small quantities of milk and meat”.

    “Serum cholesterol levels of rural Africans in the past ranged from about 3.0 to 3.5 mmol/l and remain low. The range of mean serum cholesterol levels of urban Africans was 3.5 to 4.40 mmol/l and later increased to 4.0 to 5.0 mmol/l” (3 mmol/l = 116)

    Nutrition and Heart Disease Causation and Prevention Edited by Ronald Ross Watson and Victor R . Preedy

    2) The epidemiology of coronary heart disease in South Africa

    “…..Soweto (which now has a population of 3 – 4 million), according to records of the Department of Cardiology at Baragwanath Hospital (3 200 beds), 35 blacks were diagnosed with CHD in 1992,51 in 1993, and 62 in 1994. However, of the latter number only 36 were Sowetans; the rest lived elsewhere.I’ Clearly CHD remains very uncommon in urban blacks in South Africa. To afford perspective, it could be asked how uncommon CHD is in urban blacks, compared with its occurrence in Western populations? Of the population of Soweto, almost all attend Baragwanath Hospital when serious illness occurs. If it is assumed that all the 36 patients with CHD mentioned ultimately died from the disease, CHD would be responsible for only about 0.2% of the roughly 20000 deaths occurring annually in Soweto, an extremely low proportion even allowing for uncertainties. In Europe, in the Seven Countries Study,16 for those in the Mediterranean countries and inland the age-standardised 25-year CHD mortality percentages were 4.7% and 7.7%, respectively. The proportions reported for countries in Northern Europe and for the USA were far higher, namely 16.0% and 20.3%, respectively. These comparisons with Western populations underline the very low occurrence of CHD in urban blacks”.

    Anthony Colpo was put on statins by his doctor. Guynet, Colpo etc. These are young defect people. Young guys should not have elevated cholesterol. People do not like to be diagnosed as malfunctional. Hence, the childish rebellion.

    ATP 3rd expert panel:

    “Any LDL cholesterol above 100 mg/dL appears to be atherogenic. The prevalance of elevated levels in large part accounts for the near universal development of coronary atherosclerosis in the United States and the high attendant risk for developing CHD over a lifetime—49 percent for men and 32 percent for women”
    http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf

  17. Denise Minger made a big mistake by attacking the lipid theory. She shouldn’t have gone there. I don’t have problems with her anti-vegeterian agenda, I have problem with her denialism. She screwed up a big time and she is going to pay for that.

    What she did to Colin T Campbell she will receive 10-fold back, no less.

  18. @Tom

    Stephen Guynet claimed to me poker-face that LDL cannot be lowered significantly without drugs. He probably still thinks this is so, because that’s what denialists with creationists mind-set do.

    Patients who participated in the 12 week Ornish program showed statistically significant improvements in their total cholesterol, LDL cholesterol, and triglycerdies. In fact, patients lowered their LDL-cholesterol levels by an average of 40%.

    The effectiveness and efficacy of an intensive cardiac rehabilitation program in 24 sites.
    http://www.ncbi.nlm.nih.gov/pubmed/20232608

    The LDL numbers of various low-carbers, these numbers are outright horrible, one can legitimately ask whether paleo-diet offers long-term health improvements over the SAD. I believe that this is not so. Cordain himself is obese these days.

    http://perfecthealthdiet.com/2011/03/low-carb-paleo-and-ldl-is-soaring-%E2%80%93-help/

  19. One of the best kept secrets of cholesterol denialists.

    Email this to creationists end you will be replied “that’s not double-blinded RCT, it can’t prove anything”. The science community does not agree.

    High cholesterol per se causes heart disease, and low cholesterol per se heals heart disease, animal models are killers when it comes to establishing cause-and effect. The reseachers transplanted atherosclerotic, damaged artery from a mouse with high cholesterol to a mouse with a low cholesterol. Low cholesterol is all that is required from the environment for the atherosclerotic lesions to fully heal. Inflamation, thyroid function, etc cannot be an independent cause for atherosclerosis. “It’s all about cholesterol, stupid”.

    1) Dramatic remodeling of advanced atherosclerotic plaques of the apolipoprotein E-deficient mouse in a novel transplantation model
    http://www.ncbi.nlm.nih.gov/pubmed/11533609

    Daniel Steinberg, a man who has authored over 400 on lipid metabolism.

    2) Evidence Mandating Earlier and More Aggressive Treatment of Hypercholesterolemia (2008)

    “Armstrong et al and Armstrong and Megan showed that in cholesterol-fed nonhuman primates, virtually total regression could ultimately be achieved, but it took 40 months after return to a cholesterol-free diet to undo the damage done during 17 months of prior cholesterol feeding. The remarkable thing about these studies is that not only was almost all of the lipid gone from the arteries but also virtually all signs of the inflammatory process were gone. The remains of the lesions were basically scar tissue with no signs of cellular infiltrates. In other words, it appeared that in the absence of continuing hypercholesterolemia, the inflammatory process was not self-sustaining. Simply arresting the hypercholesterolemia by reverting to a normal monkey chow diet caused virtually complete lesion regression without the need for intervention directed specifically at the inflammatory process, results recently confirmed in an elegant series of studies in rabbits.”

    “Taken together, all of these findings suggest that the inflammation associated with atherogenesis is not sufficient in itself to cause further lesion progression or even to maintain lesions at a steady state once the hypercholesterolemia has been fully corrected. In other words, many (or even most) of the inflammatory processes in the advancing lesion are downstream responses ultimately traceable to hyperlipidemia and its consequences. Consequently, early and aggressive correction of hypercholesterolemia may be sufficient. On the other hand, if hypolipidemic therapy is initiated at, say, 40 or 50 years of age, optimal intervention will no doubt also require attention to inflammation, thrombosis, and hemodynamic factors”.

    http://circ.ahajournals.org/content/118/6/672.full

    3) Excellent study for Denise Minger to blog about:

    Relationship of baseline serum cholesterol levels in 3 large cohorts of younger men to long-term coronary, cardiovascular, and all-cause mortality and to longevity.

    “These results demonstrate a continuous, graded relationship of serum cholesterol level to long-term risk of CHD, CVD, and all-cause mortality, substantial absolute risk and absolute excess risk of CHD and CVD death for younger men with elevated serum cholesterol levels, and longer estimated life expectancy for younger men with favorable serum cholesterol levels”.

    http://www.ncbi.nlm.nih.gov/pubmed/10891962

    1. Richard, I don’t need to refute your various insane statements because everyone else already has, but I will say this: I don’t mean to be a total dick (…Dick), but please, for the love of all that is good, would you stop saying ‘serie’!?!? I realize English probably wasn’t your first language, but there is no such word as ‘serie’. It’s SERIES. SERIES, SERIES, SERIES. GAH.

  20. Denise Minger = Creationist

    Evolution predicts that the shared derived features of a clade will affect all members of that clade in similar ways, because of their recent common ancestry. It predicts that the things which induce atherosclerosis in other hominoids probably do so in us, and for the same reasons. The same lipid-eating parasites that co-evolved with them also did so with us, and therefore have similar effects on us.

    This is why primate studies — especially those that focus on the hominoids — are relevant, and why they undermine the paleo/creationist diet paradigm. To argue that humans aren’t burdened by highly similar trade-offs as other hominoids is to argue that evolutionary theory has no predictive power. It is a denial of evolution, implicitly rejecting what it explicitly seeks to co-opt.

    If humans aren’t hominoids, then evolution is false. Mingers arguments on lipid theory implicitly denies this hominoid heritage, and it therefore rejects evolution itself. That’s why it’s appropriate to her position creationist.

    Even small amounts of dietary cholesterol were shown to increase atherosclerosis without evidence of a threshold beyond which a lower intake did not provide additional benefit

    Intimal Thickening in Normochoiesterolemic Rhesus Monkeys Fed Low Supplements of Dietary Cholesterol
    http://circres.ahajournals.org/content/34/4/447.full.pdf+html

    Atherosclerosis. Regression in nonhuman primates.
    http://circres.ahajournals.org/content/46/3/311.citation

    Arterial lesions and blood lipids in rhesus monkeys fed human diets.
    http://www.ncbi.nlm.nih.gov/pubmed/6832336

  21. Tom buddy,

    I got another great secret of cholesterol confusionists for you:

    This may explain why no one in the biomedical community take seriously the LDL-particle size nonsense. Aall particles in the LDL fraction are atherogenic, independent of size.

    1) LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA)

    “Thus, smallLDL was a strong confounder of the association of largeLDL with subclinical atherosclerosis, which may explain the widely-held view that larger LDL size is less atherogenic”.

    “After accounting for particle correlations, we demonstrated that the magnitude of association between small LDL and carotid atherosclerosis became equal to large LDL (on a per 1-S.D. basis) or less than large LDL (on a per particle basis). Failure to account for the strong negative correlation between small and large LDL and their different associations with other lipoproteins may underlie the belief that small LDL particles are a more potent atherogenic subclass than large LDL”.

    “There are several mechanisms that may underlie the atherosclerotic effect of both large and smallLDL[5]. At both extremes of LDL size, there is decreased receptor-binding affinity for LDL receptors [27]. Small LDL may be oxidized more rapidly and have been associated with endothelial dysfunction and metabolic dyslipidemia [28]. In comparison, large LDL predominate in patients with familial hypercholesterolemia [29] and those consuming high saturated fat diets. Large LDL have higher core cholesterol ester content, potentially delivering more cholesterol per particle to arterial walls [30], a speculation supported by our finding a greater IMT difference for large compared to small LDL on a per particle basis”.

    http://www.nypcvs.org/images/MESA.pdf

    2) Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an expert panel of lipid specialists (2011)

    “All lipoprotein particles in the LDL fraction are atherogenic, independent of size”

    http://www.lipid.org/uploads/300/Expert%20Panel%20Paper.pdf

    Everything you’ve learnt about diet online is flawed. Rescuing good science from pseudoscience,

    Richard

  22. “What is the physiological rationale for the link
    between HDL subfractions and adverse CV
    outcome?

    HDL particles are involved in reverse cholesterol transport
    and have additional antioxidant and anti-inflammatory
    properties believed to be antiatherogenic”

    http://www.lipid.org/uploads/300/Expert%20Panel%20Paper.pdf

    The financial disclosures list of that paper is horrifying, 90% of the researchers have recieved major funding from drug companies.

    “Everything you’ve learnt about diet online is flawed”

    You are online, primitive nutrition is online, all the paers you reference are online.

    I think you have been brainwashed by that vegan oddball primitve nutrition, the guy has a blatant agenda. Possibly works for a major vegan organization or statin manufacturer. The loser has nothing better to do than make videos about anthony colpo or denise minger. Heres an idea for you Richard, if you are so convinced that heart disease is all about total cholesterol and LDL, why don’t you put your effort into publishing a paper so we can stop wasting our time looking at other biomarkers such as HDL, triglycerides, LDL particle size, LDL oxidation, HA1C, CR-P, IL-1 beta, Homocysteine. That way we can carry on eating even less saturated fat and cholesterol, we can chug bottles of vegetable oil (proven to lower LDL cholesterol), we can all start taking statins to lower our LDL even more.

  23. LDL independent, causal factor in atherogensis. HDL = Leap of faith is required. All other risk factors matter in universally high risk Western population. The other risk factors matter less in a low-risk population, since atherosclerosis cannot developed independently if LDL is low enough (below 80mg/dl), an orchestra cannot perform without the conductor. At this point I’m sure you’ve heard about the immunity of CVD with TC cholesterol below 150mg/dl.

    Chant with me, babe: “Correlation does not equal causality”!

    The HDL hypothesis: does high-density lipoprotein protect from atherosclerosis?

    “It should be noted, however, that the associations between elevated LDL-C and blood pressure and increased CVD risk reflect causal relationships, whereas such a relation between low HDL-C levels and increased CVD is not undisputed”

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903818/

  24. ^Complete nonsense.

    Low-cholesterol in elderly people in high risk cohorts usually just means bad thngs, it co-founds with cancer, aggressive medication, muscle degeneration etc. Why would we care about what happens in high risk populations.

    The cholesterol-denialist are not aware of J-curve (reverse causation) and troll about low cholesterol being hamrfull because it suggest higher total mortality in epidemiologic studies, this is correct, but it does not follow, that we should not be having low cholesterol, it just follows that the cholesterol of sick, elderly Western people plummets during the last years of the their life-span due to chronic diseases and aggressive lipid lowering agents. Cholesterol levels at the age of life-span tells very little.

    Show Ray Peat these.

    1) From the Framingham

    “Under age 50 years these data suggest that having a very low cholesterol level improves longevity. After age 50 years the association of mortality with cholesterol values is confounded by people whose cholesterol levels are falling–perhaps due to diseases predisposing to death.”

    http://www.ncbi.nlm.nih.gov/pubmed/3560398

    2) Low cholesterol, mortality, and quality of life in old age during a 39-year follow-up

    “More dispute has arisen regarding the association of low cholesterol and mortality in elderly persons. For example, in the Honolulu Heart Program (5) low cholesterol was associated with greater mortality risk. Obvious explanations for the association are intervening factors that both increase mortality risk and decrease the cholesterol level. In the nine-year follow-up of the Helsinki Aging Study, mortality risk was associated with both lowered cholesterol synthesis and lowered cholesterol absorption (20), which reflect terminal decline and lead to lower serum cholesterol levels. These associations are not identified, and the relationship between cholesterol and mortality becomes distorted unless the follow-up is long enough”

    http://content.onlinejacc.org/cgi/reprintframed/44/5/1002

    3) Ornish et al. demonstrated in an intervention trial that lowering LDL was associated with increased telomerase activity, which in turn is associated with longevity.

    http://www.ucsf.edu/media/pdf/nobel/blackburn_and_ornish_lancet_2008.pdf

    4) A meta-analysis of 108 randomized controlled trials of various lipid modifying interventions found that lowering LDL cholesterol significantly decreased the risk of coronary heart disease and all-cause mortality, whereas modifying HDL provided no benefit after controlling for LDL cholesterol.

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/pdf/bmj.b92.pdf

    LDL over 50mg/dl is only Western luxury that very few Hunter Gatherer could ever afford.

    1. Are there grey clouds in the sky when it rains ? Yes

      Does it rain everytime there are grey clouds in the sky ? No

      Ornish’s intervention shows that excercise, stress reduction and increased consumption of anti-oxidants are beneficial. The LDL number on it’s own is of little importance as seen in the Lyon diet heart study.

      What is your opinion of excess linoleic acid and seed oils? Don’t you think they are somewhat responsible for heart disease rates ?

  25. There are some indications in the literature that veggie oil induce strokes (and do not provide protection for atherosclerosis) but, apart from high SFA trophical oils, they are not part of pathogensis of atherosclerosis. Remember not all strokes are due to atherosclerosis, although most are. So, strokes can occur due to other mechanism, besides atherosclerosis.

    I use veggie oils very sparingly, occasionally I use virgin canola oil for preparing chantarelle mushrooms along with whole-grain pasta.

    Saturated fats are harmfull to health, they cause elevated LDL, if isocaloric diet is maintained, this is an undisputed fact. Opposingt this is religious, not scientific at this point anymore.

  26. Normal cholesterol panel . . . no heart disease?

    http://blog.trackyourplaque.com/2011/06/normal-cholesterol-panel-no-heart-disease.html

    Small LDL particles and increased HbA1c–An evil duo

    http://blog.trackyourplaque.com/2011/10/small-ldl-particles-and-increased-hba1c-an-evil-duo.html/comment-page-2#comment-14685

    “Small LDL particles are triggered by consumption of carbohydrates. Eat more “healthy whole grains,” for instance, and small LDL particles skyrocket. ”

    Cholesterol Myths that May Surprise You

    http://health.yahoo.net/experts/dayinhealth/cholesterol-myths-may-surprise-you

  27. Nobel winners Brown & Goldstein in Stockholm, 1988

    Brown & Goldstein in Stockholm, 1988.

    A receptor mediated pathway for cholesterol homeostatis

    “Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl (Fig. 16 and ref. 120). In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels (9,119). Second, the LDL level in newborn humans is approximately 30 mg/dl (121), well within the range that seems to be appropriate for receptor binding (Fig. 16). Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies” (116,122)”

  28. Minger’s playschool China data-“analysis”. LOL

    This Swedish blog post is the best kept secret of the oaleo/real food -crew.

    1) http://translate.google.com/translate?hl=en&prev=/search%3Fq%3Dhttp://michelblomgren.blogspot.com%26hl%3Den%26biw%3D2133%26bih%3D1105%26prmd%3Dimvns&rurl=translate.google.co.jp&sl=sv&u=http://michelblomgren.blogspot.jp/2012/01/vete-och-china-study.html

    2) http://translate.google.com/translate?hl=en&prev=/search%3Fq%3Dhttp://michelblomgren.blogspot.com%26hl%3Den%26biw%3D2133%26bih%3D1105%26prmd%3Dimvns&rurl=translate.google.co.jp&sl=sv&u=http://michelblomgren.blogspot.jp/search/label/chinastudy

    Minger is a DIET-HEART theory denialis/creationist who thinks Darwins homology is a flawed premise. She also think the WHO has pulled an international conspiracy for daring to recommend plant-based diets (obs. Minger makes a big fuss for not recommending any specific diet as long as it is not vegan, except he recommends Kurt Harris archevore diet, doesn’t make any sense, but, hey, don’t blame me)..

    The World Health Organization / Food and Agriculture Organization of the Unit Nation asserted in regards to diet that:

    “Households should select predominantly plant-based diets rich in a variety of vegetables and fruits, pulses or legumes, and minimally processed starchy staple foods. The evidence that such diets will prevent or delay a significant proportion of non-communicable chronic diseases is consistent.”
    http://www.fao.org/docrep/004/Y2809E/y2809e00.HTM

  29. 1) What Can Human Genetics Teach Us About the Causes of Cardiovascular Disease?

    “If one still did not believe that LDL-C is a causal factor influencing CHD, a report in this issue of the Journal could help convince the persistent skeptic”

    Journal of the American College of Cardiology Vol. 55, No. 25, 2010

    2) PCSK9 R46L, Low-Density Lipoprotein Cholesterol Levels, and Risk of Ischemic Heart Disease: 3 Independent Studies and Meta-Analyses

    Conclusions: The PCSK9 46L allele was associated with reductions in LDL-C from 20 to 80+ years in the general population. The reduction in risk of IHD was larger than predicted by the observed reduction in LDL-C alone. This could be because genotype is a better predictor of lifelong exposure to LDL-C than LDL-C measured in adult life.

    http://content.onlinejacc.org/article.aspx?articleid=1142928

    Goldstein (Nobel prize winner for the work of LDL receptors)

    “The studies on PCSK9 mutations that lower LDL levels over a life time, as mentioned above (see answer to Question 2), show a superior effect in decreasing coronary disease as compared to the 5-year lowering of LDL levels achieved in statin trials. For example, a 15% lowering of LDL achieved after 5 years of statin treatment leads to a 15% reduction in coronary events, whereas the same 15% lowering of LDL achieved over a life time as a result of having a PCSK9 mutation leads to a 45% reduction in coronary events”.

    http://www.afernandezcruz.com/en/uncategorized-en/jl-goldstein/

  30. Minger maintains that it’s is not just so that cholesterol per se causes CAD. Well, Minger, it is just so. Coronary artery disease is multifactoral disease only in uniformly high risk society where most show non-physiological cholesterol levels due to life-long digestion of SFA and dietary cholesterol together with low-fibre context. The one gets the disease gets down to factors such as genes, smoking, diabates, issues that do not have significance in development of CAD in low-risk population.

    1) Cardiovascular Benefits of Aggressive Cholesterol-Lowering Therapy

    “In a recent editorial, William Roberts, MD, editor of the American Journal of Cardiology, succinctly summarized this complex issue into a simple phrase: “It’s the cholesterol, stupid!”

    “..in individuals with lifetime LDL-C levels reduced by approximately 28% (about 40 mg/dL) due to a nonsense mutation of PCSK9 gene, a reduction of up to 88% in the rate of coronary heart disease events has been reported.10 This 88% reduction is quite different from the 30% reduction predicted by a similar decrease in LDL-C levels noted in a meta-analysis of statin trials.11 Individuals with the PCSK9 mutations have lower LDL-C levels throughout their entire lives, which may actually triple their risk reduction compared with those whose LDL-C levels are lowered similarly but are measured for only a 5-year span”.

    http://www.jaoa.org/content/111/4_suppl_3/i.full

    2) Diagnostic Criteria for Dyslipidemia

    “Low-density lipoprotein cholesterol (LDL-C) is identified in the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) report as the most abundant and clearly causal atherogenic lipoprotein on the basis of many observational and experimental studies over several decades.1 Guidelines from the American Association of Clinical Endocrinologists (AACE) are in agreement with NCEP ATP III that LDL-C is central in the diagnosis of dyslipidemia. Any LDL-C level above 100 mg/dL appears to promote atherogenesis”

    http://www.lipidu.com/Pillars.aspx?PillarID=2&ChildID=2

    3) Evidence Mandating Earlier and More Aggressive Treatment of Hypercholesterolemia (Steinberg, 2008)

    “Armstrong et al and Armstrong and Megan showed that in cholesterol-fed nonhuman primates, virtually total regression could ultimately be achieved, but it took 40 months after return to a cholesterol-free diet to undo the damage done during 17 months of prior cholesterol feeding. The remarkable thing about these studies is that not only was almost all of the lipid gone from the arteries but also virtually all signs of the inflammatory process were gone. The remains of the lesions were basically scar tissue with no signs of cellular infiltrates. In other words, it appeared that in the absence of continuing hypercholesterolemia, the inflammatory process was not self-sustaining. Simply arresting the hypercholesterolemia by reverting to a normal monkey chow diet caused virtually complete lesion regression without the need for intervention directed specifically at the inflammatory process, results recently confirmed in an elegant series of studies in rabbits.59–61”

    “Taken together, all of these findings suggest that the inflammation associated with atherogenesis is not sufficient in itself to cause further lesion progression or even to maintain lesions at a steady state once the hypercholesterolemia has been fully corrected. In other words, many (or even most) of the inflammatory processes in the advancing lesion are downstream responses ultimately traceable to hyperlipidemia and its consequences. Consequently, early and aggressive correction of hypercholesterolemia may be sufficient. On the other hand, if hypolipidemic therapy is initiated at, say, 40 or 50 years of age, optimal intervention will no doubt also require attention to inflammation, thrombosis, and hemodynamic factors”.

    http://circ.ahajournals.org/content/118/6/672.full

    4) LDL = independent, causal factor influencing CAD. Paleo-Diet = High LDL in making. The mechanism what lowers LDL is irrelevant. Genes, surgical bypass operation of illeal (POSCH-trial), statin, excersise, diet pattern, etc they all result in lowered risk for CAD.

    5) The cause of Atherosclerosis (William Roberts, American Journal of Cardiology, editor-in-chief:)

    “In contrast to feeding cholesterol and/or saturated fat, it is not possible to produce atherosclerotic plaques in herbivores by raising the blood pressure chronically, by blowing cigarette smoke in their faces for their entire lifetimes, or by somehow raising the blood glucose levels without simultaneously feeding them an atherogenenic diet. Presently, it is commonly stated that “atherosclerosis is an inflammatory disease.” Inflammatory cells, however, are infrequent in plaques of coronary arteries studied at necropsy or in endarterectomy specimens. When present, the few mononuclear cells—even giant cells—appear to be present due to a reaction to the deposits of lipid (pultaceous debris) present in the plaque.“ Inflammation” appears to be a surrogate for elevation of serum C-reactive protein or various cytokines (interleukins 1 and 6, tumor necrosis factor, etc), not for inflammatory cells in plaques. Thus, it is a definition situation, and the morphologic definition of inflammation is not applicable”

    “Because humans get atherosclerosis, and atherosclerosis is a disease only of herbivores, humans also must be herbivores”

    http://intl-ncp.sagepub.com/content/23/5/464.full

  31. The large majority of the decline in serum cholesterol in the pre and early statin period in developed nations in the second half of the 20th century is explained by diet, and resulted in some of the largest declines in cardiovascular disease mortality in the world.

    A recent meta-analysis of mendelian randomized controlled trials including over one million individuals found that inheriting one of the nine studied genetic variants associated with life-long reduced LDL, but do not alter other known risk factors equally predicted a three-fold greater decreased risk of coronary heart disease per unit lower of LDL than statins do when started later in life. This study also found that individuals who inherit a variant of the statin drug targeted HMGCR gene that is associated with life-long reduced LDL, have an equal degree lower risk of coronary heart disease as individuals who inherited any of the other 8 studied gene variants. This provides further evidence that the primary mechanism in which statins lower coronary heart disease can be explained by its ability to lower LDL cholesterol.

    These findings demonstrates that the benefit of lowering LDL depends on both the timing and the magnitude of the LDL reduction, and that the benefits associated with lower LDL are largely independent of the mechanism in which LDL is lowered. This in-turn provides strong evidence indicating that dietary changes to reduce serum cholesterol will result in similar results as other medical based lipid modifying interventions (ie. the meta-analysis of 108 lipid modifying interventions), as has been observed in a number of nations that experienced some of the largest declines in cardiovascular disease mortality in the world.

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199603/pdf/1471-2458-11-641.pdf

    http://eurheartj.oxfordjournals.org/content/32/10/1187.full.pdf

    http://www.bmj.com/content/344/bmj.d8136

    http://www.unilever-pro-nutrition-sante.fr/wp-content/uploads/2012/06/Importance-of-reducing-SAFA-to-limit-CHD-BJN-2011-Pedersen-et-al.pdf

  32. http://omega-6-omega-3-balance.omegaoptimize.com/2010/12/03/meta-analysis-reveals-heart-healthy-omega-6-fat-increases-risk-of-heart-disease.aspx?ref=rss

    Meta-analysis Reveals “Heart Healthy Omega-6 Fat” Increases Risk of Heart Disease

    Bottom Line: The research upon which the American Heart Association based their “eat-your-omega-6-fat” advisory, is fatally flawed, according to the results of a meta-analysis study, which showed that a steady diet of omega-6 polyunsaturated fatty acids increases the risk of heart disease and death, especially for women [1]. British J Nutr. Dec 2010.

    Background: Omega-6 fats are the most commonly eaten polyunsaturated fatty acids (PUFA) in westernized countries. The top three sources are corn oil, soybean oil and cottonseed oil, which are the main ingredients in margarines, salad dressings, and mayonnaise. Many studies have shown that PUFA lower cholesterol.

    Prior to industrialization, no population has been exposed to the current high levels of omega-6 polyunsaturated fats. We evolved on a diet with a balanced proportion of omega-6 to omega-3 fats of about 1:1. Today, that ratio in westernized countries is out of whack, near 20:1 of omega-6 to omega-3 fats. Different farming practices, new food processing and the urging by health authorities to use vegetable oils in place of animal fats for heart health, triggered an onslaught of omega-6 fats into the food we eat.

    While it’s true that PUFA lowers cholesterol, cholesterol is not they key culprit in heart disease. Inflammation is the “new cholesterol” in matters of eating to protect the heart (and other chronic diseases for that matter).

  33. Evidence from over 100 randomized controlled trials, mendelian randomized control trials consisting of over one million individuals, and prospective studies consisting of several million individuals have firmly established a causal relationship between lowering LDL and non-HDL cholesterol and a decreased risk of coronary heart disease, cardiovascular disease and all-causes mortality (references below). The counter-evidence that Guynet f.ex provided is generally from studies with a significantly lower participant size without being of higher methodological quality, or some observational study that failed to sufficiently account for reverse causation.

    http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60312-2/abstract
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/pdf/bmj.b92.pdf
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2988224/
    http://circ.ahajournals.org/content/118/6/672.long
    http://www.staessen.net/publications/2006-2010/07-44-P.pdf
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3284229/
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1488755/
    http://www.ncbi.nlm.nih.gov/pubmed/19349632

  34. I would ask about the amount of K2 you recommend. On the brand you listed, is 5mg where as other brands listed is typically around the “50 mcg 30 Sgels” range. I was wondering if you take such a high concentration because of your need for recovery and if the lower concentration would be sufficient enough for prevention?

    Also, fun-fact: I get my vitamins and supplements from http://www.swansonvitamins.com they carry their own brand in addition to most popular brands and usually at a fraction of the cost. The K2 brand that you use is listed ***$20 cheaper*** through them rather than Amazon.

  35. lol, “eat real food” then the rest is anything but real food..a list of friggen supplements. if you honestly believe nature is so simple that 6 billion years can be replicated with 50 years of supplement experience then you are insane.

    1. Ignorant ^^^^^^

      I’m sorry but if you are deciding to be a vegan then you WILL need to supplement. There are many nutrients (some essential, some not) in animal products that are not found in plant foods.

  36. Umm… K2 is synthesized in the gut from K1, so there isn’t a need to supplement K2 i you are getting enough K1. This is easily attainable information.

  37. do remember that whatever diet you choose, most doctors recommend a supplement/vitamin. meat eater or veggie. in the end do what makes you feel the best and consult your doctor. i’m a recent veg head. i was doing low carb high protein lots of veg, but for me i felt bad. i gained a lot of weight, skin looked bad, hair was limp. changed that to a vegetarian diet high in leafy greens, a daily b12 and calcium supplement, nuts with breakfast daily, beans bean beans, fruit daily, whole grains (quinoa!!!!) and veggie “junkfood” only when i have no other option. i am supervised by a cardiologist at hopkins and she thinks i look wonderful, and should keep doing what i am. I feel great and look great. so it works for me. but mind you it wouldn’t work for everyone. and that is where everyone needs to know who they are and how they feel. you are your best doctor.

  38. Hey “ex-vegan girl”! You’re so beautifull! But, stop trying to unveganize the world! Your only reason to do that, is that you missed animal foods. We don’t need any “cientist” to tell us what our diet is. We feel all the benefits in ourselves. 😉

    1. Agreed. Husband and I are vegan athletes in our mid-50s. All health prblems (asthma, arthritis onset, breast lump, etc.) subsided after switching to vegan diet (mostly plants, fruits, seeds/flaxseeds/quinoa, beans…very little processed grains) supplemented only with vitamin B12 ten years ago. Never have been healthier, and have more energy and endurance than most athletes half our age.

  39. Everything You Know About Saturated Fat Is Wrong

    One of the most prominent proponents of rewriting the book on saturated fat is cardiologist Dariush Mozaffarian, an associate professor of medicine at Harvard Medical School and the author of more than 100 scientific papers on nutrition and health. We asked him to explain why the conventional wisdom on saturated fat is misleading—and how eating it, in moderation, can sometimes be the healthiest move you could make.

    http://www.more.com/health/healthy-eating/saturated-fat-good

    Q: What has been the effect of the move to cut down on saturated fat in the United States?

    A: In the last few decades, total-fat and saturated-fat consumption has gone down, but consumption of refined carbohydrates has soared. Low-fat versions of packaged foods, loaded with refined carbohydrates, sugars and salt, now flood the market. When people replace saturated fat with refined carbohydrates, they are unlikely to improve their health and may worsen it. That’s because these kinds of carbohydrates are more likely than saturated fat to raise the risk of heart disease and type 2 diabetes.

  40. Avoiding SFA is a no-brainer. Just because an item a is perceived to be better than item b, does not establish that item a is good.

    1) Jeremiah Stamler wrote an excellent piece over the ideas harboured by Krauss and Mozzafarian, it’s here:
    http://ajcn.nutrition.org/content/91/3/497.full

    2) The co-author of Siri-Tarino Meta-Analysis in 2012:

    “Why is red meat harmful? “Saturated fat, which can lead to cardiovascular disease, is really just the beginning of the story,” explains Hu”
    http://harvardmagazine.com/2012/01/a-diabetes-link-to-meat

    3) Harvard School of Public Health:

    “Choose foods with healthy fats, limit foods high in saturated fat, and avoid foods with trans fat”
    http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/fats-and-cholesterol/

    4) Fresh paper about the Inuits:

    Consumption of omega-3 fatty acids is not associated with a reduction in carotid atherosclerosis: the Genetics of Coronary Artery Disease in Alaska Natives study

    “Dietary intake of omega-3 FAs in a moderate-to-high range does not appear to be associated with reduced plaque, but is negatively associated with IMT. The presence and extent of carotid atherosclerosis among Eskimos is higher with increasing consumption of saturated FAs”

    http://www.ncbi.nlm.nih.gov/pubmed/18054937

    4) Denise Minger wants us to believe that malfunction in the thyroid is the CAUSE of coronary artery disease. That’s is ridiculous nonsense and based on really old & poorly presented speculations. If even small but relavent bunch of those who died as result of CAD got first problems with thyroid, then this would be reflected in the large body of high quality prospective studies that have corrected for regression dilution bias. There’s absolute no hint of such events taking place. Even the few who develope malfunction in the thyroid and end up dyeing due to CAD develope CAD because of elevated LDL.

    Increased Oxidizability of Low-Density Lipoproteins in Hypothyroidism
    http://jcem.endojournals.org/content/83/5/1752.short

    5) CAD is shown to be develope in linear relationship to serum cholesterol concentration even within population that have low cholesterol concentration to begin with, and even in the context regression dilution bias has been corrected with follow-up blood-lipid measurements.
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1670480/?page=1

    Cholesterol, coronary heart disease, and stroke in the Asia Pacific region

    “Numerous other observational studies, particularly in men, have demonstrated a strong, continuous, graded, and independent association between cholesterol and the risk of CHD.1–,6 The current data clearly extend these findings to Asian populations with substantially lower average levels of cholesterol, and confirm that effects are similar in men and women”

    http://ije.oxfordjournals.org/content/32/4/563.long

    6) Elevated total cholesterol: its prevalence and population attributable fraction for mortality from coronary heart disease and ischaemic stroke in the Asia-Pacific region.

    “Conventional methods for estimating disease burden severely underestimate the effect of TC. Cholesterol-lowering strategies could have a tremendous effect in reducing cardiovascular deaths in this populous region”

    http://www.ncbi.nlm.nih.gov/pubmed/18677162

    7) According to the anti-darwinist denialists such as Denise Minger we should eat the “archevore diet” ala Kurt Harris and have total and LDL cholesterol levels far exceeding those found in wild animals, human infants, and groups of people well-documented to have no atherosclerosis. They want to believe that adult humans need /benefit from having TC more than 50% and LDL at least 200% above known required and physiologically normal levels. LOL

    For some reason, they clearly understand that a blood sugar level 50-200% above physiological levels is harmful, and that a body fat level 50+% above physiological levels is harmful, but they believe that a blood lipid level 50-200% above physiological levels is not only not harmful, it is, according to them, positively beneficial. LMAO.

  41. Tell me Dennis,

    if significant proportion of those who died in CAD had malfunction in thyroid, then why high quality prospective cohorts corrected for regression dilution bias have failed to show this? How is this possible? Instead these high quality cohorts have firmly establish the independent, continuous, positive and log-linear, nature of the associations between TC and both CHD and Ischemic Stoke even within population that have very low serum cholesterol concentrations compared to Westerners!

    In fact, this great review discusses eloquently how regression dilution (systematic error) has failed to show the real association of serum cholesterol concentrations to coronary heart disease in many Western cohorts characterized with very high population-wide cholesterol concentrations.
    http://aje.oxfordjournals.org/content/150/4/341.full.pdf

  42. First let me say that this article is a very nice summary and has good information.

    But I also wanted to make a general point. The vegan diet is scrutinized so much and people are obsessed with “if their doing it right” and if their daily fluctuations in how they feel is a result of their diet changes.

    For some reason people think meat is some multi-vitamin of something. If you have dietary issues eating meat is not a magical cure. People walk around deficient in all kinds of things because of a poor diet and that doesn’t have to do with eating meat or not, its about eating right or genetic issues (which the author mentions briefly). There are tons of things we could do to be at PERFECT health. Eating all of these supplements might get you closer to that. But this article makes it seem like if you don’t supplement with all these things then you can’t be vegan and feel fine. This would be a fallacy.

  43. I should also comment to Denise that “squashing out bad science” with opinions or reinterpretations of data that themselves have no data doesn’t make any sense.

  44. Creationist-minded debators like Minger deny the independent & causal role of LDL in coronary artery disease.

    Atherosclerosis can be induced in a great variety of animal species including vegetarian and carnivore species (e.g. insects, birds, cats, dogs, non-human primates etc.) by raising serum cholesterol high enough and maintaining it long enough. Atherosclerosis can also be reversed by lowering TC enough and maintaining it long enough. The lipid deposits and foam cells disappeared but some fibrous tissue remained. Some species, such as the dog and rat, do not get elevated TC from a diet high in saturated fat and cholesterol. But when a way was found to elevate their TC they also developed atherosclerosis. This is so consistent no matter which species is tested that it appears to be a scientific law that elevated LDL can cause atherosclerosis. ) This can’t be explained away by stress, inflammation or some infectious agent. In clinical trials, Dr. Esselstyn’s group did better than Dr. Ornish’s group even though Dr. Ornish used stress reduction and Dr. Esselstyn didn’t. However Dr. Esselstyn’s patients had lower LDL. And although inflammatory factors like infection can speed up atherosclerosis, oxidized LDL, foam cells and cholesterol crystals inside the artery wall provide their own inflammation

    Here are findings from reviews that demonstrate that LDL concentration is a causal risk factor for coronary heart disease and all-cause mortality:

    Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis

    The meta-regression analysis included 108 randomised trials involving 299 310 participants at risk of cardiovascular events. All analyses that adjusted for changes in low density lipoprotein cholesterol showed no association between treatment induced change in high density lipoprotein cholesterol and risk ratios for coronary heart disease deaths, coronary heart disease events, or total deaths. With all trials included, change in high density lipoprotein cholesterol explained almost no variability (<1%) in any of the outcomes. The change in the quotient of low density lipoprotein cholesterol and high density lipoprotein cholesterol did not explain more of the variability in any of the outcomes than did the change in low density lipoprotein cholesterol alone. For a 10 mg/dl (0.26 mmol/l) reduction in low density lipoprotein cholesterol, the relative risk reduction was 7.2% (95% confidence interval 3.1% to 11%; P=0.001) for coronary heart disease deaths, 7.1% (4.5% to 9.8%; P<0.001) for coronary heart disease events, and 4.4% (1.6% to 7.2%; P=0.002) for total deaths, when adjusted for change in high density lipoprotein cholesterol and drug class.

    To take into account non-lipid effects of specific drugs (such as potential pro-thrombotic effects of hormone therapy), we included a categorical variable of drug class in the meta-regression model and did a meta-regression analysis stratified by drug class. We used R2 to measure the proportion of the variability in the log risk ratio of an outcome explained by the statistical model.

    Similarly, we found no association between change in triglycerides and risk of coronary heart disease events whenever the model included an adjustment for the change in low density lipoprotein cholesterol (data available from the authors). Change in low density lipoprotein cholesterol, however, remained a significant predictor in a multivariable model adjusting for change in high density lipoprotein cholesterol, change in triglycerides, and class of intervention, with a 7.4% (4.4% to 10.4%; P <0.001) relative risk reduction for coronary heart disease events.
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/

    A Mendelian Randomized Controlled Trial of Long Term Reduction in Low-Density Lipoprotein Cholesterol Beginning Early in Life

    Number of participants in meta-analysis = 1,003,207

    Prolonged exposure to lower LDL-C beginning early in life associated with 3-fold greater clinical benefit for each unit lower LDL than treatment with a statin started later in life (Mean age at randomization in statin trials: 63 years; p = 0.00000000000000000843)

    Absence of Heterogeneity: Suggests the effect of each of included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL-C, rather than through some other pleiotropic effect.

    The increased clinical benefit associated with lowering LDL-C beginning early in life appears to be independent of the mechanism by which LDL-C is lowered. Diet and exercise are probably as effective as other therapies at reducing the risk of CHD (per unit reduction in LDL-C)

  45. Campbell & Junshi reported,

    “There appears to be no treshold of plant-food enrichment or minimization of fat intake beyond which further disease prevention does not occur”

    “Mean intakes of animal protein (about one-tenth of the mean intake in the United States as energy percent), total fat (14.5% of energy), and dietary fiber (33.3 g/d) reflected a substantial preference for foods of plant origin. Mean plasma cholesterol concentration, at approximately 3.23-3.49 mmol/L, corresponds to this dietary life-style”

    “These findings suggest that even small intakes of foods of animal origin are associated with significant increases in plasma cholesterol concentrations, which are associated, in turn, with significant increases in chronic degenerative disease mortality rates”.

    Minger does not believe that LDL-cholesterol concentrations of +200% above physiological levels can cause problems per se. LDL-cholesterol concentrations of +200% above physiological levels are the norm in Western societies. Physiological LDL-levels are those levels we are designed to have by evolution, which are essentially the levels found in all mammalian species that do not develope atherosclerosis, healthy neonates and those societies that face absence of coronary artery disease as well as other chronic disease. Campbell & Junshis findings may be provocative, but essentially the authors observed that even small amount of animal products can cause abnormal cholesterol concentration in human in the studied eco-niche. In turn, abnormal cholesterol concentrations may a catalysator for chronic disease. Observe that high quality prospective cohorts that have adjusted for regression dilution bias have firmly established positive, inpendent, continuous and log-linear association of serum cholesterol to coronary artery disease and ischemic stroke for both sexes even among populations that have low cholesterol concentrations as a base-line. These associations opf seum cholesterol to coronary heart disease are inpendent of thyroid function.

    Minger claim that she has refuted the findings in China. I find these claims outrageously ridiculous. Everyone can clinically observe for themselves how much animal foods they can tolerate in order to hit the 3.23-3.49 mmol/l the cholesterol treshold observed in rural Chinese villages. The values observed matches nicely to the cholesterol concentrations observed in Western people consuming whole-food, plant-based diets.

  46. Confirmed Again: Statin Drugs Accelerate Cardiovascular Disease

    http://articles.mercola.com/sites/articles/archive/2012/10/15/statin-drugs-on-coronary-disease.aspx

    What You Need to Know About Cholesterol in Order to Understand the Dangers of Statins

    Statin drugs work by preventing the formation of cholesterol and reduce LDL cholesterol, which is considered the “bad” cholesterol. There is no argument that these drugs can effectively lower your cholesterol levels. However, what has NOT been proven is that they significantly lower your risk of dying from heart disease. In no way, shape or form do they treat the underlying cause of your problem. They are nothing more than a toxic band-aid.

    So just what makes statins so dangerous, and why are they not the answer for managing your cholesterol levels?

    First you need to understand the biological workings of cholesterol. In fact, there is no such thing as “good” or “bad” cholesterol. Both HDL and LDL cholesterol perform vital functions in your body, which is why it’s actually dangerous to bring your LDL levels down too low.

    HDL (high density lipoprotein) and LDL (low density lipoprotein) are actually proteins that transport the cholesterol to and from your tissues. Cholesterol in turn is a precursor to your steroid hormones, bile acids, cell membrane walls and vitamin D. For example, cholesterol is essential for you to make testosterone or estrogen, cortisol, DHEA or pregnenolone, or a multitude of other steroid hormones that are necessary for health, without cholesterol. Even more importantly, your cells cannot regenerate their membranes without it.

    The reason you have LDL to begin with is to transport the cholesterol to the tissues in order to make new cells and repair damaged ones. However, there are different sizes of LDL particles and it’s the LDL particle size that is relevant, and statins do not modulate the size of the particles. Unfortunately, most people still don’t know about that part, and very rarely, if ever, get tested for particle size. The particles are sticky, so very small LDL’s can easily get stuck in different areas, and the build-up eventually causes inflammation and damage.

    The only way to make sure your LDL particles are large enough to not cause damage is through your diet. In fact, it’s one of the major functions of insulin.

    Conveniently enough, a healthy diet is also the answer for type 2 diabetes, so by focusing on what you eat, you’re treating both your diabetes and your cholesterol levels, and reducing your associated risk of heart disease. If you eat properly, which is really the only known good way to regulate LDL particle size, then it does the right thing; it takes the cholesterol to your tissues, the HDL takes it back to your liver, and no plaque is formed.

  47. LOL!

    Don’t you think it’s perfectly natural that those prescribed to statins have most plaque? Second, calcium-dense plaques are the most mild form of plaque, the lipid-dense plaque are the real nightmare. Statins have an ability to stabilize the plaque and change its composure.

    You didn’t seriously think statin shave cause-effect relationship in increasing plaque-build up? As Minger would say: “correlation does not equal causation”. What would be the biological mechanism which would cause HMG-CoA inhibitors to produce more plaque?

  48. View this picture:

    You can see that Rosuvastatin produced significant changes to the plaque composure. Altering its constitution from more lipid-dense to more fibrous as well slightly more calcified. Lipid-dense plaques are the most rupture prone. Calcified and fibrous plaques more stabil and safer. Moreover, pay attention that Rosuvastatin not only produced changes in the plaque form but significantly reduced its size as well.

    Early intervention with rosuvastatin decreases the lipid components of the plaque in acute coronary syndrome: analysis using integrated backscatter IVUS (ELAN study).
    http://www.ncbi.nlm.nih.gov/pubmed/21266787

    I find it weird that the cholesterol denialist/creationist -fringe online neglect these findings. The take-home message is that low LDL does a lot of good things for us.

  49. http://blog.trackyourplaque.com/

    Why small LDL particles are the #1 cause of heart disease in the US

    9/15/2011, Dr. William Davis

    Ask your doctor: What is the #1 cause of heart disease in the US?

    Let’s put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

    High cholesterol or high LDL cholesterol
    Too much saturated fat
    Obesity

    Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.
    I’d tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

    –Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

    –In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here’s a 2006 review.

    –Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to “cut fat and eat more healthy whole grains.” Conventional diet advice has therefore triggered an explosion in small LDL particles.

    –When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

    If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either “pattern B,” meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus “pattern A,” meaning falling below that same arbitrary threshold.

    Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called “pattern A.”

    If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with “pattern B” small LDL particles would go much higher.

    I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat (“wheat belly”) to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet

  50. This large study found that all LDL particle sizes are atherogenic and big fluffy particles, those carried by FH patients, were even more atherogenic, partly because of its abilty to deliver more cholesterol per particle to arterial walls.

    1) LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA)

    “Thus, smallLDL was a strong confounder of the association of largeLDL with subclinical atherosclerosis, which may explain the widely-held view that larger LDL size is less atherogenic”.

    “After accounting for particle correlations, we demonstrated that the magnitude of association between small LDL and carotid atherosclerosis became equal to large LDL (on a per 1-S.D. basis) or less than large LDL (on a per particle basis). Failure to account for the strong negative correlation between small and large LDL and their different associations with other lipoproteins may underlie the belief that small LDL particles are a more potent atherogenic subclass than large LDL”.

    “There are several mechanisms that may underlie the atherosclerotic effect of both large and smallLDL[5]. At both extremes of LDL size, there is decreased receptor-binding affinity for LDL receptors [27]. Small LDL may be oxidized more rapidly and have been associated with endothelial dysfunction and metabolic dyslipidemia [28]. In comparison, large LDL predominate in patients with familial hypercholesterolemia [29] and those consuming high saturated fat diets. Large LDL have higher core cholesterol ester content, potentially delivering more cholesterol per particle to arterial walls [30], a speculation supported by our finding a greater IMT difference for large compared to small LDL on a per particle basis”.

    http://www.nypcvs.org/images/MESA.pdf
    ——————————————————————————————–
    This expert panel reviewed the data and did not recommend particle-size count for any patient group. Particle number count was recommended for diabetics, in order to define the degree of intensiveness of LDL-lowering theraphy for them.

    2) Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an expert panel of lipid specialists (2011)

    “All lipoprotein particles in the LDL fraction are atherogenic, independent of size”

    http://www.lipid.org/uploads/300/Expert%20Panel%20Paper.pdf

  51. Anyone who wants to put their faith on the many monetary interest on the promotion of grains, statins and the “official” advice can do so. But the simplistic approach to arthrosclerosis is foolish this is a disease that is just a superficial label for a cluster of symptoms not yet fully understood by medical science. You can have studies pointing in multiple directions because the science is very complex and has yet to be settle, regardless of what you may hear. The reality is that what little is known about the cholesterol theory has been changing with time.

    If you want to read how complex the science is read:

    http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-i

  52. Potato, tomato and rice lectins may cause as much inflammation as wheat

    http://www.naturalnews.com/037597_wheat_lectins_inflammation.html

    Inflammation and osteoarthritis common

    Sayer Ji, founder of GreenMedInfo.com, says tomatoes, rice and potatoes are particularly lectin-heavy. That’s especially problematic, he says, because “while the ‘nightshade’ (potato and tomato) connection with inflammation has been known about for quite some time anecdotally, rice has rarely been considered problematic and has become something of a poster child for the wheat/gluten free industry which often substitutes it for gluten-containing ingredients.”

    “The discovery that chitin-binding lectin is broadly distributed throughout cereal grasses sheds light on how the grain-free diet produces health results superior to that of eliminating wheat and gluten containing grains alone,” he continued.

    These three foods are extremely prevalent in the West’s diet, which could help explain another phenomenon: why the incidence of osteoarthritis, a degenerative joint disease, is so widespread, Ji says.

    It all begins with gluten, however.

    “Gluten’s inflammatory effect in the gut causes intestinal cells to die prematurely and causes oxidation on those cells,” writes health enthusiast Sebastien Noel at Paleo Diet Lifestyle. “This effect creates a leaky gut and a leaky gut can allow bacterial proteins and other toxic compounds to get in the blood stream, which can also lead to autoimmune attacks on the body. A leaky gut also means that food as not digested properly and nutrients are not absorbed fully, which can lead to nutrient deficiencies.”

  53. @Charlie,

    the nonsense about “little is known” was very well utilized by the cigarette and asbestos industries. Peter Attia is another anti-science figure and is on par with William Davis. Typically the societies where atherosclerosis does not exist show very low levels of serum cholesterol which are maintained throughout the life. These cultures are almost essentially grain-cultures where staple food is maize, sorghum, rice, millet, wheat, etc.

    While you are doing your succesfull “research” on the pathophysiology of atherosclerosis, I leave you with these two reviews. I personally have the statin and grain industries anytime over obese, anti-science low-carb/paleo spin-doctors.

    LDL-cholesterol is the direct, causal factor influencing artery disease. This notion has similar consensus among the biomedical community as any great idea has within its respective experts, e.g. the theory of evolution.

    1) Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis

    The meta-regression analysis included 108 randomised trials involving 299 310 participants at risk of cardiovascular events. All analyses that adjusted for changes in low density lipoprotein cholesterol showed no association between treatment induced change in high density lipoprotein cholesterol and risk ratios for coronary heart disease deaths, coronary heart disease events, or total deaths. With all trials included, change in high density lipoprotein cholesterol explained almost no variability (<1%) in any of the outcomes. The change in the quotient of low density lipoprotein cholesterol and high density lipoprotein cholesterol did not explain more of the variability in any of the outcomes than did the change in low density lipoprotein cholesterol alone. For a 10 mg/dl (0.26 mmol/l) reduction in low density lipoprotein cholesterol, the relative risk reduction was 7.2% (95% confidence interval 3.1% to 11%; P=0.001) for coronary heart disease deaths, 7.1% (4.5% to 9.8%; P<0.001) for coronary heart disease events, and 4.4% (1.6% to 7.2%; P=0.002) for total deaths, when adjusted for change in high density lipoprotein cholesterol and drug class.

    To take into account non-lipid effects of specific drugs (such as potential pro-thrombotic effects of hormone therapy), we included a categorical variable of drug class in the meta-regression model and did a meta-regression analysis stratified by drug class. We used R2 to measure the proportion of the variability in the log risk ratio of an outcome explained by the statistical model.

    Similarly, we found no association between change in triglycerides and risk of coronary heart disease events whenever the model included an adjustment for the change in low density lipoprotein cholesterol (data available from the authors). Change in low density lipoprotein cholesterol, however, remained a significant predictor in a multivariable model adjusting for change in high density lipoprotein cholesterol, change in triglycerides, and class of intervention, with a 7.4% (4.4% to 10.4%; P <0.001) relative risk reduction for coronary heart disease events.
    http://www.ncbi.nlm….les/PMC2645847/

    2) A Mendelian Randomized Controlled Trial of Long Term Reduction in Low-Density Lipoprotein Cholesterol Beginning Early in Life

    Number of participants in meta-analysis = 1,003207 million

    Prolonged exposure to lower LDL-C beginning early in life associated with 3-fold greater clinical benefit for each unit lower LDL (1mmol/l) than treatment with a statin started later in life ( p = 0.00000000000000000843, Mean age at randomization in statin trials: 63 years;)

    Absence of Heterogeneity: Suggests the effect of each of included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL-C, rather than through some other pleiotropic effect.

    The increased clinical benefit associated with lowering LDL-C beginning early in life appears to be independent of the mechanism by which LDL-C is lowered. Diet and exercise are probably as effective as other therapies at reducing the risk of CHD (per unit reduction in LDL-C)

    3) "The most commonly used statins are off patent, which means the drug companies no longer have any financial incentive expanding the market. It's the medical community who is pushing for wider use of statins since they are convinced by the evidence this will reduce heart attacks and strokes in the future"

    –Peter Weissberg, British Heart Foundation

  54. Here’s a nice textbook on atherosclerosis:

    Dyslipidemia & Atherosclerosis Essentials (2009). The authors note that normal cholesterol in Americans is twice that of physiological levels. In the page 8 they have picture showing mean cholesterol levels in various hunter-gatherer groups (which are similar to those found in quasi-vegan agriculturalists in rural Asia, South-America and Afrika), wild primates and other mammals.

    Most people realize that blood pressure above 200% of physiologicl levels are harmfull. We also realize that BMI 50% over physiological levels can be harmfull as such. Dennis Minger is a denialist who thinks tht LDL -cholesterol levels 200% above physiological levels, the “normal” ,cannot be harmfull as such. According to her we need to explain heart disease through thyroid function & oxidation independent of elevated cholesterol. Big LOL!

    Dietary cholesterol oxidizes LDL:

    The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis.
    http://www.ncbi.nlm.nih.gov/pubmed/16270280

    Consumption of eggs with meals increases the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation
    http://www.ncbi.nlm.nih.gov/pubmed/9001684

    “Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels. Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies”.

    –Brown & Goldstein, Nobel lecture

    Of the various atherosclerotic risk factors, which one is an absolute prerequisite for development of atherosclerosis?

    “The answer is hypercholesterolemia. What level of total cholesterol and specifically LDL cholesterol is required for atherosclerotic plaques to develop? Symptomatic and fatal atherosclerosis is extremely uncommon in societies where serum total cholesterol levels are <150 mg/dL and serum LDL cholesterol levels are <100 mg/dL (8). If the LDL cholesterol level is <100— and possibly it needs to be 150 mg/dL and the LDL cholesterol is >100 mg/dL, the other risk factors clearly accelerate atherosclerosis”.

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1312295/

    Diagnostic Criteria for Dyslipidemia

    Low-density lipoprotein cholesterol (LDL-C) is identified in the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) report as the most abundant and clearly causal atherogenic lipoprotein on the basis of many observational and experimental studies over several decades.1 Guidelines from the American Association of Clinical Endocrinologists (AACE) are in agreement with NCEP ATP III that LDL-C is central in the diagnosis of dyslipidemia. Any LDL-C level above 100 mg/dL appears to promote atherogenesis”

    http://www.lipidu.com/Pillars.aspx?PillarID=2&ChildID=2

  55. This quote went in as erranous: here’s the correct citation

    Of the various atherosclerotic risk factors, which one is an absolute prerequisite for development of atherosclerosis?

    “The answer is hypercholesterolemia. What level of total cholesterol and specifically LDL cholesterol is required for atherosclerotic plaques to develop? Symptomatic and fatal atherosclerosis is extremely uncommon in societies where serum total cholesterol levels are <150 mg/dL and serum LDL cholesterol levels are <100 mg/dL (8). If the LDL cholesterol level is <100— and possibly it needs to be 150 mg/dL and the LDL cholesterol is >100 mg/dL, the other risk factors clearly accelerate atherosclerosis”.

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1312295/

  56. Very weird, the text still came as flawed. Hopefully this one works. If not check out the original source: P

    The answer is hypercholesterolemia. What level of total cholesterol and specifically LDL cholesterol is required for atherosclerotic plaques to develop? Symptomatic and fatal atherosclerosis is extremely uncommon in societies where serum total cholesterol levels are <150 mg/dL and serum LDL cholesterol levels are <100 mg/dL (8). If the LDL cholesterol level is <100— and possibly it needs to be 150 mg/dL and the LDL cholesterol is >100 mg/dL, the other risk factors clearly accelerate atherosclerosis.

  57. Extremely weird, but the this platform just screws the whole above citation. Minger, can you removed the above two posts. As everyone can see the tesxt is completely illogical because of the artificial cut-point of the text. Perhaps this happens because of the frequent use of symbols in the original text.

    “The answer is hypercholesterolemia. What level of total cholesterol and specifically LDL cholesterol is required for atherosclerotic plaques to develop? Symptomatic and fatal atherosclerosis is extremely uncommon in societies where serum total cholesterol levels are <150 mg/dL and serum LDL cholesterol levels are <100 mg/dL (8). If the LDL cholesterol level is <100 – and possibly it needs to be 150 mg/dL and the LDL cholesterol is >100 mg/dL, the other risk factors clearly accelerate atherosclerosis”.

  58. “A typical Western diet is rich in oxidized fats and therefore could contribute to the increased arterial atherosclerosis in our population”

    Thats very true. This supports low temperature cooking and avoiding excess PUFA consumption. How many healthy populations have a high consumption of PUFA’s, especially linoleic acid ?

    Cooking with vegetable oil is a bad idea.

    It’s worth noting that the Lyon diet heart study was the most successful CVD intervention of all time and serum lipids did not differ between the control group and intervention group.

    Focusing on biomarkers like LDL and total cholesterol may not be an optimal measure to prevent and reverse heart disease unless the levles are supraphysiological which could indicate FH or other diseases. Eating a diet rich in fruits, vegetables and quality meats and balancing the omega 3 to 6 ratio is a good enough intervention

    As Lalonde explains at the 3.30 mark, you can use drugs to lower LDL to really low levels but you can still get progression of atherosclerosis and the methods by which statins work when they do work is still up for debate. They have anti-inflammatory properties, antioxidant properties, anti-clotting properties and the interfere with Rho signalling.

  59. Lyon trial showed difference in LDL between intervention group and the control, this difference was very small, though. Not a single one participated in the Lyon intervention group had the progression of their coronary artery disease halted let alone regressed. What happened was that the disease progressed slower in the intervention group as opposed to control group. These are not really good results compared to the work of Ornish and Esselstyn, who is soon out with a larger study involving over 200 patients. Last, the Lyon intervention group based their diet in lacto-ovo-vegeterian style mediterranian diet rich in canola oil. This approach clashes pretty much 180-degree with approach chosen by the spindoctors around the internet, including Dennis Minger and yourself.

  60. If you can show me a (animal) model where coronary disease was regressed without the change in LDL, I’d like to see that, so far I’ve encountered on such papers.

  61. Great paper by O’Keefe and Loren Cordain.

    Optimal low-density lipoprotein is 50 to 70 mg/dl: Lower is better and physiologically normal
    http://www.sciencedirect.com/science/article/pii/S0735109704007168

    Good luck for those who’ve read the paleo-solution and think they can show off equally healthy metabolic-parameters as been observed in Hadza, f.ex. Eating meat in parasitic-rich, non-sanitized eco-niche is different than eating meat in an eco-niche where cholesterol lowering parasites do not exist.

    I am glad to know my diet has resulted in physiological LDL -cholesterol for me. Whole-food vegan diet seems to do the trick.

  62. “Lalonde explains at the 3.30 mark”….LOL

    The mean age of randomization in statin trials is 63-years of age. The mean lenght of the trial is 5-year. By the age of 63-year most hypolipidemic individuals have managed to accumulate an atherosclerotic burden where LDL-lowering drug theraphy alone may not be enough, especially if a potent statin is not used. Even though, potent statins can induce slight regression in the plaque and change its composure from more lipid-dense to more fibrous and calficied, the plaque even when smaller and more stabile can cause a ruprure in these people. In order to tackle the residual risk, health bureacrats want people to start taking statins earlier. Because the benefits of LDL-lowering theraphy depends on both magnitude and durance.

    Cholesterol Treatment Trialists’ (CTT) Collaborators. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet 2012;380:581–90

    Give statins to all over-50s: Even the healthy should take heart drug, says British expert
    http://www.dailymail.co.uk/health/article-2194892/All-50s-statins-regardless-health-history-says-Oxford-professor.html

    When you keep your LDL-low throughout the life you get more benefits than statins can give when started at the mean age of 63. (60% reduction per each 1mmol/l reduction in LDL-fraction as opposed to 20% reduction with a statin)

    A Mendelian Randomized Controlled Trial of Long Term Reduction in Low-Density Lipoprotein Cholesterol Beginning Early in Life

    Number of participants in meta-analysis = 1,003207 million

    Prolonged exposure to lower LDL-C beginning early in life associated with 3-fold greater clinical benefit for each unit lower LDL (1mmol/l) than treatment with a statin started later in life ( p = 0.00000000000000000843, Mean age at randomization in statin trials: 63 years;)

    Absence of Heterogeneity: Suggests the effect of each of included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL-C, rather than through some other pleiotropic effect.

    The increased clinical benefit associated with lowering LDL-C beginning early in life appears to be independent of the mechanism by which LDL-C is lowered. Diet and exercise are probably as effective as other therapies at reducing the risk of CHD (per unit reduction in LDL-C)

  63. Actually the thing that makes the lyon diet heart study unique is that it reduced lionoleic acid consumption to minimal levels. I’m sure denise and many others would agree that this is a good idea. The intervention group also ate fruits, vegetables, poultry and fish. I don’t see a major clash.

    What do you think about the rose corn oil trial ?

    “Eighty patients with ischaemic heart disease were allocated
    randomly to three treatment groups. The first was a control
    group. The second received a supplement of olive oil with
    restriction of animal fat. The third received corn oil with
    restriction of animal fat. The serum-cholesterol levels fell in
    the corn-oil group, but by the end of two years the proportions
    of patients remaining alive and free of reinfarction (fatal or
    non-fatal) were 75 %, 57 %, and 52 % in the three groups respectively”

    Does saturated fat increase LDL number in the long term ?

    “The low-carbohydrate group had a lower
    intake of carbohydrates (P<0.001) and higher
    intakes of protein (P<0.001), total fat (P<0.001),
    saturated fat (P<0.001), and total cholesterol
    (P = 0.04) than the other groups."

    What happened to their lipids by the end of the study ?

    After 6 months LDL levels were higher in the low carb group but by 24 months they dropped.

    The authors conclude

    "Mediterranean and low-carbohydrate diets may be effective alternatives to low-fat diets. The more favorable effects on lipids (with the low-carbohydrate diet) and on glycemic control (with the Mediterranean diet) suggest that personal preferences and metabolic considerations might inform individualized tailoring of dietary interventions."

    There is a reason why harvard now agree that saturated fats are not the problem. Taking all the observational studies and RC'sT into account, saturated fats do not cause dyslipidemia and dietary interventions should now focus on the reduction of refined carbohydrates and reduction in central adiposity.

  64. “Thus, although recommendations to replace SFA with PUFA appear appropriate, the much larger CVD burdens caused by other dietary factors (e.g., low omega-3, low fruits and vegetables, high trans fat, and high salt appear to warrant much more attention”

    Dariush Mozafarrian

    I very much agree with this except the evidence supporting substituting SFA for PUFA is far from conclusive as shown in a 2010 christopher ramsden paper

  65. There are some preliminary evidence that oils can induce heart disease with a mechanism that the LDL-cholesterol (and HDL) fail to track. Pay attention that not all heart disease is of atherosclerotic in origin, although most are.

    As Bill Roberts, the editor in chief of American Journal of Cardiology put it:

    “….The lower the LDL cholesterol the better, and this principle has been established repeatedly despite the voices of the anticholesterol, antistatin fallacy mongers! It’s the cholesterol, stupid!”
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3012294/

  66. “I don’t see a major clash”

    Really? You don’t see the hefty use of canola oil-laden margharines and the removal of SFA’s such as butter as a major clash to the recommendations made by the spin-doctors? And, no the intervention group in Lyon did not consume heart-disease causing palm and coconut oils recommended by Minger.

    1) Differences in all-cause, cardiovascular and cancer mortality between Hong Kong and Singapore: role of nutrition.

    “The ratio of animal to vegetal fat was higher in Singapore (2.24) than in Hong Kong (1.08). Singapore had higher serum concentrations of total cholesterol and low-density lipoprotein cholesterol than Hong Kong, but the opposite result was observed for high-density lipoprotein cholesterol”.

    “There are striking differences in all-cause and cardiovascular mortality between Hong Kong and Singapore. These differences can be most reasonably and plausibly explained by their differences in dietary habits, for example, a higher consumption of coconut and palm oil, mainly containing saturated fat, in Singapore”

    http://www.ncbi.nlm.nih.gov/pubmed/11855581

    2) Consumption of omega-3 fatty acids is not associated with a reduction in carotid atherosclerosis: the Genetics of Coronary Artery Disease in Alaska Natives study

    “Dietary intake of omega-3 FAs in a moderate-to-high range does not appear to be associated with reduced plaque, but is negatively associated with IMT. The presence and extent of carotid atherosclerosis among Eskimos is higher with increasing consumption of saturated FAs”.

    http://www.ncbi.nlm.nih.gov/pubmed/18054937

  67. In response to the hong kong and singapore study

    http://www.ncbi.nlm.nih.gov/pubmed/9066473

    “•
    Mortality from coronary heart disease in 50-54 year old men is four times higher in Lithuania than in Sweden


    Differences in traditional risk factors for coronary heart disease in 50 year old men in LinkÖping (Sweden) and Vilnius (Lithuania) were small–systolic blood pressure was higher in men from Vilnius, but total and low density lipoprotein cholesterol concentrations were lower and smoking habits similar


    The resistance of low density lipoprotein to oxidation was lower in men from Vilnius and remained after adjustment for antioxidant vitamin concentrations


    Plasma concentrations of the antioxidant vitamins, ß carotene, lycopene, and lipid adjusted tocopherol were lower in men from Vilnius; tocopherol did not differ

    Mechanisms related to antioxidant state may be important in explaining the much higher mortality from coronary heart disease in Lithuanian compared with Swedish middle aged men”

    Do you buy Esselstyn’s argument that you are heart attack proof below 150 ?

  68. A huge blow to cholesterol nihilist. No matter what the mechanism is used, they all work differently in lowering circulative LDL-C in serum, however the end result is highly identical.

    Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease
    A Mendelian Randomization Analysis

    Results: All 9 polymorphisms were associated with a highly consistent reduction in the risk of CHD per unit lower LDL-C, with no evidence of heterogeneity of effect (I2 = 0.0%). In a meta-analysis combining nonoverlapping data from 312,321 participants, naturally random allocation to long-term exposure to lower LDL-C was associated with a 54.5% (95% confidence interval: 48.8% to 59.5%) reduction in the risk of CHD for each mmol/l (38.7 mg/dl) lower LDL-C. This represents a 3-fold greater reduction in the risk of CHD per unit lower LDL-C than that observed during treatment with a statin started later in life (p = 8.43 × 10−19).

    Conclusions: Prolonged exposure to lower LDL-C beginning early in life is associated with a substantially greater reduction in the risk of CHD than the current practice of lowering LDL-C beginning later in life.

    Importantly, we evaluated 9 polymorphisms located in 6 different genes, including polymorphisms in the genes that encode for the targets of both statins and monoclonal antibodies directed against PCSK9. Although each of these polymorphisms presumably affects circulating LDL-C levels by a different mechanism, and the per-allele effect of these SNPs on LDL-C levels varied by more than 6-fold; all 9 polymorphisms were associated with a highly consistent reduction in the risk of CHD when measured per unit lower LDL-C. This finding suggests that the effect of long-term exposure to lower LDL-C on the risk of CHD appears to be independent of the mechanism by which LDL-C is lowered. Therefore, the method of lowering LDL-C is likely to be less important than the magnitude and timing of LDL-C reduction. As a result, diet and exercise are probably as effective at reducing the risk of CHD as are statins or other treatments that lower LDL-C when started early in life (and when measured per unit lower LDL-C).
    http://content.onlinejacc.org/article.aspx?articleid=1379036

    Do I buy Esselstyns idea? Esselstyn hasn’t come up with any ideas of heart disease immunity with TC cholesterol under 150, kept consistently! This is what biomedical community at large maintains, he merely echoes the message. This not about buing, this is about consistency of evidence, science that is. Atherosclerosis is a cholesterol problem, and when cholesterol levels are maintained low (TC cholesterol under 150 and LDL preferably under 80) the disease cannot iniate or progress despite of glucose abnormalities, cigarette smoking, stress, etc. They factors can only exacerbate the problem, not cause the artery disease.

    National Cholesterol Education Program, ATP- third expert panel:

    “Only populations that maintain very low levels of serum cholesterol, eg. total cholesterol below 150mg/dl throughout the life do we see a near-absence of clinical CHD”.

    “Any LDL cholesterol above 100 mg/dL appears to be atherogenic”

    http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf

    Diagnostic Criteria for Dyslipidemia

    “Low-density lipoprotein cholesterol (LDL-C) is identified in the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) report as the most abundant and clearly causal atherogenic lipoprotein on the basis of many observational and experimental studies over several decades.1 Guidelines from the American Association of Clinical Endocrinologists (AACE) are in agreement with NCEP ATP III that LDL-C is central in the diagnosis of dyslipidemia. Any LDL-C level above 100 mg/dL appears to promote atherogenesis”

    http://www.lipidu.com/Pillars.aspx?PillarID=2&ChildID=2

    1) This great review discusses eloquently how unadjustment for regression dilution (systematic error) has failed to show the real association of serum cholesterol concentrations to coronary heart disease in many uniformly high-risk Western cohorts characterized by very high population-wide cholesterol concentrations.
    http://aje.oxfordjournals.org/content/150/4/341.full.pdf

    2) High quality prospective cohorts which have corrected for regression dilution bias have firmly establish the independent, continuous, positive and log-linear nature of the associations between TC cholesterol and both CHD and Ischemic stoke even within population that have low serum cholesterol concentrations to begin with!

    Cholesterol, coronary heart disease, and stroke in the Asia Pacific region

    “Numerous other observational studies, particularly in men, have demonstrated a strong, continuous, graded, and independent association between cholesterol and the risk of CHD.1–,6 The current data clearly extend these findings to Asian populations with substantially lower average levels of cholesterol, and confirm that effects are similar in men and women”

    http://ije.oxfordjournals.org/content/32/4/563.long
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1670480/?page=1

    3) Elevated total cholesterol: its prevalence and population attributable fraction for mortality from coronary heart disease and ischaemic stroke in the Asia-Pacific region.

    “Conventional methods for estimating disease burden severely underestimate the effect of TC. Cholesterol-lowering strategies could have a tremendous effect in reducing cardiovascular deaths in this populous region”

    http://www.ncbi.nlm.nih.gov/pubmed/18677162

  69. Cholesterol denialist refer to cross-sectional studies and observational studies on saturated fat and serum lipids, the nonsense often mentioned by the denialists were already refuted several decades ago.

    It was estimated over four decades ago that in order to estimate within 20% of the actual dietary intake, there is a requirement of at least 22 days of 24-hour dietary recalls for saturated fat. Inaccurately measuring intraindividual variation has been shown to lead to a miss-classification of subjects into ranges of usual dietary intakes, and biasing correlation coefficients towards null. The majority of the observational studies cited by denialists used single 24-hour dietary recalls and therefore a null association between saturated fat and serum cholesterol is to be expected. Furthermore, the denialists often fail to cite numerous observational studies that used higher quality dietary measurement methods with a larger participant size that found a positive association between saturated fat and serum cholesterol.

    Another issue with the observational studies that you and others have cited is that many only used single measurements of serum cholesterol. Several measurements of serum cholesterol are required to measure mean cholesterol due to the substantial intraindividual variation in concentrations, and therefore would have likely biased the association between saturated fat and serum cholesterol towards null.

    One more major issue with observational studies, as was noted in the Chicago Western Electric Company study is that the cross-sectional association between saturated fat and serum cholesterol can be biased towards the opposite direction due to participants lowering intake of saturated fat in response to elevated serum cholesterol, which is similar to the “sick quitter effect”, this would have likely biased the association between saturated fat and coronary heart disease towards null in meta-analyses of prospective studies.

    http://ajcn.nutrition.org/content/24/3/304.full.pdf
    http://ajcn.nutrition.org/content/37/6/986.full.pdf
    http://www.ncbi.nlm.nih.gov/pubmed/7041632
    http://ajcn.nutrition.org/content/65/5/1597S.full.pdf
    http://www.ncbi.nlm.nih.gov/pubmed/17982164

    Cholesterol denialists try to mislead their readers into believing that a hand-full of poor quality cross-sectional studies are more informative to address the association between saturated fat and serum cholesterol than that of hundreds of controlled feeding trials which have produced an irrefutable strong positive association.

    Now, are suggesting to me that people in Lithuania with mean LDL -choelsterol of 127mg/dl had healthy, physiological cholesterol levels to begin with? In fact the LDL-fraction of the Lithuanian men was about 200% above what is physiologically normal LDL cholesterol present in healthy neonates, wild mammalians who not develope atherosclerosis and among people living in societies where chronic disease are near absent.

  70. Anyways,

    couple word about your Sweden-Lithuania paper. Both cultures had huge amount of CHD. The fact that Lithuania had lot more, was because people, especially men in post-Communist socities live more plaque-rupture prone lifestyle, alcoholism, stress, lack of medical care, (and perhaps a poor antioxidant status). Moreover, th cross-sectional study did not even control the amount of care received by Swedish high risk patients, assuming that most poor high risk Lithuan were left out from such medical care.

    Instead of uniformly high risk cross-sectional studies from Western societies where non-physiological cholesterol concentration are the norm, I find studies on low-risk people much more beneficial from the standpoint of healthy lifestyle decisions.

    Studying pooulation with very low serum cholesterol concentration as a baseline, Campbell and Junshi (1994) reported that the chief correlate to all diseases of affluence was elavated TC cholesterol (p = 0.01), which in turn was associated with intake of meat & total fat and inversely associated with intake of legumes and certain fiber extractions
    http://ajcn.nutrition.org/content/59/5/1153S.full.pdf+html

  71. Cholesterol theory is one of the few theories in medicine which is bullet-proof.

    In fact it would not even require much evidence. LDL -cholesterol levels over 200% above to what is physiologically normal is a norm in Western socities. By physiological levels is meant by those LDL- levels which are seen in healthy neonates, all wild mammalians who do not develope atherosclerosis and members in socities where chronic disease including atherosclerosis is near absent.

    Normal, non-retarded humans are perfectly able to gather that blood-pressure or BMI above 200% of the physiological norm is harmfull. Normal non-retarded people are also able to conclude and deduce that LDL +200% above to what is physiologically normal cannot be too good.

    IMO very good paper by O’Keefe and Loren Cordain:

    Optimal low-density lipoprotein is 50 to 70 mg/dl: Lower is better and physiologically normal

    “People with heterozygous hypobetalipoproteinemia have total cholesterol levels as low as 80 mg/dl and LDL cholesterol levels as low as 30 mg/dl (30). This condition is associated with longevity (31), presumably due to the absence of atherosclerosis, but the lack of other adverse effects that might have accompanied a low LDL level suggests that such low levels of LDL are safe”.

    http://content.onlinejacc.org/article.aspx?articleid=1135650

  72. Is this the same T colin campbell who said

    “The highest blood cholesterol levels in the Chinese were associated with DHA and fish consumption but with the lowest risk of heart disease”

    and

    “it is the largely vegetarian, inland communities who have the greatest all risk mortalities and morbidities and who have the lowest LDL cholesterols”

    Why don’t you post this kind of stuf on masterjohn’s blog ? You will probably get a much better debate out of him

  73. LOL! Cholesterol denialists haven’t advanced much from the 1970.s. All risk mortality in China correlated with wealth and access to antiobiotics, well sanitized loo’s and health care. All that was lacking in the plant-based rural parts where LDL levels were low. The idea of China Study was not to study all-cause mortality but diseases of affluence. In other words, the scholars weren’t too interested in 12-girls with low cholesterol dying because of infection. This because of diet had no role in it. Lack of antibiotics had.

    High fish consumption protects high risk communities. The benefits of fish consumption becomes less clear in low-risk groups.

    “Shekelle et al. [382] reported a significant inverse correlation between fish consumption and 25 year CHD mortality in Chicago. This also appeared to be independent of other risk factors (The 30-year follow up of this cohort, with the same overall result was reported in detail in 1997) [383]. Eleven cohort studies had reported by the end of the century. They were critically reviewed by Marckmann and Gronbaek [384], who concluded: “Of 4 studies judged to be of high quality, the 2 largest were performed in populations at low risk of CHD. They found no protective effect of fish consumption. The other two high-quality studies were relatively small and included individuals at higher risk. They found an inverse relationship between fish consumption and CHD death, suggesting that 40–60 g fish/day is optimal and associated with a risk reduction of 40–60%. Results of 4 studies of intermediate quality support that fish consumption is inversely associated with CHD mortality in high-risk populations only”

    Stewart Truswell., Cholesterol & Beyond (textbook)

    If you are worried about LDL peroxidation as Masterjohn is, I advice a cut on the fish department

    Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in eastern Finnish men

    “These data suggest that a high intake of mercury from nonfatty freshwater fish and the consequent accumulation of mercury in the body are associated with an excess risk of AMI as well as death from CHD, CVD, and any cause in Eastern Finnish men and this increased risk may be due to the promotion of lipid peroxidation by mercury”

    http://www.ncbi.nlm.nih.gov/pubmed/7828289

  74. Arterial endothelial dysfunction in baboons fed a high-cholesterol, high-fat diet

    “In summary, our results clearly show that the HCHF (high cholesterol and high fat) diet resulted not only in increased serum cholesterol concentrations but also in inflammation and endothelial dysfunction”

    http://www.ncbi.nlm.nih.gov/pubmed/16210703

  75. Passwater: Is it accurate to say that only oxidized-LDL starts the plaque process?

    Steinberg: No, it seems to me very likely that other modified forms of LDL are involved in plaque formation. What we know so far is that the use of antioxidants can decrease the rate of progression of lesions by 50-80%. That would speak to a major involvement of oxidation, but other things can also lead to foam cell formation. Studies by Dr. John C. Khoo in my laboratory have shown that aggregation of LDL with itself markedly increases the rate of uptake by macrophages. [15] The uptake in that case occurs by way of the native LDL receptor, not the acetyl LDL receptor or oxidized LDL receptor.

    Studies by Drs. J. S. Frank and A. M. Fogelman at UCLA have demonstrated the generation LDL aggregates in the subendothelial space. [16] Aggregation does not depend upon prior oxidative modification. So here is a quite distinct mechanism by which LDL uptake into the macrophages can be accelerated and can perhaps initiate the fatty streak lesion.

    Studies by Dr. Joseph L. Witztum and others in our laboratory have shown that minor modifications in the structure of LDL can render it immunogenic. Autoantibodies against oxidized LDL have been demonstrated in rabbits and in humans as well. Therefore, a complex of a modified LDL particle and an antibody against it can be taken up into macrophages by way of a completely different receptor, the receptor for immunoglobulins (the FC receptor).

    So, there are at least two or three alternative modifications of LDL that could account for foam cell formation. These have not yet been studied in vivo as intensively as oxidative modification, and so we are not in a position to say with any confidence how important they may be.

    http://www.healthy.net/scr/interview.aspx?Id=197

  76. Richard,

    You should really write these to your own blog / free-online-book. This is great work you are doing. I just wonder how somebody manage to write so much! Keep up the great work! Example blogspot.com is great and very simple platform.

  77. Bill,

    In the other hand there’s Peter Attila, who has studied lipids 9 months, saying “All cholesterol is good!” and in the other hand there’s T. Colin Campell proving with the best studies in nutrition world that cholesterol kills… hmm wonder who’s right.

  78. Thanks Toni,

    why would anyone listen to denialists spindoctors such as Masterjohn or P. Attia who aim to confuse and sabotage the truth around cholesterol and heart disease by spreading infantile nonsense that everyone abobe the age 12 can easily debunk by using google, when one can just listen real scientists who do actual research on the given topic. Daniel Steinberg has authored over 400 articles on cholesterol metabolism and served in several expert panels and review board of scientific journals.

    Anyways, that was great interview with Steinberg who revealed us that oxidized LDL is just one form of modication process that can ininiate the foam cell formation together with the two of three additional modification process where one is simply the aggregation of LDL with itself.

  79. Cholesterol denialists such as Denise Minger/Colpo/Masterjohn/Guyenet wants mislead our attention from a meta-analysis regression curve consisting of 108 randomized controlled trials showing that lowering LDL cholesterol significantly reduces coronary events and all cause mortality independent of changes in triglycerides, HDL or the non-lipid lowering effects of various drugs to a epidemiologic studies that are either cross-sectional and suffer from a signficant regression dilution bias and/or or show major weakness in the form of imprecise dietary assessment methods without even mentation the limitations and shortcomings of these kind of studies. In short, denialists often recite studies without a discussion about the methdologic strenght/weakness inherent in these studies and thus confuse their readers into believing that all studies are made equal.

    Moreover, denialists such as Denise Minger/Guyenet wants to confuse their audience into believing that TC cholesterol as risk marker is not relevant by citing studies that are cross-sectional by nature and suffer from a signficant regression dilution bias. Simultaneously, the cholesterol denialists miss the opportunity of discussing studies that have used superior methodology by adjusting for regression dilution bias and showed a powerfull, consistent, independent, positive and log-linear association of TC cholesterol and coronary heart disease and ischemic stroke, even within populations that have very low cholesterol as baseline compared to high risk Western populations.

    Lastly, cholesterol denialists such Denise Minger fail to discuss the evidence from mendelian randomized controlled trials consisting over the one million people that have showed highly consistent and major reduction in coronary heart disease risk, independent of mechanism by which LDL cholesterol is lowered, in people who’ve born and maintained low LDL cholesterol levels throughout the life, without showing any other inherent differences in other biomarkers.

    Finally, cholesterol denialist like Denise Minger wants to confuse her readers into believing that thyroid dysfunction is a root cause for coronary heart disease independent of cholesterol levels (eventhough elevated cholesterol are part of the pathology of thyroid malfunction) without the evidence from high quality prospective cohorts that would indicate that the majority of coronary heart disease patients FIRST developed thyroid dysfunction prior to the diagnosed heart disease. The lack of such evidence from high quality prospective cohort studies consisting millions of people, and showing the independent and causal nature of elevated cholesterol to coronary heart disease risk, strongly indicates that Denise Minger utilizes the common tactiques of denialists as described by Diethelm (2009)
    http://eurpub.oxfordjournals.org/content/19/1/2.full

    References:

    http://content.onlinejacc.org/article.aspx?articleid=1379036
    http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60312-2/abstract
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/pdf/bmj.b92.pdf
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2988224/
    http://circ.ahajournals.org/content/118/6/672.long
    http://www.thelancet.com/journals/lancet/article/PIIS0140673607617784/abstract
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3284229/
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1488755/
    http://www.ncbi.nlm.nih.gov/pubmed/19349632
    http://ije.oxfordjournals.org/content/32/4/563.long
    http://www.ncbi.nlm.nih.gov/pubmed/18677162

  80. Couple typing and grammatical errors there. English not my first language, anyways, I am sure the message will be understood by those who do not posses the typical denialist/crank psyche.

  81. Continues…

    Elevated LDL cholesterol induces atherosclerosis and coronary artery disease mortality in every mammalian specimen (birds and insects included). Humans in Western societies typically show LDL cholesterol levels that are +200% above to what is physiologic, that is, levels that has been observed in a) free-ranging mammalians that do not develop atherosclerosis, b) healthy neonates and c) members living in societies where chronic disease including atherosclerosis is near-absent.

    In free-ranging non-human primates, consuming only food founds in their natural habitat higher cholesterol concentrations (LDL > 70mg/dl) have been associated with atherosclerosis despite having cholesterol concentrations that are much lower than in humans living in Western societies and despite consuming a diet rich in antioxidants.

    Perhaps the considerations expressed above influenced this article, published in a peer-reviewed scientific journal.

    Cholesterol myth club on par with flat earth society
    http://www.ncbi.nlm.nih.gov/pubmed/2296560

    Dennis Minger does not want to share the opportunity for her readers to find about the +100 hundred experiments demonstrating that dietary cholesterol induces experimental atherosclerosis in virtually any animal model that it elevates serum cholesterol in, even when the elevation is considered to be small, this includes omnivorous non-human primates. There was no evidence of a threshold for dietary cholesterol with respect to an adverse effect on arteries. This persisted even when researchers made sure that micronutrient intake requirements were being met.

    Dennis Minger who is mentally invested in the appeal-to-nature fallacy, is suggesting that virtually all the major health authorities around the world who warn against the dangers of dietary cholesterol, saturated fatty acids and elevated serum LDL concentrations are participating in a worldwide conspiracy. For Denise Minger, LDL cholesterol level that is +200% above to what is biologically normal and (unfortunately) a norm in societies where saturated fats and dietary cholesterol are customarily ingested in every meal, cannot cause harm as such. Her arguments are based on imaginary science and denialism, shunning the evidence from over one hundred randomized controlled trials and animal models.

    1. Richard, the article ‘Cholesterol myth club on par with flat earth society’ may have been published in a ‘peer-reviewed scientific journal,’ but it’s an editorial . . . written by a medical student . . . in 1990.

      Your skepticism is healthy, however I do not understand why a) you make your attacks so personal (it really detracts from your arguments) b) you use such lousy references and bad science to support your arguments. If the question were so clear cut, you wouldn’t have to and c) if you are indeed a man of science, I don’t understand how you can be so confident that you are right. Scientific understanding, particularly where it comes to health and disease, is changing literally all the time. In my experience, the key attribute that separates the truly scientific mind from the angry amateur is humility. After all, we’re all trying to explain something that none of us fully understands.

  82. @melkoppelman

    I don’t need humility nor patience since I am not pushing a fringe beliefs in regards to first class theories that are globally accepted by every major health organization. Thus, it’s clear that I can afford to be more confident than cholesterol denialists such as Denise Minger who advocate the consumption saturated fat laden trophical oils for vegans.

    Please, provide a detailed explanation why my references are lousy. My references include a) meta-analysis regression curve consisting of 108 randomized controlled trials showing that lowering LDL cholesterol significantly reduces coronary events and all cause mortality independent of changes in triglycerides, HDL or the non-lipid lowering effects of various drugs, b) high quality prospective cohort studies including millions of participants showing a positive, independent and log-linear association of TC cholesterol and coronary heart disease and ischemic stroke even within population with very low serum cholesterol levels as the baseline, c) mendelian randomized controllod trials consisting over million people showing the causal nature of LDL cholesterol to coronary heart disease risk, and d) evidence from over 100 experimental models, including evidence from omnivorous non-human primates, demonstrating that dietary cholesterol induces experimental atherosclerosis in virtually any animal model that it elevates serum cholesterol in, even when the elevation is considered to be small. In addition, my sources include the findings from Campbell and Junshi (1994) showing that elevated TC cholesterol is the most important correlate to all chronic disease (p=0.01) in a low-risk population with low serum cholesterol concentrations as the baseline.

    I am not angry I simply try to do atleast 0.01% of that what Dennis did to Colin T Campbell.

    Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease:

    Number of participants in meta-analysis = 1,003,207

    Prolonged exposure to lower LDL-C beginning early in life associated with 3-fold greater clinical benefit for each unit lower LDL (1mmol/l) than treatment with a statin started later in life (Mean age at randomization in statin trials: 63 years; p = 0.00000000000000000843)

    Absence of Heterogeneity: Suggests the effect of each of included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL-C, rather than through some other pleiotropic effect.

    The increased clinical benefit associated with lowering LDL-C beginning early in life appears to be independent of the mechanism by which LDL-C is lowered. Diet and exercise are probably as effective as other therapies at reducing the risk of CHD (per unit reduction in LDL-C)

    http://content.onlinejacc.org/article.aspx?articleid=1379036

    1. Hi Richard,

      I think the biggest issue I have with your references (aside from you citing them inconsistently, it’s helpful to start with the author and year so everyone is singing from the same hymn sheet, or at least this is generally how it’s done int he academic community), is relevance. Most of your references seem to link high LDL and heart disease. I may have missed it, but I didn’t see where in this article Denise claims otherwise. If she’s done so elsewhere, I’d love to see what she says accurately quoted and in context.

      What most of your references do not do is link the diet advice that Minger actually recommends to elevated cholesterol or, more importantly, CVD, in any convincing way. This is a diet blog, after all. You realize that dietary cholesterol has very little effect on serum cholesterol? I’m pretty sure at this point (2012), you’d no longer considered this a ‘fringe belief’?

      I’m sure some of your points are valid but their effect gets lost in your misquoting and ranting. Is your point that a vegan diet is safer or better for your health than an omnivorous diet?

      1. The impact of dietary cholesterol to serum lipids is not pronounced for most people who already have suprafysiologic levels to begin with. Dietary cholesterol as a dose-dependent, linear relationship to serum lipids for all who follow low-cholesterol diets. This is a well established fact. Moreover, there’s evidence showing that dietary cholesterol damages arteries independently of their effect to serum lipids. To make a case for dietary cholestrol and pretending its health promoting substance for humans is nothing pushing fringe beliefs.

        1. Dietary cholesterol has a dose-dependent…

          To make a case for dietary cholestrol and pretending its health promoting substance for humans is nothing BUT pushing fringe beliefs.

  83. According to Denise Minger, Caldwell Esselstyn shoul’ve focused in raising the HDL in his patients. Denise Minger, mentally invested in the appeal-to-nature fallacy, clearly forgor her “correlation is not causation” mantra. While HDL function may be causally related to coronary heart disease (still unclear) there’s no indication that HDL volume is.

    The causal nature of LDL cholesterol volume was established not only in meta-analysis regression curve consisting of 108 randomized controlled trials showing that lowering LDL cholesterol significantly reduces coronary events and all cause mortality independent of changes in triglycerides, HDL or the non-lipid lowering effects of various drugs and high quality prospective cohort studies including millions of participants showing a positive, independent and log-linear association of TC cholesterol and coronary heart disease and ischemic stroke (starting from somewhere around 3.2mmol/l/122mg/dl) even within population with very low serum cholesterol levels as the baseline, but also in mendelian randomized controlled trials consisting of over million genotypes and showing 55% reduction for heart disease per every 1mmol/l (38mg/dl) reduction in LDL fraction beginning early in life. The independence of mechanism (each of the studied mutations in different SNPs lower LDL with different mechanism) and lack of heteogenity suggest that dietary patterns and excerise have similar effect.

    While similar mendelian randomized trial was performed on HDL cholesterol, what happened? No indication of causality.

    CONCLUSION: “Some genetic mechanisms that raise plasma HDL cholesterol do not seem to lower risk of myocardial infarction. These data challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction”.

    http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60312-2/abstract

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