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Coconut Oil

In a former life, when I was an Air Force doctor, one of my duties was to give “Healthy Heart” briefings with a script furnished by Air Force experts. It covered the scientific consensus of the time (the early 80s) about diet. It recommended a low fat diet, restricted cholesterol and saturated fat, and demonized tropical oils like palm oil and coconut oil. (Trans fats weren’t yet on the agenda.)

Times have changed. Today we are more lenient about cholesterol in the diet, less concerned about total fat and saturated fat, and more concerned about trans fats. While many major health organizations still discourage its use, coconut oil has not only been rehabilitated in the public mind, but all kinds of health benefits are being claimed for it.

The fats in coconut oil
Coconut oil is high in saturated fats; it contains more saturated fatty acids than any other non-hydrogenated oil. It is stable and has a long shelf life. It is used in movie theaters to pop popcorn and in South Asian cuisine for dishes like curries. A hydrogenated version of coconut oil is an ingredient in non-dairy creamers. Much of the research done on coconut oil studied hydrogenated or partially hydrogenated forms. According to an article in the New York Times:

Partial hydrogenation creates dreaded trans fats. It also destroys many of the good essential fatty acids, antioxidants and other positive components present in virgin coconut oil. And while it’s true that most of the fats in virgin coconut oil are saturated, opinions are changing on whether saturated fats are the arterial villains they were made out to be. “I think we in the nutrition field are beginning to say that saturated fats are not so bad, and the evidence that said they were is not so strong,” Dr. Brenna said.

Coconut oil contains lauric acid, which raises both HDL and LDL cholesterol levels. This may improve the cholesterol profile, although there are concerns that it may promote atherosclerosis by other means. Virgin coconut oil contains medium-chain triglycerides, which are not as risky as some other saturated fats.

Health Claims
Any number of health claims have been made for lauric acid. According to proponents, it’s a wonder substance with possible antibacterial, antimicrobial, antiviral properties that could also, in theory, combat HIV, clear up acne and speed up your metabolism. Researchers are skeptical:

“There are a lot of claims that coconut oil may have health benefits, but there is no concrete scientific data yet to support this,” said Dr. Daniel Hwang, a research molecular biologist specializing in lauric acid at the Western Human Nutrition Research Center at the University of California, Davis.

The hype comes from unreliable sources. Joe Mercola says it is the smartest choice for cooking, is good for your heart, contains the kind of fat found in mothers’ milk, enhances immunity, and helps with weight loss by stimulating metabolism. And of course he sells it. Dr. Oz says it is a heart healthy food that helps resist viruses, bacteria, yeast, fungi, and candida; boosts thyroid function; improves blood sugar control and reduces the need for insulin; increases energy and endurance; increases digestion and improves absorption of vitamins; lowers cholesterol; helps control weight; has anti-aging effects; is good for skin and hair; and is quite safe to take in reasonable amounts. The Wellness Mama website lists 101 uses for coconut oil, including treating sunburns, athlete’s foot, Alzheimer’s disease, nasal allergies, arthritis, insomnia, autism, heartburn, hemorrhoids, depression, acne, cellulite, mosquito bites, and lice.

Alzheimer’s Disease
The Wellness Mama website provides a link to a reference for Alzheimer’s disease but it is only a case study showing that the writer’s husband improved and was able to draw a more accurate picture of a clock after adding coconut oil to his diet. Natural News says coconut oil can prevent and reverse Alzheimer’s. Naturopath Bruce Fife has several books touting the benefits of coconut oil and coconut water. One title claims you can “Stop Alzheimer’s Now!”

A clinical query search for “Alzheimer’s coconut oil” on PubMed yielded no results. Snopes has evaluated the claims for coconut oil and agrees that “there are no peer-reviewed articles addressing research on coconut oil as a treatment for Alzheimer’s disease.” Even the Alzheimer’s Association says: “A few people have reported that coconut oil helped the person with Alzheimer’s, but there’s never been any clinical testing of coconut oil for Alzheimer’s, and there’s no scientific evidence that it helps.”

Coconut water
The liquid inside a coconut is being promoted as a sports drink and as a miracle food. They claim it is so compatible with the human body that it can be infused directly into the bloodstream (indeed, it is likely sterile and there are reports of its use as an intravenous fluid substitute in emergencies when medical saline was unavailable). As with coconut oil, there are a few suggestive studies in animals and test tubes, but no credible evidence for clinical benefits in humans.

Conclusion
Coconut oil is probably not as bad as once thought, but it’s no “miracle” food either. It is probably safe to use it in reasonable amounts to replace other oils in the diet, and doing so may have a favorable effect on lipid profiles; but it’s not clear whether that will actually reduce the risk of cardiovascular events. There is no justification for adding it to the diet on top of the usual consumption of other fats. There is no credible evidence to support any of the many health benefits claimed for using it as a supplement.

Posted in: Herbs & Supplements, Nutrition

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143 thoughts on “Coconut Oil

  1. TsuDhoNimh says:

    (indeed, it is likely sterile and there are reports of its use as an intravenous fluid substitute in emergencies when medical saline was unavailable)

    My dad, a combat medic in WWII, sometimes used it as a wound wash because it was a lot cleaner than the water they usually had available. That doesn’t make it a wonder-drug, it merely makes it an adequate emergency substitute for something.

    ========
    It’s a very nice hair conditioner. So is Pantene!

    1. Cheryl says:

      What HARMFUL CHEMICALS are in Pantene though?

      1. WilliamLawrenceUtridge says:

        Are there any? Most ingredients in cosmetics are tested.

  2. elburto says:

    Coconut oil is the new Tea Tree oil- lots of grand claims of ‘miraculous properties’ without the hard data to back it up.

    However, it smells lovely, makes a great skin and hair moisturiser, and is a very good lubricant.

    For fun I recommend going onto Amazon and reading reviews/testimonials for various brands of coconut oil. Some of the claims made are hilarious!

  3. goodnightirene says:

    “…may have a favorable effect on lipid profiles.”

    I improved my lipid profile substantially–by losing 40 lbs–by eating sensibly and reducing my caloric intake (I was already exercising and eating a decent diet). Lowered my bp and normalized my glucose as well. There’s little room for fat in my world and I limit it to painfully small amounts of olive oil or peanut butter.

    No matter how many idiotic diet books are touted to “speed up metabolism” or “lose weight with ‘good’ fat” hit the market, few people lose weight beyond some initial phase, let alone keep it off for any length of time. Coconut oil is just the latest fad, along with the anti-gluten craze. Sometimes I try to guess what will be next! It’s tempting to find some obscure berry or exotic oil, locate a study somewhere of any old quality, write a book, get a snazzy website, perhaps garner an appearance on “Oz” and get filthy rich,

    It’s the calories, stupid (not you, Dr. Hall) :-)

    I would add that citing a lack of evidence for something, and especially admitting that it hasn’t been studied, doesn’t go very far to convince believer-types. The comeback to that is always, “see, it hasn’t been studied because no one (especially BigPharma) wants to bother studying something natural that they can’t patent and make a bazillion dollars off of”. And yet, the purveyors of coconut products are making bazillions–go figure.

    1. Jack says:

      Understand that an individuals ‘practiced based research’ would be far more accurate that a “double blind” peer reviewed study! You do your own study to open your mind! If not then have a look at Ray Peats work!
      By the way…those peanuts and probably destroying your gut ;) (PUFA)

    2. Chris Young says:

      Whilst I agree there is a lack of scientific evidence and so, based on past experience, we have to be very sceptical about the claims, I have to disagree with your comment: “few people lose weight beyond some initial phase”. I switched to a low carb, paleo diet (grass fed meat and animal products) and I eat a LOT of fat including plenty of coconut oil. Whilst my weight has stayed the same (and I didn’t really need to lose any anyway) I visibly leaned up and lost a lot of stomach fat. The main thing I have found is that I feel better without ever feeling hungry, which I have always done on every other kind of “diet” I have tried. As long as I stick to this lifestyle then I don’t see that the weight will ever go back on and I have no intention to add carbs back in as I have no cravings for them any more and I a few stomach issues that I used to have have also cleared up.

    3. Cheryl says:

      @goodnightirene it is apparent that you do not have Celiac’s Disease. They problem here in the US that isn’t in other countries are GMO’s.

      1. WilliamLawrenceUtridge says:

        For one thing, there are GMOs in other countries. For another, GMOs don’t seem to present any inherent or empirically-recognized risks beyond what their component genes would contain, and they are tested for allergenicity (more so than conventionally-bred cultivars).

  4. DevoutCatalyst says:

    In her book Gorillas in the Mist, Dian Fossey said the one thing she missed from civilization was “nummy Triscuit wafers”. Triscuits were made with tropical oils back then and in my recollection tasted insanely good. My assertion is that the current soybean oiled Triscuits taste like cardboard by comparison and Dian is spinning like a lathe. If the current enthusiasm for coconut oil brought back a little sin to our cracker boxes that wouldn’t necessarily be such a bad thing. Maybe would have to go to Whole Foods to get proper junk food these days.

  5. WilliamLawrenceUtridge says:

    I’m curious what “increases digestion” is supposed to mean – like, you get more micro and macro nutrients from your food? Or is it just one of those CAM word salads that sounds good but is meaningless.

    Ah, I just answered my own question.

  6. Angora Rabbit says:

    WLU: You got it. Yet another example of someone listening to their nutritional biochem lecture in a twilight state. :) FAs that are C10 or shorter are semi-water soluble so are inefficiently packaged into chylomicrons by the intestinal mucosa. Instead they move directly into the bloodstream (by-passing the lymph) and travel on albumen etc. IIRC endothelial lipoprotein lipase has faster preference for medium chain triglycerides and thus are preferred for TPN solutions. But having said that, pancreatic LPL prefers unsaturated over saturated and larger than C16 lengths, which coconut oil is not, and that’s the enzyme relevant for lipid digestion. Oops, curse those pesky facts.

    I like also how coconut oil “increases vitamin absorption.” Well, only for the fat solubles and at high intakes could inhibit the water soluble absorption. Whoops, cherry-picking facts again!

  7. tuck says:

    “There is no justification for adding it to the diet on top of the usual consumption of other fats. There is no credible evidence to support any of the many health benefits claimed for using it as a supplement.”

    The active ingredient in coconut oil that is hypothesized to affect Alzheimer’s disease are the medium-chain trigclyercides.

    “Coconut oil is composed of approximately 66% medium-chain triglycerides.”
    http://en.wikipedia.org/wiki/Medium-chain_triglycerides

    They’ve been used for quite some time in the construction of ketogenic diets for the treatment of epilepsy.

    “Medium-chain triglyceride (MCT) ketogenic therapy.”
    http://www.ncbi.nlm.nih.gov/pubmed/19049583

    “Medium-chain triglyceride ketogenic diet, an effective treatment for drug-resistant epilepsy and a comparison with other ketogenic diets.”
    http://www.ncbi.nlm.nih.gov/pubmed/23515148

    Ketogenic diets have been found to be protective against various neurological conditions, including in models of Alzheimer’s:

    “d-β-Hydroxybutyrate protects neurons in models of Alzheimer’s and Parkinson’s disease.”
    http://www.pnas.org/content/97/10/5440.short

    MCTs are metabolized differently from other fats. They’re metabolized directly into ketones, regardless of the other components of the diet. This means that you don’t have to practice the extreme carbohydrate restriction typical of a ketogenic diet.

    “Insulin and Ketone Responses to Ingestion of Medium and Long-chain Triglycerides in Man”
    http://diabetes.diabetesjournals.org/content/18/2/96.short

    Based on those results, a ketogenic diet was proposed as a potential treatment for AD.

    “Ketone Bodies, Potential Therapeutic Uses”
    http://onlinelibrary.wiley.com/doi/10.1080/152165401753311780/full

    A company was founded, and it formulated a medical food based on MCTs (coconut oil, purified), and it tested the hypothesis:

    “Higher ketone values were associated with greater improvement in paragraph recall with MCT treatment relative to placebo across all subjects (P=0.02). Additional research is warranted to determine the therapeutic benefits of MCTs for patients with AD and how APOE-4 status may mediate beta-OHB efficacy.”

    “Effects of beta-hydroxybutyrate on cognition in memory-impaired adults.”
    http://www.ncbi.nlm.nih.gov/pubmed/15123336

    “In the second phase 2 trial, 152 patients with mild-to-moderate AD received AC-1202 (containing 20 g MCT) or placebo for 90 days in a double-blind, randomized design [52]. Results from this study were consistent with those of the earlier phase 2a study; AC-1202 produced a rapid onset of significant improvements in cognition, as measured using AD Assessment Scale-cognitive subscale (ADAS-cog), which were maintained throughout the study, correlated with blood levels of BHB, and were most apparent in ApoE4-negative patients.”

    “Hypometabolism as a therapeutic target in Alzheimer’s disease”
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2604900/

    Testing continues, based on early successes:

    “As a result of several positive research findings, in March 2009, the U.S. Food and Drug Administration (FDA) decided to regulate Axona® as a medical food available by prescription for the “dietary clinical management of the metabolic processes associated with mild to moderate Alzheimer’s disease”.”

    “Coconut Oil for Alzheimer’s Disease?”
    http://article.sapub.org/10.5923.j.cp.20120102.01.html#Sec2.2

    “AC-1204 26-Week Long Term Efficacy Response Trial With Optional Open-label Ext (NOURISH AD)”
    http://clinicaltrials.gov/show/NCT01741194

    Meanwhile, a substance that increases ketone uptake also seems to have benefits:

    “Sodium butyrate improves memory function in an Alzheimer’s disease mouse model when administered at an advanced stage of disease progression.”

    http://www.ncbi.nlm.nih.gov/pubmed/21593570

    Butyrate is the chemical root of the ketones produced

    But, as Alzheimer’s doesn’t wait for clinical confirmation, many people are using coconut oil directly, without waiting for the trial results. Given that the downside is diarrhea, one can hardly blame them.

    MCTs are generally recognized as safe, and have been used for decades in treating neurological disfunction.

    That’s not “no evidence”, or “no justification”. That’s reasonable behavior based on emerging scientific evidence.

    I’ll be interested to see how you incorporate this new evidence into your post.

    1. Mayan Fox says:

      Bam!

  8. stanmrak says:

    “The hype comes from unreliable sources. Joe Mercola says it is the smartest choice for cooking, is good for your heart, contains the kind of fat found in mothers’ milk, enhances immunity, and helps with weight loss by stimulating metabolism. And of course he sells it. ”
    “One could say the same for most prescription drugs advertised on TV. The “hype “comes from the drug companies — completely “unreliable sources” as they have been caught lying over and over and over again, and who “of course sell the drugs!”

  9. weing says:

    “The “hype “comes from the drug companies — completely “unreliable sources” as they have been caught lying over and over and over again, and who “of course sell the drugs!”

    Thank goodness! I was worried, but now you’ve set me straight and know that they are lying when they report all the side effects, including death.

    1. spacialist says:

      Sarcasm doesn’t illuminate a thing and neither does insinuating things in your lame rebuttal that were not claimed in the above comments. I am not name calling but simply identifying the degree of effort, or lack thereof, to offer a relevant response, and further, to dramatize the discussion by countering with “…side effects including death”. You claim that because they report on side effects that are sometimes negative they could have no profit motive but fail to offer any evidence on why this proves they are paragons of virtue and could never be unreliable. Just a tad simplistic and if you try logical deconstruction of the authors comments you find that they do not amount to claiming that they never tell the truth but simply that they cannot always be relied upon to tell the truth and this is a matter of record.

      1. weing says:

        “You claim that because they report on side effects that are sometimes negative they could have no profit motive but fail to offer any evidence on why this proves they are paragons of virtue and could never be unreliable.”

        Why would I even want to suggest, never mind prove, that they are paragons of virtue? Do you believe the sellers of coconut oil are such paragons?

      2. weing says:

        “if you try logical deconstruction of the authors comments you find that they do not amount to claiming that they never tell the truth but simply that they cannot always be relied upon to tell the truth and this is a matter of record”

        “The “hype “comes from the drug companies — completely “unreliable sources”

        You set me straight. I didn’t know what completely and always meant. I will correct my understanding of English language.

  10. Scott says:

    I’m also not aware of anyone here who considers TV ads as good evidence for the benefits of drugs to begin with.

  11. Harriet Hall says:

    @stanmrak,

    “One could say the same for most prescription drugs advertised on TV.”
    One could say that. One could also look for reliable peer-reviewed studies to find out whether there is scientific evidence that the drug works, and whether the claims of Mercola are true. One could also realize that for patients to get a prescription drug, they have to see their doctor, so there is a reality check.

  12. WilliamLawrenceUtridge says:

    I can see why Stan would be concerned, since my TV has a prescription pad built in, automatically dispensing a prescription every time a Pfizer commercial comes on.

    Question – why is it “lying” when drug companies misrepresent benefits and fail to recognize risks, but when CAM promoters do it, it’s just fine? Oh, that’s right, because you’re a hypocrite.

  13. WilliamLawrenceUtridge says:

    @tuck

    It looks like certain components of coconut oil have promising properties for future investigations. It’s a candidate for pharmacognosy study. However its properties are mostly extrapolated from proxy studies. Coconut oil and AD don’t show many results on pubmed, you’re relying primarily on MCT, ketones, sodium butyrate and related purified compounds – which aren’t the same thing as coconut oil, though they might be derived from it, in the same way ASA can be derived from willow bark. Rat studies and epilepsy research are good starting points for the investigation of AD, certainly they are not end points. And hopefully any benefits that might exist outweigh the risks of long-term supplementation outlined in one of the articles you linked to (“acidosis, hypocalcemia, hyperlipidemia, orcarcinogenesis“, though I’m rather surprised to see the author citing naturebath.com instead of something peer-reviewed).

    If purified components of coconut oil are proven to improve the cognitive performance of people with AD, that’s fantastic (so long as it’s something a little more meaningful than repeated clock-drawing) but it would only justify its use for AD, not the myraid other conditions it is claimed to treat.

    Medicine must await proof, not promise.

  14. ConspicuousCarl says:

    If 20% of your claims are unsupported, it’s a Big Pharma crime. If 100% of your claims are unsupported, it’s like a different philosophy, maaaaan.

    1. spacialist says:

      ? C’mon tell us. You know you want to! :)

  15. Harriet Hall says:

    @tuck,

    “I’ll be interested to see how you incorporate this new evidence into your post”

    I don’t need to incorporate this evidence, because as you yourself have pointed out: “But, as Alzheimer’s doesn’t wait for clinical confirmation, many people are using coconut oil directly, without waiting for the trial results.”

    Some of the studies you listed are suggestive, but we don’t yet have any actual credible evidence for clinical benefit of coconut oil for Alzheimer’s disease.

  16. elburto says:

    Oh Stan, never change. You should take to the stage, sunshine, ‘cos you’re hilarious.

    Hmm… maybe some coconut oil could lubricate your rusted head and neck?

    I wish we had prescribing TVs here in Blighty. OTOH we only get advertising for off the shelf stuff like Nurofen or Tixylix* anyway, so it’s not worth shelling out the extra for PrescriboVision.

    On a tangent, I’m surprised at how huge print pharmaceutical ads are. I subscribe to an American magazine in a digital format, and some of the ads are four full pages, with three of those being side effects. Hardly an example of Big Pharma hiding the truth.

  17. For Alzheimers prevention I recommend omega-3 fatty acids supplements, increased antioxidant intake, and natural weight-loss program as obesity increases alzheimer risk by 500%.

    Alzheimers prevention has to be treated as a holistic approach for overall body health, best served by naturopathic methods.

    The only thing you are getting from the druggie allopaths for alzheimers is an extremely toxic Aricept pill that does absolutely nothing to prevent the disease. The FDA of course refuses to remove this junk out of the pharmacy because it generates 1 billion dollars a year to Pfizer, and the first principle of allopathic care is to “do no harm” to the income statement,

    1. Mary says:

      It would be interesting to correlate the spike in Alzheimer’s And other neurological diseases, especially in younger people, with the advent of the “low fat diets.” Sometimes modern medicine makes claims that are later disputed. For 20 years I have been treated for glaucoma drugs which gave me all sorts of problems, only to be told last year that there has been a revision on how they assess glaucoma and I do t have it, I only have a thick cornea which shows a false positive for high eye pressure. They now think that cholesterol is not the baddie in heart disease, inflammation is the problem. Perhaps in the future they will re-think how they view coconut oil. In the meantime, having had a mother die of Alzheimer’s I would do anything to try and avoid it.

  18. goodnightirene says:

    @elburto

    “…some of the ads are four full pages, with three of those being side effects.”

    I always like to mention that those lists include every single side effect that has ever been REPORTED. Not investigated, verified, or found to be related to the drug in question, just reported.

    @tuck

    The epilepsy high fat diet you refer to is considered a last ditch effort and it does make people who use it fat. With advances in surgery for some drug-resistant epilepsies, the use of this diet will probably become even rarer. Dr. Novellal can correct me if I’ve misstated anything here. My knowledge comes from wide reading when one of my kids had an unexplained seizure–no recurrence happily, and a cousin who was severely affected.

    One more thing: People are not mice and vice versa. I wouldn’t start consuming something that could make me fat or clog my arteries just because it helped mice.

    1. Seamus says:

      So let’s do it the correct way, Show us the peer-reviewed clinical studies that being in ketosis (I.E a high fat, low-carb diet) to treat epilepsy makes you fat. Actually, all studies show the opposite.

      Most studies actually found out that in ketosis you loose weight, and you lower the bad cholesteroll and stablize the good one(so long for cloging your arteries on the diet).

      And for the sake of it, a clinical study done on about 300 patients found out that being on a low-carb diet helps against tumors, particulary brain tumors.

    2. James says:

      I was sitting next to a doctor on a plane who specializes in epilepsy and asked why the diet is never tried first. His response was because it is too hard for most people to implement.
      However seeing two of my nieces struggle with getting the dosage and medication for their epilepsy correct this took years. The idea of hard is lost to me.
      Given it could be very hard to find proper dosage and which medication would work for an individual.

      This begs the question, why are people not given the option of the diet first at first?

      I am not saying people should never go on medication.
      However given the fact the diet does work for some people in my opinion it should be given as an option at first instead of last.

      1. WilliamLawrenceUtridge says:

        The thing is, a pill is much easier and quicker than a massive dietary adjustment that severely restrics what you can eat, for the rest of your life, that must be maintained constantly, that requires the help of a dietician, that takes time to take effect but can be undone with a life saver (that the patient will desperately want to eat), that may permanently stunt a child’s growth, that doesn’t obviate the need for medication, and also does not lack the negatives of the medication – it doesn’t necessarly render you siezure-free, it doesn’t work for all patients and it has a host of complications (which would be side effects if it were a medication; kidney stones, high cholesterol, dehydration, constipation, slowed growth or weight gain, bone fractures). From here.

        I don’t know enough about epilepsy to say whether the medications are better or worse, I know they have a reputation for being brutal, but I can quite see why it might not be a first choice. Given the multitude of conditions that fall under the umbrella “epilepsy”, it seems like no matter what it is a rather complicated diagnostic and treatment issue. Rather than being a first choice, keeping it as a possible option would seem to make sense.

        1. James says:

          Thank you for your reply. I do agree it is easier to just give a pill.
          There are times I feel the convenience is for the doctor.
          However it is the patient who has to live with the consequences of the treatment drug or diet.
          I did not mean that as a slight to doctors in general. We all take short cuts at times.

          I guess what I am try to say simply this doctors should treat their patients like a science experiment.
          The should make no assumptions on what will work and validate their treatments.

          I seen doctors just give some drugs and expect you should be ok.
          Dismissing patients as a complainer (which I could understand why after work customer service for many years)
          Never really trying to find the true cause of the problem just instead of placing a bandaid.
          I heard many friends complain about having push their doctor to get anything done.
          The trust of doctors is on the decline partially because of the unrealistic expectations of the patient.
          And feeling that doctors do not care about their health.
          I do not envy the positions that doctors are in now.
          However I seen many doctors just reenforce those stereotypes of being that doctors are uncaring.

          Thank You Again for the reply

          1. WilliamLawrenceUtridge says:

            I can’t imagine the ketogenic diet oculd could ever be called “convenient” for the patient. I wonder what the long-term compliance rate is, in the one article I could find in a lazy pubmed search, it was just over 50% (7/12). A lot of the review articles I saw suggested making it more of a first-line option. I don’t know if it’s a question of doctors being lazy or taking short-cuts, I would more expect it to be a recognition of the difficulties the diet presents.

            I’ll also point out that the diet is more of a band-aid than pills are – you eat one candy and you’re done, meanwhile a long-acting pill can take days to wash out of your system (in general, I don’t know about epilepsy meds).

            I agree, I don’t envy the position of doctors. I’m very glad I live in Canada where we have a public health care option. I have never had a doctor come across as uncaring, or convey a sense of urgency. Several have broken their clinic rules in my favour, being willing to address more than one complaint per visit. In the managed care environment of the US, I’m not surprised to hear complaints like yours.

            1. James says:

              Thank You for the reply. You are right the diet is not convenient. However it is not convenient to be overweight, have brain fog, being manic or depressed which are some of the side effects that my nieces have to deal with. Also a 50% success rate is not that bad in my eyes. So one or two years of an inconvenient diet or years of fighting with doctors trying to counteract the side effects of the convenient pill.
              I am not saying diets can cure everything however they are powerful tool that doctors should use help people achieve good health.

  19. stanmrak says:

    The drug industry has been convicted of lying in the courts… GlaxoSmithKline lied for 11 years to the public and FDA about the risks of their drug Avandia. Merck lied for nearly as long about the increased risk of heart attacks caused by their block-buster drug Vioxx, which lead to an estimated 120,000 heart attacks, and 48,000 patients dying. Lilly lied to or withheld information from doctors about the risks and side effects of Zyprexa. The list goes on and on.

    Deaths are deaths, no excuses.

  20. ConspicuousCarl says:

    Glaxo’s CEO could juggle cats while standing on a puppy, and yet homeopathy would still be nonsense.

  21. annappaa says:

    I’ll tell you one thing, and that is that coconut oil makes a hell of a pie crust.

    1. spacialist says:

      Greeeaat pancakes too!

  22. morris39 says:

    A datum point. I use coco oil b/c of its high smoke point and know that lauric acid constitutes about half of its weight. I ran across a paper from Japan (cannot find the link) which claimed that lauric acid plus some co-factor was effective against antibiotic-resistant staphylococcus aureus. I tried it on my rough heels and within 3 weeks there was very significant reduction in skin cracks/roughness. I stopped for about 6 months and the roughness returned but not nearly the same extent. Now 4 months after starting again, the roughness is mostly gone but not likely to disappear completely (symptoms return if I stop for longer than a week). Commercial preparations had no effect.

    1. Carlos Oliveira says:

      Yes , Morris

      Lauric acid is present in a concentration of of 50% (fifty percent) in the extra virgin coconut oil.

      There are a lot of articles that proof that both, lauric acid and it byproduct of metabolization, the monolaurin can gives some protection against virus, fungus,bacterias, and others “bugs” , as in the references of articles that I pasted bellow .

      Lauric acid and monolaurin (derivative of metabolization of lauric acid from EVCO), protects too OUR BODIES from that dangerous microorganisms .This it is a very important propíertie of coconut oil to benefit aged dementia persons.

      The scientis Homung and others, wrote in na scientificarticle of 1994 that “the antiviral action attributed to monolaurin (a substance found only in coconut oil) turns “fluid” the structure in the envelope of the vírus ( it), causing the disintegration of the microbial membrane and that another antimicrobial effect in viruses is due to lauric acid’s interference with virus assembly and viral maturation .
      Witcher and others in 1993 wrote that another mode of action of lauric acid and monolaiurin (that you get from coconut oil) ,it is the enhancing of the immune system itself .

      The researcher Kabara in 1978 and the researchers Boddie and Nickerson in 1992 , wrote scientific articles about the propierties of derivatives of EVCO , the lauric acid and monolaurin , that INACTIVATE the dangerous bacterias Listeria monocytogenes, Staphylococcus aureus, Streptococcus agalactiae, groups of streptococci, gram-positive organisms, and some gram- negative organisms (including the Clamydia and H.Pylori).

      The researcher Isaacs and others ,wrote in 1991 scientific articles that the substances that you can find in large amounts in Extra Virgin Coconut Oil that are the lauric acid and monolaurin can INACTIVATE a large number of fungi, yeast, and protozoa ..and can inactivate too the yeast Candida albicans . The fungi include several species of ringworm .

      Considering that some scientific articles in pubmed relate the evolution (and starting ) of Alzheimer disease and other dementias , to some types of bacterial infections , that antibacterial propierties of extra virgin coconut oil substances , as lauric acid and monolaurin can be very useful to dementia patients.

  23. tuck says:

    @WilliamLawrenceUtridge: “…ASA can be derived from willow bark…”

    That’s pretty obtuse, as we derived ASA from willow bark *because* willow bark had the effects that we desired. We extracted the active ingredient, as they’re doing with MCTs and coconut oil.

    “…And hopefully any benefits that might exist outweigh the risks of long-term supplementation…”

    There are many, many studies in the medical literature demonstrating the complete, long-term safety of MCTs and ketogenic diets. Case is closed on that…

    @goodnightirene: “The epilepsy high fat diet you refer to is considered a last ditch effort and it does make people who use it fat.”

    It’s a last ditch effort only because the medical profession is remarkable obtuse (there’s that word again!) about it’s preference for treating symptoms rather than root causes. If fixing the diet resolves the condition, then any engineer would tell you that’s the first course of action: you don’t apply a band-aid, which is the drug approach. And the primary trait of the ketogenic diet is reduction in obesity, not weight gain. Spend a little time reading the literature, and you’ll find that to be the case.

    @Harriet Hall: “…we don’t yet have any actual credible evidence…”

    We have a “…randomized, double-blind, placebo-controlled, parallel-group study…” showing efficacy. According to you, in this post: http://www.sciencebasedmedicine.org/index.php/antibiotics-for-low-back-pain/ this is what we look for. And the company conducting these studies is not a whack-job “alternative” bunch, they’re PhDs and venture capitalists out of Novartis’s medical-food division (now part of Nestle).

    You seem grossly unfamiliar with the science and the people involved in this line of work. I suggest you spend a little more time looking into it before you dismiss it.

    Oh, and it’s well-demonstrated that coconut oil has the same effect on blood ketone levels as MCTs; replacing one with the other is common in medical interventions.

    “Coconut oil is acceptable in replacing medium chain triglycerides for ketogenic diet therapy in childhood epilepsy.”

    http://ncp.sagepub.com/content/23/6/589.short

    “MCT can be given in the diet as oil, as coconut oil, or as an emulsion (Liquigen, SHS, Liverpool, U.K.)”

    http://onlinelibrary.wiley.com/doi/10.1111/j.1528-1167.2008.01765.x/full

    Due to FDA regulations, a medical food must be processed, it cannot be the natural version, regardless of efficacy. Got to protect the guild, above all!

    Clearly it’s already been demonstrated that coconut oil has the same effects, whatever they may be, as the MCTs do. Hanging your hat on a regulatory quirk as a lack of “credible” evidence is ridiculous.

    1. spacialist says:

      Well stated Tuck. I find it amusing that an institution that is noted for it’s ‘education intensive’ nature, cannot escape the collective intellectual capacity of dullards, in that if they haven’t seen it yet, they can not grasp its full potential and begin talking instead of designing studies to verify, or disprove the ambient anecdotal claims. Such close minded ness amongst so called scholars yet history has shown many anecdotal conclusions to have merit upon close scrutiny. In spite of many claims being found without merit, where would humanity be if we gave up investigating that which we have yet to thoroughly understand or, indeed when new information confronts and challenges our understanding of old findings. There is a lot of bias being expressed here against something that is not a matter of controversy in the manner of two verifiable and confounding findings but merely as a result of what is not known because it has yet to be examined.

      1. WilliamLawrenceUtridge says:

        Asking for and expecting data before making sweeping recommendations is not “closed mindedness”. If coconut oil is such a health boon, then surely it would be easy to demonstrate, no? Until it’s demonstrated, it’s rather unreasonable to expect medical authorities to start recommending significant increases in consumption.

  24. Coot says:

    Clearly it’s already been demonstrated that coconut oil has the same effects, whatever they may be, as the MCTs do.
    LOL.

  25. Harriet Hall says:

    @tuck,

    “We have a “…randomized, double-blind, placebo-controlled, parallel-group study…”
    I’m not sure which study you mean. I didn’t find any such study using actual coconut oil in the way recommended by its enthusiasts. If I missed one, please point it out to me.

    I wrote about how science should be done. Even if you can come up with one good study, one good study is not enough. We know not to hang our hat on any single study without replication and confirmation. And I clearly said that in the article you linked to.

    I didn’t “dismiss” coconut oil; I said the evidence is insufficient. If future studies bear out current claims, I’ll follow the evidence.

  26. jt_512 says:

    Harriet Hall wrote:

    It is probably safe to use it in reasonable amounts to replace other oils in the diet, and doing so may have a favorable effect on lipid profiles…

    Why do you think replacing other oils in the diet with coconut oil would improve serum lipid profiles. Most other oils in the diet are high in polyunsaturated fatty acids. Coconut oil consists almost entirely of saturated fatty acids. Since about half of these fatty acids are lauric acid, then maybe you get a break-even on the total- to HDL-cholesterol ratio compared with typical vegetable oils. But an improvement? I doubt it.

    Jay

  27. Harriet Hall says:

    @jt_512,

    “Why do you think replacing other oils in the diet with coconut oil would improve serum lipid profiles.”

    I didn’t claim that it “would.” I said “Coconut oil contains lauric acid, which raises both HDL and LDL cholesterol levels….Virgin coconut oil contains medium-chain triglycerides, which are not as risky as some other saturated fats.”

    We don’t have the evidence to know for sure how replacing other oils with coconut oil would affect lipid profiles, or whether that would relate to a decrease in cardiovascular risk, but I think is is fair to say what I did: it “may” improve lipid profiles.

  28. jt_512 says:

    “I think is is fair to say what I did: it “may” improve lipid profiles.”

    But it’s equally fair, if not more fair, to say that it would not, and would be at least as likely to make serum lipid profiles worse. Look up the Mensink and Katan saturated-fatty-acid-specific equations and do the math. I think writing that substituting coconut oil for other dietary oils “may” improve serum lipids, when it is at least as likely to have the opposite effect, is sending the wrong message.

    1. Harriet Hall says:

      @jt_512,

      No, it would not be “equally fair to say that it would not.” It would be equally fair to say that it “may” not. Neither of us can legitimately say what it “would” do until it is properly studied.

      1. Mie says:

        Dr Hall, this in no way counters the point made by “jt_512″. By stating that

        “It is probably safe to use it in reasonable amounts to replace other oils in the diet, and doing so may have a favorable effect on lipid profiles”

        you very explicitly hypothesize on something which – in the light of what we know about the effects of different kinds of fat on blood lipids – is very, very unlikely. So the word “probably” shouldn’t be there, nor in fact the whole sentence.

        If you want to make a hypothesis that is based on what we know, that is.Of course you’re entitled to make whatever random guesses you wish.

        1. spacialist says:

          This is not a compelling argument when you rest on the ‘likelihoods’ of your eventuality being efficacious as opposed to Harriets ‘probabilities’. Neither are proof and both are hypothetically stated without any warranty of truth. No way to know without doing the research folks. Me? I’m just waiting for folks like y’all to stop the egocentric parrying and navel gazing and do the research!

          1. Mie says:

            Please read the exchange between “jt_512″ and Dr Hall in detail. What you stated has already been addressed.

            As for “stop yakking and do the research” bit: oh please.

      2. spacialist says:

        Exactly so Harriet!

  29. WilliamLawrenceUtridge says:

    There are many, many studies in the medical literature demonstrating the complete, long-term safety of MCTs and ketogenic diets. Case is closed on that…

    Then why are you posting on a discussion about coconut oil? Coconut oil =/= MCT and ketogenic diets just like willow bark =/= aspirin. If MCT are safe and effective, that doesn’t prove that coconut oil, a much dirtier, mixed and nonspecific substance, works. There could be a component of it that causes harms in a different way, intereferes with any health benefits of MCT, or otherwise renders all the positive studies on MCT completely moot.

    Science involves carefully-advanced steps to a conclusion that is repeatedly tested. While you may (and I emphasize may, and in my case I woudn’t) recommend MCT as a neutraceutical or even outright drug for certain conditions, coconut oil is leagues away from being the same thing as MCT and even further from being a recommended treatment for anything as far as science is concerned. It’s a food, it’s not a drug. Hopefully it does work, coconut is lovely and delicious. We’re just pretty far from knowing enough about it to say it’s a cure for AD.

    @FBA

    For Alzheimers prevention I recommend omega-3 fatty acids supplements, increased antioxidant intake, and natural weight-loss program as obesity increases alzheimer risk by 500%.

    You wouldn’t happen to conveniently sell omega fatty acids as part of your practice, would you?

    What exactly is a “natural” weight loss program? A diet high in fruits, vegetables and whole grains and low in red meat and refined foods, plus daily exercise? Like, oh, I don’t know, every health agency in the world recommends?

    Also, are you a naturopath or a vet? Because the study you linked to was in inbred obese mice. Do you recommend thalidomide to your clients? It’s perfectly safe for rodents.

  30. jt_512 says:

    OK, fine, “may” not. My point, which you seem intent on missing, is that if there is a lack of evidence of benefit over harm, then it is misleading to say that it “may have a favorable effect on lipid profiles,” because it also may have a negative effect on lipid profiles. And the onus is on coconut oil proponents to show otherwise, something they have not done.

    Whether you see it or not, your statement gives the one-sided impression that substituting coconut oil for other dietary oils carries no risk. What you should have said is that its effect on blood lipids is unknown.

  31. Harriet Hall says:

    @jt_512,

    “your statement gives the one-sided impression that substituting coconut oil for other dietary oils carries no risk”

    Read again. I said, “This may improve the cholesterol profile, although there are concerns that it may promote atherosclerosis by other means.”

    I don’t think most readers would interpret that to mean it carries no risk. You are quibbling about the exact meaning of the word “may” taken out of context, a word that I intended one way and you read another way. The whole thrust of my post was that we don’t have enough evidence.

  32. DavidRLogan says:

    @jt_512: “look up the Mensink and Katan…and do the math.”

    Here is Mensink himself in 2003 AJCN: “the favorable effects on this (Tot:HDL) ratio by such factors as coconut fat, which is rich in lauric acid, do not exclude the possibility that coconut fat may promote CAD through other pathways, known or as yet unknown.” Or rather, regarding CAD, coconut oil “may” promote but we need more evidence. And regarding the RATIO it sounds (to me) like Mensink has conceded the favorable change (you claim he would compute otherwise?).

    At any rate, your confidence in meta-analyses (problems often discussed on this-here blog), upon diets studied by regression (do you honestly think this is a method that can license the phrase “do the math”?) is not shared by me.

    Thanks WLU and Dr. Hall for the moderate and thoughtful considerations (and Angora Rabbit for a heroic level of nerdiness.) I owe my own moderate view on this subject to you both.

  33. jt_512 says:

    @DRLogan:

    The favorable effect of coconut oil that Mensink et al (2003) are referring to is for when it is substituted for carbohydrate. There is no favorable effect when coconut oil is substituted for polyunsaturated fat, the predominant type of fat in other dietary oils, which is what Dr. Hall was talking about.

    The meta-analysis upon which the Mensink and Katan equations are based is reliable. It’s not like typical meta-analyses that combine somewhat disparate outcomes from studies of variable quality. Every study in the meta-analysis was a tightly controlled metabolic trial. If you look at Figure 2 in the paper you can see how consistent all the included studies are.

  34. jt_512 says:

    @Dr. Hall:

    You wrote, “This may improve the cholesterol profile, although there are concerns that it may promote atherosclerosis by other means.”

    Once again, based on the actual evidence (or lack thereof), what you should have said is that substitution of coconut oil for other dietary oils on the cholesterol profile is unknown. It may improve it or make it worse. There are also concerns that it may promote atherosclerosis by other means.

    1. spacialist says:

      Again, you are simply argumentative. May is a conditional word meaning ,possibility. not definitely! I don’t know if you have noticed or not but you are arguing with someone who also has reservations about the efficacy of claims made by proponents of coconut oil and I find you both dismissive, also without ‘proof’, only she isn’t willing to claim proof positive as you tend to imply that your conclusions are correct without producing studies on coconut oil that prove it’s proponents wrong.

      1. weing says:

        “…you tend to imply that your conclusions are correct without producing studies on coconut oil that prove it’s proponents wrong.”

        I think you are getting close to the gist of the problem. Speaking for myself only, it’s not really that we imply that our conclusions are correct. It’s more that the default setting is that we need proof. It is not our job to prove the proponents wrong. It’s the proponents job to prove to us that they are right. You are making the assumption that we don’t want to believe them. Some of us may not, others may. Our wants are irrelevant to the proof. Anecdotes are not proof. They are a good starting point for hypothesis testing. When Bernie Madoff tells you he’ll turn your $10,000 into $10 million in a year, I’m sure you want to believe him. But you’d be a fool if you did without proof. Even if he supplied the proof of testimony of happy clients, you would be well advised to maintain your skepticism and search for alternative explanations.

  35. DavidRLogan says:

    @jt_512

    We may have a disagreement (I’m not sure.) I can’t tell, in the discussion of that (2003) paper, if he is in fact saying what you attribute to him. The subheading under which that quote appears seems only relevant to coconut oil’s effect on the ratio generally, not only to the replacement of carbohydrates (as far as I can tell), and the paper’s objective and design seem to me not unified on the theme you suggest. Any help?

    More to the point, you write there is “no favorable effect” when substituting for PUFAs. Is there evidence for that, or is that what is supposed to come from the equations? If there is evidence I would agree with you against Dr. Hall (obviously a FT citation would probably end this.) Otherwise I will probably still agree with her it “may” have the relevant effect (the questions on the modeling seem to large. The table to which you refer-the regression coefficients?-seems vulnerable to the “colinearity” objection, which seems like a really long painful argument if that’s right.)

    BTW you caught me on a pretty small technicality in the argument and I was impressed. Nice.

  36. jt_512 says:

    DavidRLogan wrote:

    We may have a disagreement (I’m not sure.) I can’t tell, in the discussion of that (2003) paper, if he is in fact saying what you attribute to him. The subheading under which that quote appears seems only relevant to coconut oil’s effect on the ratio generally, not only to the replacement of carbohydrates (as far as I can tell), and the paper’s objective and design seem to me not unified on the theme you suggest. Any help?

    A general principle in nutritional epidemiology is that absolute effects of energy-providing macronutrients are meaningless. Therefore, the effect of one macronutrient can only be measured relative to the effect of another, reference, macronutrient. This is true for two reasons. First, if you were to add calories from a macronutrient to a diet, the effect of the macronutrient would be confounded with the effect of the extra calories themselves. Second (the obesity epidemic notwithstanding), energy intake is under (albeit imperfect) homeostatic control; if you attempted to add calories from a macronutrient to someone’s diet, they would, to a good first approximation, offset the additional calories by reducing intake from other macronutrients. (This may sound implausible, given trends in obesity, but energy intake agrees with energy expenditure to within 1 or 2 percent, which cannot be an accident.) Therefore, well-designed studies of the effect of macronutrients on blood lipids substitute one macronutrient for another while maintaining equal total energy intake, and report the effect of the substitution.

    Over the years, carbohydrate has evolved to be the standard reference macronutrient for these studies. This is reflected in Mensink et al (2003) in Tables 1–3, in which results are presented as the effects on blood lipids for isocaloric substitution of each type of fat or fatty acid for carobhoydrate (Tables 1 & 2) or vice versa (Table 3).

    In the Discussion section of the paper, although the authors do not make it explicit, they are most certainly talking about the effect of lauric acid vs an isocaloric amount of carbohydrate, since the effect of any macronutrient can only meaningfully be stated in terms of isocaloric substitution for another macronutrient, the effect depends on which macronutrient is used as the referent, carbohydrate is the de facto standard referent in the field, and every result in the paper is presented as an effect of isocaloric substitution for carbohydrate.

    More to the point, you write there is “no favorable effect” when substituting for PUFAs. Is there evidence for that, or is that what is supposed to come from the equations?

    I meant that the paper shows no favorable effect for substitution of lauric acid for PUFA. From Tables 1 and 2, the effect on the ratio of total- to HDL-cholesterol of substituting 1% of total energy from lauric acid for 1% of total energy from carbohydrate is –.037, and for making a similar substitution of PUFA for carbohydrate is –.032. Adding the two figures together after changing the sign of the latter, gives the effect of substituting 1% of total energy from lauric acid for 1% of total energy from PUFA: –.005. The confidence interval (CI) for this result must be at least as wide as the CIs for the terms we added together; that is, the CI for lauric acid vs PUFA is –.005 ± .01 (at least), and therefore the result is completely indistinguishable from an effect of 0—no effect. Moreover, the confidence interval admits the possibility of deleterious effects on the total- to HDL-cholesterol ratio. That is why I think a statement like “it may improve your lipid profiles” gives the wrong impression. The little evidence there is suggests that it is basically just as likely to make your lipid profile worse.

    Otherwise I will probably still agree with her it “may” have the relevant effect.

    Yes, it “may.” But based on the evidence, it “may” also have the opposite effect.

    The table to which you refer-the regression coefficients?-seems vulnerable to the “colinearity” objection, which seems like a really long painful argument if that’s right.)

    I don’t know what you mean by “the collinearity objection.” The authors state that they tested for collinearity and found none.

  37. DavidRLogan says:

    @jt_512 (!!!)

    I was unaware that carbohydrate substitution was the assumed standard. I really appreciate your lucid and friendly explanation.

    Point conceded, is it fair for me to complain? The exact thing they wrote was “the favorable effects on this ratio by such factors as coconut fat, which is rich in lauric acid.” If, as you suggest in an earlier post, the other SFA in CO will raise the ratio, then they should not have written this. And if they only meant LA they should not have said “coconut fat, which is rich in LA.” Those, plus the assumption you mention, and you can probably see why I was confused.

    The argument you give in the second paragraph was very persuasive. I appreciate the time you took to type it out.

    At least part of the colinearity problem (and if I am wrong in calling it “colinearity problem” it is still a worry for regression) is that we are adding SFA, but also decreasing CHO, and also there *may* be a metabolic relation between the two (for instance, speculating wildly and only to illustrate the point, PUFA may interfere with CHO metabolism.) So, we have cholesterol as a function of SFA (changing), and CHO (changing), and SFA and CHO as *maybe* functions of eachother. Sometimes this means it is very hard to compute coefficients, or that new, independent variables will need to be introduced, variables that may or may not strongly resemble the originals.

    But that is the worry. Thanks again for going into the detail you did.

  38. Kaku says:

    Bio-chemistry is clear that the human body cannot convert the fatty acids in fats into energy. Only the glycerol in the fat molecule serves as a source of energy molecules. The theory on virgin coconut oil that the short and medium chain saturated fatty acids turn into energy quickly through ketones is wrong. The short and medium chain saturated fatty acids in virgin coconut oil are converted into saturated palmitic, saturated stearic and mono unsaturated palmitoleic and oleic acids, which are used to improve the performance of the cells for its many activities.
    Alzheimer’s disease, like most of the neural diseases, is caused by the destruction of the myelin covering of the nerves and impairment of the cell walls by high levels of poly unsaturated fatty acids and trans-unsaturated fatty acids, which harm the cells in a number of ways including: -
    • Trans-unsaturated fatty acids impair the cell walls causing poor insulation and short circuiting of signals, which then fail to reach their destinations.
    • Poly unsaturated fatty acids are easily converted into prostaglandins generating free radicals. PROSTAGLANDINS and free radicals have been identified as creating conditions for the onset of most of the autoimmune, metabolic and neural diseases afflicting children and grown-ups.
    • Prostaglandins can puncture the membrane of cells making it easier for microorganisms e.g. fungi, viruses, bacteria etc. to attack the cells and organs. Fungi cause a lot of diseases, especially skin diseases including whites. Bacteria are involved in a variety of diseases. Viruses can cause the mutation of the cells and distort genes damaging the yet to be born.
    • Prostaglandins disturb the movement of protein, thereby retarding or obstructing the processing of nutrients including vitamins and minerals for the organs, resulting in a number of debilitating ailments and diseases.
    • Prostaglandins expand and contract anyhow causing pain e.g. migraine, dysmenorrhea, cramps.
    • Poly unsaturated fatty acids are easily elongated. The elongated poly unsaturated fatty acids impair the myelin of the nerves and the cell walls resulting in poor insulation around the nerves and cells. Signals get short circuited and fail to go to the intended destination. This has been identified as the underlying cause of AUTISM and EPILEPSY.
    Poly unsaturated fatty acids accumulate in the body, when we eat food containing processed unsaturated vegetable oils often. Processed unsaturated vegetable oils include margarine, shortening, soy oil, canola, sunflower oil, corn oil cottonseed oil, safflower oil, etc. Under the conditions generated by poly unsaturated fatty acids, any of the organs of the body can get diseased, either by the destruction of the myelin /cell wall or invasion by microorganisms.
    As fatty acids are not converted into energy, during the VIRGIN COCONUT OIL DIET (KETOGENIC DIET), the glycerol in the accumulated fats is used to produce energy and the free and inappropriate poly unsaturated fatty acids are excreted. The short and medium chain saturated fatty acids are converted into saturated palmitic, saturated stearic and mono unsaturated palmitoleic and oleic acids, which replace the poly unsaturated fatty acids in the myelin and cell walls. If the cells or organs are not damaged beyond repair, then with the avoidance of all foods that contain some quantities of poly unsaturated (both cis- and trans-) fatty acids such as processed unsaturated vegetable oils and unfermented grains while ensuring the ingestion of foods that contain short and medium chain saturated fatty acids and palmitoleic and oleic acids such as organic milk butter, virgin coconut oil, virgin palm kernel oil, virgin palm oil, virgin olive oil, fruit cider vinegar and fermented foods. Such foods will assist the cells and associated organs to get rejuvenated naturally.
    The consumption of the short and medium chain saturated fatty acids in those foods while avoiding any food item that contains processed unsaturated vegetable oils enhances the production of the fatty acids which are suitable for the cells, thus improving the chances of preventing and even healing autoimmune, metabolic and neural diseases.
    Molecular biology, chemistry, physics and neural science have spelt out the principles and theories underlying the harmful effect of poly unsaturated fatty acids (both cis- and trans-) and the healing properties of short and medium chain saturated fatty acids.
    In view of this, sufferers of a number of autoimmune and metabolic diseases such as lupus, HIV, epilepsy, autism, diabetes, Alzheimer’s disease, migraine, cramps, menstrual pains, etc. etc. have benefited from the use of virgin coconut oil and organic butter, consumed in handsome quantities and the avoidance of foods containing poly unsaturated fatty acids.
    Virgin coconut oil, organic butter and many of the saturated fats and virgin olive oil as part of the normal food support good and healthy life of anyone and everyone, including pregnant women, lactating mothers, babies, old people and all.

  39. illogicalscience says:

    There is a fundamental bias and illogic at work in a lot of the literature on this topic. So much it makes the entire medical/research edifice look inept.

    As a coconut promoting website argues, contrary to the repeated claims that there is not a lot of research on coconut oil, there is actually quite a lot. Add MCT oil into the mix and there is even more. But people here are stressing coconut oil is not MCT oil. Why? Are there studies showing the two have generally different effects? Olive oil is not 100% monounsaturated oleic but that doesn’t stop medical commentators for all practical purposes using the two interchangeably. The comments from the cardiologists are given great weight even though they have an embarrassing history of giving bad advice while conclusions from other researchers like biochemists are ignored. One such researcher Hans Kaunitz whose research generally supports coconut oil even had an award dedicated to his memory. Cardiologists may no little about coconut oil but that doesn’t mean others are as ignorant.

    Also while the generic statements from organizations say there is no evidence for coconut oil they keep saying saturated fats are bad and saying low-fat diets are good—based on what evidence? Why don’t we turn the tables around and ask where is the evidence for low-fat diets? After a succession of comparative diet studies that repeatedly keep showing low-fat diets performing worse than low-carb high-protein diets, low-fat diets are still recommended. Where’s the evidence to support this? The past 30 years of low-fat propaganda have only resulted in an obesity and diabetes epidemic.

    Let’s talk about Alzheimer’s. True there is a dearth of rigorous studies showing coconut oil is a beneficial treatment, but then what treatment is? It is considered a terminal incurable disease. Aricept and Namenda will not stop it despite whatever studies may have showing their negligible benefits. How many are there? Indeed should anyone believe either of them superior to coconut oil based on those studies alone? Coconut oil has been used for centuries as an herbal medicine and is a food product ingested by millions. Yet it seems there are doctors more comfortable issuing medicines like Aricept and Namenda over coconut oil despite their own set of side effects most of which are more immediate and severe and many likely still unknown. Is this logical? The situation makes a mockery of the medical profession. Even more, instead of acknowledging the ludicrous state of affairs, “experts” have decided to hide behind the “there isn’t enough evidence” fig leaf.

    If there is a lack of studies on coconut oil it is an indictment not on coconut oil but the patent failure of the research system that should be studying it. But then again the saturated fat is dangerous myth dissuaded serious research didn’t it? Doctors should own up to their mistakes if they are to be taken seriously. That they fail to do so justifies skepticism of them.

  40. @WilliamLawrenceUtridge

    You wouldn’t happen to conveniently sell omega fatty acids as part of your practice, would you?

    I do happen to have a few in stock, how many do you need? We can start your treatment plan immediately.

    What exactly is a “natural” weight loss program? A diet high in fruits, vegetables and whole grains and low in red meat and refined foods, plus daily exercise? Like, oh, I don’t know, every health agency in the world recommends?

    Every health agency? I wish that was true but the current drug-based-medicine consensus is that there is NO proven prevention recommendation for Alzheimer’s disease. They recommend absolutely no preventative care for it. I wish it was different!

  41. jt_512 says:

    Kaku wrote, “Bio-chemistry is clear that the human body cannot convert the fatty acids in fats into energy.”

    Thanks for starting out your tome with a sentence that immediately shows you’re a kook. Saves us from having to read to read any further.

  42. illogicalscience says:

    jt_512 wrote:
    The favorable effect of coconut oil that Mensink et al (2003) are referring to is for when it is substituted for carbohydrate. There is no favorable effect when coconut oil is substituted for polyunsaturated fat, the predominant type of fat in other dietary oils, which is what Dr. Hall was talking about.

    I think you are wrong. Lauric acid raises HDL the most of any kind of fatty acid and consequently improves the HDL/TC ratio the most. It would also be better if you specified which polyunsaturated fat in particular you would wish to compare coconut oil to. I’d refer you to Thijssen and Mensink, Fatty Acids and Atherosclerotic Risk, (2005) which rehashes the earlier material but is apparently no longer available online for free.

    When the Mensink and Katan paper adds “do not exclude the possibility that coconut fat may promote CAD through other pathways, known or as yet unknown” they are basically covering their butts because they are aware of the prevailing dogma and their results are contradicting it. It is clearly speculation only because their experiments do not address the question. If their paper was truly free of bias they would have refrained from commenting on it.

    Perhaps when you state that “[t]here is no favorable effect when coconut oil is substituted for polyunsaturated fat” you are referring to the received wisdom based on other studies. The main problem is that specificity with a particular PUFA is usually lacking in such comparisons. The updated results to the Sydney Diet-Heart Trial would show that coconut oil has better results than safflower oil for example. On the other hand showing superiority over fish oil would be harder.

  43. illogicalscience says:

    jt_512 wrote:
    The favorable effect of coconut oil that Mensink et al (2003) are referring to is for when it is substituted for carbohydrate. There is no favorable effect when coconut oil is substituted for polyunsaturated fat, the predominant type of fat in other dietary oils, which is what Dr. Hall was talking about.

    I think you are wrong. Lauric acid raises HDL the most of any kind of fatty acid and consequently improves the HDL/TC ratio the most. It would also be better if you specified which polyunsaturated fat in particular you would wish to compare coconut oil to. I’d refer you to Thijssen and Mensink, Fatty Acids and Atherosclerotic Risk, (2005) which rehashes the earlier material but is apparently no longer available online for free.

    When the Mensink and Katan paper adds “do not exclude the possibility that coconut fat may promote CAD through other pathways, known or as yet unknown” they are basically covering their butts because they are aware of the prevailing dogma and their results are contradicting it. It is clearly speculation only because their experiments do not address the question. If their paper was truly free of bias they would have refrained from commenting on it.

    Perhaps when you state that “[t]here is no favorable effect when coconut oil is substituted for polyunsaturated fat” you are referring to the received wisdom based on other studies. The main problem is that specificity with a particular PUFA is usually lacking in such comparisons. The updated results to the Sydney Diet-Heart Trial would show that coconut oil has better results than safflower oil for example. On the other hand showing superiority over fish oil would be harder.

  44. WilliamLawrenceUtridge says:

    I do happen to have a few in stock, how many do you need? We can start your treatment plan immediately.

    Oh, I don’t want any. I’m in excellent health – low blood pressure, low cholesterol, no arthritis, no major health complaints really, and no real minor ones either. Because I follow my doctor’s advice – a diet rich in fruits and vegetables, lean proteins, prepared by me from simple ingredients. Plus, regular exercise, low stress and avoiding medication if I don’t need it. I see no reason to supplement it with obesogenic, unnecessary, unproven tropical oils.

    My actual point was – selling something that you recommend is a conflict of interest. Arguably worse than Big Pharma, since you benefit much more directly than they do. Unless you sell at or below cost, you’re pocketing cash on each and every sale. So tell me again how evil Big Pharma is because they make a profit, you hypocrite.

    Every health agency? I wish that was true but the current drug-based-medicine consensus is that there is NO proven prevention recommendation for Alzheimer’s disease. They recommend absolutely no preventative care for it. I wish it was different!

    I wish it was different too, but that doesn’t change the fact that there is no proven form of prevention for Alzheimer’s – drug or nondrug. Pretending you’ve got the “secret cure”, selling that “secret cure” without proof, selling false hope based on a long chain of specious, unproven reasoning, is contemptible. Your study, in heavily inbred rats, didn’t prove anything about Alzheimer’s disease in humans. Did you know thalidomide is perfectly safe for rats? Are you OK with recommending it to your patients? But it’s really about pretending to be on the cutting edge of science, not actually being on it.

    Can you show me any major health agency that doesn’t recommend a diet rich in fruits, vegetables and lean proteins? This is major, mainstream agencies, not the Atkins clinic. Does the Mayo Clinic, CDC, WHO, FDA or NHS?

    Of course not, because your entire practice is based on a dishonest portrayal about what medicine is. Your practice is based on 50% dishonest criticism of medicine, 25% unproven claims and 25% pretending mainstream advice is somehow unique to naturopathy. Which makes it 100% lies.

    You should really get off your high horse since you’re really just a dishonest hypocrite.

    1. spacialist says:

      Even more compelling than unsubstantiated claims, name calling! I am guessing you are heavily invested in ‘big pharma’?

      1. WilliamLawrenceUtridge says:

        Nope, not even a little. Just finished Bad Pharma and found it a little scary. I just find it extremely hypocritical that people claim Big Pharma has a conflict of interest, but some guy selling you coconut oil does not.

        Do you have such a double standard? Why?

  45. jt_512 says:

    illogicalscience wrote, illogically:

    Perhaps when you state that “[t]here is no favorable effect when coconut oil is substituted for polyunsaturated fat” you are referring to the received wisdom based on other studies.

    Nope. As I explained in great detail in my post, the results of Mensink et al (2003) indicate that the effect on the total- to HDL-cholesterol ratio of substituting lauric acid for PUFA is essentially 0. Obviously, you did not understand my post.

  46. illogicalscience says:

    I understand it, but conflated it with other concerns admittedly beyond the scope of Mensink et al.

    Let’s put it this way: if coconut oil can be substituted for omega 6 PUFAs with all omega 6s’ supposed advantages yet none of their disadvantages, I’d call that a favorable effect.

    The once extravagant claim that coconut oil is possibly the healthiest cooking oil is tenable and remains to be debunked. If there are any common omega 3 cooking oils, however, that might change the odds.

  47. jt_512 says:

    @illogicalscience:

    That would be canola oil. Its ω6:ω3 ratio is 2:1. Since the ω6:ω3 in typical Western diets is 10:1 or more, substituting canola oil for other dietary oils (including coconut oil) would reduce the ω6:ω3 ratio of the diet.

  48. illogicalscience says:

    Better but, if aiming for a ω6:ω3 ratio of 1:1, canola still wouldn’t be the best choice. Now if canola has properties comparable to increasing thermogenesis, disabling lipid-coated viruses, and providing alternative energy that facilitates a reduction in carbohydrate intake, then its case would be even stronger. Even then if coconut oil is ever shown to slowdown the onset of cognitive diseases like Alzheimer’s, Parkinson’s, or epilepsy, or be more beneficial in the treatment of diabetes, how much of a debate would there be?

  49. jt_512 says:

    An ω6:ω3 ratio of 1:1 is unattainable, and there is zero evidence that it would be beneficial. Furthermore, none of those other benefits you insinuate can be attributed to coconut oil have been established.

  50. illogicalscience says:

    Are you familiar with the argument made here>?

    1. Mie says:

      That argument is an excellent case of n-6 alarmism. That old post by Guyenet isn’t relevant since meta-analyses on the consumption of pufa/n-6 fatty acids point very clearly that adverse effect simply do not occur unless the consumption is way, way higher than currently.

      As for coconut oil itself: I suppose you can use it in moderation. But then again, that’s the case with almost everything. As for coconut oil being healthy/healthier than high quality vegetable oils, nuts or fatty fish … Forget about it.

  51. illogicalscience says:

    Depends on what you mean by established. More interestingly, I haven’t heard any of them being disproved.

  52. Artour says:

    It is probably not a bad fat choice, but there is a much better coconut product that becomes popular: coconut yogurt that is now sold in health food stores around the world.
    It is quite cheap in the USA (e.g., in Whole Foods), but is still expensive in Europe and Australia probably due to newness of the product. Coconut yogurt can become even more common due to increasing rates of allergies to milk and soy products.
    As with other probiotic products, coconut yogurt helps to improve gut flora, reduce toxic load from the gut, boost immunity and slow down breathing naturally while increasing body oxygenation.

  53. WilliamLawrenceUtridge says:

    Boost the immunity you say…does it come with a warning for people with allergies?

  54. Dr. Mark says:

    I think where we go wrong is in treating food like it’s some kind of remedy for our diseases. When we view food in this way, it becomes just another treatment. We eat to nourish our bodies, and the best way to consume it is the way it grew in nature in most cases, to give our cells what they need to live and thrive. We should be focusing on nutrition for the nourishment it gives, not in how it affects this or that condition.

    1. Chris says:

      “We eat to nourish our bodies, and the best way to consume it is the way it grew in nature in most cases, to give our cells what they need to live and thrive.”

      Yeah, sure. I guess you don’t eat many cashews nor tapioca. And certainly no blue corn, nor tofu or miso. Also to get coconut oil from coconuts is a long process using lots of coconut meat.

      I love it when folks make pronouncements on having food that has “not been processed”, but then forget that much of the food we eat needs a certain amount to actually be edible, or to even release the nutrients (like blue corn). Of course my favorite was one “raw food” enthusiast had tofu and miso in her recipes. Um, they start out as soybeans that need to be cooked.

  55. J_N says:

    Coconut oil is not a drug. It’s been a part of ancestral diets of several different peoples for centuries. Vegetable oils which are purported to be healthier are actually a new invention and were never a part of the human diet.

    The burden of proof is not on proponents of coconut oil to prove it’s safety since it has been consumed traditionally throughout history. The burden of proof is on those who suggest PUFA rich vegetable oils are healthier to make their case. When I say vegetable oils, I mean corn, sunflower, safflower, canola, etc. Olive oil is a traditional oil and definitely separate from this class of industrial oils.

    Just because a diet rich in PUFA results in lower cholesterol levels than a diet rich in coconut oil or other SFAs, we cannot come to the conclusion that the latter is unhealthy. Coconut oil is not hypercholestoremic, rather PUFA rich oils are hypocholestoremic. There is an underlying assumption that lower cholesterol is better, when there is no real evidence to back this claim, just a hypothesis. Lower cholesterol is associated with higher risk of stroke and illnessess associated with mental decline, depression, suicide, etc. The 200 cutoff value for cholesterol is not scientific, it’s an arbitrary value designed to increase the amount of people who can be medicated. There is no evidence to suggest that 190 is healthier than 240 for example. The cholesterol range associated with lowest all cause mortality is something like 220-240, IIRC.

    The theory goes that SFAs raise LDL (supposedly at least in short term trials) and high LDL is associated with CHD so high SFA consumption must be associated with CHD. Yeah, not quite. SFA consumption has not been associated with increased incidence of CHD in recent meta-analyses.

    The evidence that high LDL ’causes’ CHD is lacking and there are other factors at play which are beyond the scope of this discussion. But anti-SFA proponents conveniently forget to mention that SFAs lower Trigylcerides and raise HDL as well, hence resulting in a ‘better’ lipid profile and keeping the Total Cholesterol/HDL ratio at worst the same or at best better (depending on the actual SFAs consumed) than a diet rich in PUFAs. PUFAs (n6 and n3) are beneficial when one is deficient in them and we only need a small amount of n6/n3 in our diets. There are much healthier foods to get them from than vegetable oils. Omega-3 from marine animals is better than that from canola oil, not least because it’s unprocessed and EPA + DHA rather than inferior ALA in canola oil. Also, nuts a healthier source of n-6 than any industrial vegetable oil.

    Whoever came up with the idea that a cooking oil is supposed to be rich in PUFA? PUFA are by definition least stable to heat and hence not suitable for cooking. Cooking oils should be able to stand upto heat and SFA rich oils fit this criterion best. Hence, the use of Ghee, Coconut and Palm oils in traditional cultures.

    I accept that those on the other end of the spectrum, i.e. claiming coconut oil to be some sort of panacea are yet to provide evidence and are jumping on the bandwagon, but there can be no doubt about coconut oil’s place in a human diet. A diet is not obesogenic when it’s high in fat; it’s obesogenic when it’s high in processed foods which tend to provide high calories and low nutrition, be they high in fat or carbs. Eating a whole foods diet rich in animal fat, tropical oils, organ meats, vegetables, fruits, nuts,full fat dairy, etc. is not only healthful in theory, it has several living examples.

    Reading this article made me feel like we somehow have to come up with a justification for consuming coconut oil, because it may somehow promote heart disease by other means even if it improves lipid profile. This is the sort of attitude which we need to get out of. This is not the 80s anymore. Self-experiment. I did and found coconut oil to not only improve my lipid profile vastly (my HDL went to 84 with a Total/HDL ratio below 3.5) but also improve my immunity to common illnesses. It’s anecdotal evidence but I’m not waiting around for a study to tell me that it’s ‘safe’ whereas canola oil is being sold on shelves like it’s the healthiest thing ever invented. No thanks. I trust nature more than man-made, highly processed foods.

    1. Mie says:

      “The burden of proof is not on proponents of coconut oil to prove it’s safety since it has been consumed traditionally throughout history. The burden of proof is on those who suggest PUFA rich vegetable oils are healthier to make their case. When I say vegetable oils, I mean corn, sunflower, safflower, canola, etc. Olive oil is a traditional oil and definitely separate from this class of industrial oils.”

      BS, plain and simple. The burden of proof rests on those making positive claims such as “coconut oil is healthy”. This question cannot be answered by looking at historical and/or ecological data. As for PUFA oils, the quality and amount obviously matter: e.g. Ramsden’s meta-analysis showed that when one’s diet contains both n-3 and n-6 fatty acids, the effects on CV health are good. And we’ve got results showing the health effects of n-6 fatty acids, too. Only when the consumption of n-6 oils increases considerably do we see some problems – and these results date mostly back to “old school” vegetable oils.

      “There is an underlying assumption that lower cholesterol is better, when there is no real evidence to back this claim, just a hypothesis. Lower cholesterol is associated with higher risk of stroke and illnessess associated with mental decline, depression, suicide, etc. The 200 cutoff value for cholesterol is not scientific, it’s an arbitrary value designed to increase the amount of people who can be medicated. There is no evidence to suggest that 190 is healthier than 240 for example. The cholesterol range associated with lowest all cause mortality is something like 220-240, IIRC.”

      Once again, plain ol’ bullshit. Lower LDL-cholesterol (which is what you meant, right?) being associated with the abovementioned is merely an association with no viable mechanism to back up the assumption. It’s the same case as with e.g. the elderly: low cholesterol is associated with excess mortality due to e.g. increase of cancer and malnutrition. Excluding these: there’s simply no evidence to suggest that e.g. physiological (around 1,5 mmol/L) LDL levels are detrimental to health, on the contrary.

      “The theory goes that SFAs raise LDL (supposedly at least in short term trials) and high LDL is associated with CHD so high SFA consumption must be associated with CHD. Yeah, not quite. SFA consumption has not been associated with increased incidence of CHD in recent meta-analyses.”

      Yes. However, when SAFA is replaced with PUFA, the risk of CVD goes down. It’s not a matter of SAFA being deadly, no matter the context. It’s precisely a matter of dose and context. And of course, no all SAFAs are created equal.

      “The evidence that high LDL ’causes’ CHD is lacking and there are other factors at play which are beyond the scope of this discussion.”

      Ahem, have you heard of the term “risk factor”? And what about terms “sufficient” and “necessary cause”? Abnormal LDL levels is clearly a risk factor in CVD. To claim otherwise is – simply put – religious nonsense a la THINCS and other denialists.

      “But anti-SFA proponents conveniently forget to mention that SFAs lower Trigylcerides and raise HDL as well, hence resulting in a ‘better’ lipid profile and keeping the Total Cholesterol/HDL ratio at worst the same or at best better (depending on the actual SFAs consumed) than a diet rich in PUFAs.”

      BS, onge again. SAFA raises LDL much more than HDL which results in tot. chol.: HDL ratio becoming worse than when substituting SAFA for PUFA or MUFA (both oh which lower LDL and raise HDL). If your claim were true, we’d be seeing evidence showing the benefits of diets rich in SAFA both in cohort and experimental studies. Such studies don’t exists – wherease the abovementioned meta-analyses show the exact opposite.

      1. J_N says:

        For someone who likes to use the term ‘BS’ a lot, your arguments are ironically poor. Like I said, historical evidence is much more reliable for human health than anything else. Individual health claims of coconut oil can be studied to death but no one needs to wait for these studies to be affirmed of it’s safety or health. What evidence was used to push PUFA rich vegetable oils on us? Where is the foolproof evidence that they should replace the traditional oils in our diet? Coconut oil is not something new in my part of the world, it’s been consumed forever. The burden of proof is on those who insist I take it out of my kitchen and replace it with vegetable oils. I cannot be anymore clear than that.

        One’s diet should contain n-6 and n-3, but in minimal amounts. And not from vegetable oils, but unrefined sources. The evidence for benefits from n-3 is plentiful, but n-3 is not meant to replace cooking oils like coconut, not should it because it is highly unstable and prone to oxidation and rancidity. N-6 is beneficial as long as one is deficient in it, but in a normal diet anywhere in the world, you do not need vegetable oils to overcome a n-6 deficiency. You will get enough n-6 from eggs, poulry, nuts, etc. There are several studies cited in favour of n-6 rich oils replacing SFA rich oils but the benefit seems to arise when the original diet was deficient in n-6/n-3 or when the markers used to assess the benefit is a middle man like serum cholesterol. It’s just taken for granted that higher cholesterol is unhealthy, another assumption. Ramsden’s analysis is quite good and in line with my take. Here is a post analysing it:

        http://wholehealthsource.blogspot.com/2010/12/diet-heart-controlled-trials-new.html

        The point I made with cholesterol is that lower is associated with other diseases and the association needs to be studied further and it is irresponsible to lower levels without considering these. Such low levels are not the result of a normal diet anyway, they are obtained through drugs mostly. Just like higher LDL cholesterol is merely associated with heart disease (the association with HDL is actually stronger than with LDL and inverse, but there aren’t many drugs which can raise HDL so everyone sticks to the lower is better theme). The mechanism for heart disease via raised LDL is not clear at all. There are hypotheses and theories, nothing concrete. To say that lower cholesterol is merely associated while higher cholesterol ’causes’ disease is just bias. Scientists do not know either way. The most compelling argument for the real cause of heart disease is made by Chris Masterjohn. In summary, he talks about the oxidation of LDL as being key, not LDL-C per se. What increases oxidation of LDL is not SFA intake.

        http://www.cholesterol-and-health.com/Does-Cholesterol-Cause-Heart-Disease-Myth.html

        You talk about the replacement of SFA with PUFA lowering risk. If the studies you mention measure risk as cholesterol, then I have nothing to say except the fact that it’s an assumption with very little evidence to back it up. SFAs are not harmful in any context, except in case of a n6/n3 deficiency which itself has nothing to do with SFA intake.

        For risk factors and LDL levels being a risk factor, I again refer you to the link above where Chris Masterjohn dissects the lipid hypothesis in it’s current form. The negative association of CHD with HDL is stronger than it’s positive association with LDL. Nothing raises HDL as much as SFAs, especially those in Coconut oil.

        And finally, in response to your point about SFAs not improving the ratio and replacement of SFAs with PUFA/MUFA improving the ratio, I would like to say that humans don’t replace particular fatty acids in their diet, they replace oils/foods. Even coconut oil has some MUFA and PUFA and the effect of replacing it with another oil or vice versa would involve a synergistic effect. I invite you to read the following which confirms that lauric acid in coconut oil improves the ratio more than any other fatty acid, saturated or unsaturated:

        “How Do Dietary Fats Affect the Total-to-HDL Cholesterol Ratio?

        The second study was a meta-analysis published in 2003 of sixty trials testing the effect of feeding different types of fats to humans on the total-to-HDL cholesterol ratio.

        The study found that saturated fats did not change the ratio when substituted for carbohydrates. Carbohydrates, however, did raise triglyceride levels and shift LDL to the small, dense pattern associated with atherosclerosis when they were substituted for saturated fats.

        Unsaturated fats, especially polyunsaturated fats, decreased the ratio. But so did specific saturated fats like stearic and lauric acids. “As a result,” the authors wrote, “lauric acid had a more favorable effect on total:HDL cholesterol than any other fatty acid, either saturated or unsaturated.”

        They pointed out further that even highly saturated fats like dairy and tropical oils contain some unsaturated fat, so they will all decrease the ratio relative to carbohydrate. And since coconut oil is rich in lauric acid, it would be especially effective in reducing the ratio.

        In contrast to all of these fats, trans fats raised the ratio.”

        You may read the source article here:

        http://blog.cholesterol-and-health.com/2009/01/total-to-hdl-cholesterol-ratio-what.html

        1. weing says:

          “The 200 cutoff value for cholesterol is not scientific, it’s an arbitrary value designed to increase the amount of people who can be medicated.”

          What is your evidence for this claim?

          I recommend you check out the 7 countries study to begin with. Then check out
          http://www.ncbi.nlm.nih.gov/pubmed/6361299

          While HDL cholesterol is associated with lower CAD risk, I know of no studies that show raising HDL levels is beneficial. Quite the contrary.

          1. Mie says:

            “While HDL cholesterol is associated with lower CAD risk, I know of no studies that show raising HDL levels is beneficial. Quite the contrary.”

            This is because raising HDL seems to be – generally speaking – more difficult than lowering LDL and because RCTs that have attempted this have produced very minor changes (usually way less than 5-10%, excluding torcetrapib etc. the problems of which aren’t related to HDL as such). Evidence from observational studies and HDL infusion therapy clearly points the benefits of having high & functional HDL.

          2. J_N says:

            The 200 cutoff value for cholesterol was politically motivated. See here:

            http://www.second-opinions.co.uk/enig_chol.html

            Lowest all cause mortality is associated with a cholesterol range of 200-240. See here:

            http://healthcorrelator.blogspot.com/2009/12/total-cholesterol-and-cardiovascular.html

            I have read the seven countries study by Ancel Keys and also the several articles debunking it. I suggest you google it.

            The study you linked to shows a modest benefit of lowering serum cholesterol. This is explained in great detail by Chris Masterjohn here:

            http://blog.cholesterol-and-health.com/2011/03/how-conflating-lipid-hypothesis-with.html

            Few studies attempt to raise HDL cholesterol because it’s quite difficult to do so with drugs. Easiest way is to have coconut oil, but why would anyone ever propose eating a SFA rich food? :)

            Masterjohn explains the role of HDL and why a trial aiming to raise HDL failed to find benefit:

            Where does HDL fit in? Much has been made of its role in reverse cholesterol transport, but that has little to do with the oxidation of LDL or the oxidized derivatives of linoleic acid that have been shown to turn on the “foam cell” genes in the monocytes that first swallow them up. As described in the article I linked to above, when the contribution of oxidized LDL was first discovered in the late 1970s and early 1980s, researchers found that HDL or vitamin E both prevented the oxidation that would occur when LDL was exposed to the cells that line the blood vessels for a prolonged period of time. As I have pointed out on my site elsewhere, HDL is responsible for delivering vitamin E to these cells.

            So that suggests a protective, causal effect of HDL, but not HDL cholesterol. And in fact, interventions to try to specifically boost HDL cholesterol have not been terribly successful. The most notorious case was torcetrapib, a drug that was designed to block the transfer of cholesterol from HDL particles to LDL particles. Not only was it toxic, but a recent trial concluded the following:

            The absence of an inverse relationship between high-density lipoprotein cholesterol change and cIMT progression suggests that torcetrapib-induced high-density lipoprotein cholesterol increase does not mediate atheroprotection.

            In other words, keeping the level of cholesterol in the HDL particles high does not reduce the progression of atherosclerosis. This suggests that while HDL protects against atherosclerosis by preventing the oxidation of LDL, HDL cholesterol does not protect against atherosclerosis by transporting cholesterol away from peripheral tissues and back to the liver. This is unsurprising, considering it is the oxidation of LDL and not the transport of cholesterol to peripheral tissues that contributes to atherosclerosis.

            Source article for the above is here:

            http://blog.cholesterol-and-health.com/2009/01/total-to-hdl-cholesterol-ratio-what.html

        2. Mie says:

          “Like I said, historical evidence is much more reliable for human health than anything else.”

          And like I said, this is false. You may keep on repeating it if you wish, I shall not address it (or any of the same BS claims again).

          “One’s diet should contain n-6 and n-3, but in minimal amounts … Ramsden’s analysis is quite good and in line with my take. Here is a post analysing it:”

          It isn’t in line with your take. Guyenet’s post has two key points (and I quote):

          1) Interventions that replaced animal and trans fat with seed oils that were rich in LA but low in omega-3 caused a non-significant trend toward increased heart attacks (13% increase) and overall mortality.

          2) Interventions that replaced animal and trans fat with a combination of LA and omega-3 fats significantly reduced heart attacks (by 22%). The numbers for total mortality followed a similar trend.

          Even when looking at excessive intake of n-6, there was no statistically significant effect on MI and total mortality. So much for the dangers of PUFA. The second point was exactly what I stated earlier. Now, you may want to read your sources through next time, unless you wish to prove what your opponents state. :-)

          “The point I made with cholesterol is that lower is associated with other diseases and the association needs to be studied further and it is irresponsible to lower levels without considering these.”

          Oh, but it has been studied quite a bit. Just like LDL lowering medication like statins, which do not increase CDV mortality nor total mortality – which would be the case, if lower LDL had a causal link to these.

          “The most compelling argument for the real cause of heart disease is made by Chris Masterjohn. In summary, he talks about the oxidation of LDL as being key, not LDL-C per se. What increases oxidation of LDL is not SFA intake.”

          Masterjohn is partly claiming something that isn’t backed up by data (PUFA oxidation & n-6 link has no evidence, on the contrary as various meta-analyses show) and partly attacking a strawman. Yes, LDL oxidation is a problem. However, this happens in the arterial intima and the risk INCREASES when LDL levels get higher and higher.

          “You talk about the replacement of SFA with PUFA lowering risk. If the studies you mention measure risk as cholesterol, then I have nothing to say except the fact that it’s an assumption with very little evidence to back it up.”
          You may wish to have a look at virtually any meta-analysis on the issue, conducted since 2000. They all show beneficial effects from such a “trade”.

          “The negative association of CHD with HDL is stronger than it’s positive association with LDL. Nothing raises HDL as much as SFAs, especially those in Coconut oil.”

          Err, no. Tot.cholesterol:HDL -ratio is the most meaningful, and this doesn’t improve when SAFA replaces unsaturated fatty acids.

          “And finally, in response to your point about SFAs not improving the ratio and replacement of SFAs with PUFA/MUFA improving the ratio, I would like to say that humans don’t replace particular fatty acids in their diet, they replace oils/foods. Even coconut oil has some MUFA and PUFA and the effect of replacing it with another oil or vice versa would involve a synergistic effect.”

          Well I’ll be! Finally a point that has sense.

          “I invite you to read the following which confirms that lauric acid in coconut oil improves the ratio more than any other fatty acid, saturated or unsaturated.”

          Yes, Mensink et al (2003) shows that lauric acid raises HDL. And LDL, twice as much. However, the change was beneficial only when compared to carbohydrates and other SAFAs.

          And, since you brought up the issue of foods vs individual fatty acids, notice figure 4 in the same meta-analysis: the effect of coconut fat on tot.cholesterol:HDL ratio is virtually insignificant. A health benefit? Hardly.

          1. J_N says:

            “And like I said, this is false. You may keep on repeating it if you wish, I shall not address it (or any of the same BS claims again).”

            You can choose to ignore historical evidence completely and base your nutritional opinions on whatever studies tickle your fancy. Dismiss everything which points to the possibility that you may be wrong. No BS recommendations ever came from scientists.

            “It isn’t in line with your take. Guyenet’s post has two key points (and I quote):

            1) Interventions that replaced animal and trans fat with seed oils that were rich in LA but low in omega-3 caused a non-significant trend toward increased heart attacks (13% increase) and overall mortality.

            2) Interventions that replaced animal and trans fat with a combination of LA and omega-3 fats significantly reduced heart attacks (by 22%). The numbers for total mortality followed a similar trend.

            Even when looking at excessive intake of n-6, there was no statistically significant effect on MI and total mortality. So much for the dangers of PUFA. The second point was exactly what I stated earlier. Now, you may want to read your sources through next time, unless you wish to prove what your opponents state. ”

            Err, yes. Now you are going to tell me what is in line with my take. Brilliant.

            Point 1 clearly states that replacing animal and trans fats with seed oils rich in LA (n-6) resulted in an INCREASED incidence of heart attacks and overall mortality. That’s not making much of a case for n-6 rich oils, is it?

            Point 2 is basically saying that IF you are deficient in n-3, replacing animal and trans fat with a combination of LA and omega-3 fats reduces incidence of heart attacks and overall mortality. This shows the benefits of NOT being deficient in omega-3, that’s about it. It’s not a vindication of replacing SFA rich oils with PUFA. It’s clear I read my sources, Guyenet says what I just said and you would know if you bothered to read the rest of his post.

            “Oh, but it has been studied quite a bit. Just like LDL lowering medication like statins, which do not increase CDV mortality nor total mortality – which would be the case, if lower LDL had a causal link to these.”

            The benefits of statins are not due to cholesterol lowering. They are because of their anti-inflammatory and pleotropic effects. Uffe Ravnskov has had a paper published where he shows that there is no dose-response effect of cholesterol lowering by statins on atherosceloric plaque, which would be expected if there was any causal link between LDL and heart disease. Statins have a number of negative side effects including cognitive decline, muscle pain, CoQ10 depletion, etc. There are numerous health issues associated with low cholesterol. The causality with low LDL needs to be established but the association does exist. Emily Deans, a well-known Psychiatrist has blogged about the importance of cholesterol for the brain and the implication of cholesterol lowering on brain related illnesses. It is pertinent to note that there has been no causality established for high LDL and heart disease either.

            “Yes, Mensink et al (2003) shows that lauric acid raises HDL. And LDL, twice as much. However, the change was beneficial only when compared to carbohydrates and other SAFAs.

            And, since you brought up the issue of foods vs individual fatty acids, notice figure 4 in the same meta-analysis: the effect of coconut fat on tot.cholesterol:HDL ratio is virtually insignificant. A health benefit? Hardly.”

            If Lauric acid raises HDL by 10 and LDL by 20, that’s very good for the ratio. A LDL/HDL ratio of 2:1 is great. That’s why the authors state lauric acid has the best effect on TC/HDL ratio of ANY fatty acid.

            As Chris Masterjohn quoted from the study: “As a result,” the authors wrote, “lauric acid had a more favorable effect on total:HDL cholesterol than any other fatty acid, either saturated or unsaturated.” It appears you again didn’t read the article of his which I linked to. If you did, you also wouldn’t say the Total/HDL ratio itself is any sort of ‘health benefit’. It is at best a proxy for the amount of time LDL spends circulating the in blood, which is important because oxidation of LDL is what is implicated in heart disease, as per Masterjohn. The mere concentration of cholesterol in LDL, i.e. LDL-C does not tell us much. Which is why the lipid hypothesis in it’s current form does not tell us anything close to the complete story.

            The following part of Masterjohn’s analysis (which I linked to earlier as well) is relevant before concluding health benefits based solely on the Total/HDL ratio findings of this study (which considered cholesterol levels to stabilize within 13 days by the way):

            What Does This Tell Us About Dietary Fat?

            Before we conclude anything about what type of fat we should eat, we must remember that correlation does not prove causation. As I pointed out above, evidence suggests that the total-to-HDL cholesterol ratio is a marker for the time LDL spends in the blood rather than a causal factor itself. So we cannot conclude that PUFA oils and coconut oils are the best fats to prevent heart disease based on this meta-analysis by itself.

            The latest edition of the widely respected textbook Modern Nutrition in Health and Disease states that linoleic acid (a PUFA found abundantly in vegetable oils) decreases cholesterol levels because the enzymes that store cholesterol by connecting it to fatty acids, called esterification, will selectively use linoleic acid. Thus, while liver cells get stuffed with cholesterol linoleate esters, their level of free cholesterol declines and they produce more LDL receptors on their surface, which bring LDL in from the blood.

            Increased expression of the LDL receptor is good. But this meta-analysis considered blood lipids to reach a steady state by 13 days. Maybe cholesterol linoleate can accumulate in the liver for 13 days without adverse effects, but what happens over the long term when cholesterol esters progressively accumulate in that organ? Can that go on forever? Longer studies would be needed to find out.

            It isn’t quite clear how some saturated fats decrease the total-to-LDL cholesterol ratio. Perhaps they enhance LDL receptor function by decreasing oxidative stress, but there could be many possibilities.

            As the authors of this meta-analysis pointed out, we should rely on controlled trials testing the effects of dietary fats on heart disease risk rather than extrapolating from surrogate markers. They cite several trials showing that unsaturated fats reduce heart disease risk compared to saturated fats.

            These trials, however, were often poorly conducted or deceptively interpreted. Moreover, a number of trials showed the opposite, like the Rose, et al. (1965) trial that found corn oil to quadruple the risk of heart disease when substituted for butter over the course of two years. I have discussed those trials here.

          2. J_N says:

            “Masterjohn is partly claiming something that isn’t backed up by data (PUFA oxidation & n-6 link has no evidence, on the contrary as various meta-analyses show) and partly attacking a strawman. Yes, LDL oxidation is a problem. However, this happens in the arterial intima and the risk INCREASES when LDL levels get higher and higher.”

            PUFA oxidation & n-6 link has no evidence? Meta-analyses? You mean those observational studies that have been dissected several times by both Masterjohn and Guyenet? Right. LDL oxidation depends on many factors. As Masterjohn points out, the time LDL spends circulating in the blood is key. A standard lipid panel measures LDL-C, i.e. the amount of cholesterol in LDL particles. There can always be discordance between LDL-P and LDL-C and the former is more relevant to LDL oxidation as Peter Attia has painstakingly pointed out in his series of blog posts. That’s why you have those French and Swiss people eating loads of saturated fat and having higher or the same cholesterol levels than the US, but still having a fraction of the rate of heart disease. An LDL-C level can only tell you so much. For people on high PUFA diets, like Americans, lower LDL-C levels still result in greater heart disease. Maybe because the PUFA makes their LDL more prone to oxidation. But that can’t be right, can it?

          3. J_N says:

            Living longer, yes. Due to better healthcare, better hygiene, less poverty, etc. But living healthier? Don’t think so. In my country, despite being much more modern now, our grandparents and great-grandparents were much healthier in their old age, made fewer trips to the doctor and did not get sick as frequently as we do.

        3. weing says:

          You are giving blogs for references instead of articles to review. One even asks us to rely on hearsay and not on studies.
          I hope you realize it is LDL cholesterol that I am talking about. There are numerous published interventional studies if you care to look at them. If you aren’t swayed by them, I can’t help you.

          As I said before, there are plenty of observational studies of HDL and and TC:HDL but I am not aware of any positive interventional studies. HDL is more complicated than you think, and probably its function is more important than its level as shown by the work of Dan Rader. If you care to learn what HDL is, I recommend http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2959168/

          Back to coconut oil, my understanding is that the MCTs lead to a mildly ketotic state and those ketones are utilized by the brain as fuel. There are claims that there is impaired glucose utilization by the brain in Alzheimer’s and the ketones are an alternative pathway for the brain to get the needed fuel in these patients. Interesting hypotheses. I don’t know if I am convinced, I am willing to entertain them. Further studies are needed. But that may be only because of my ignorance of what’s been done.

          1. Mie says:

            “As I said before, there are plenty of observational studies of HDL and and TC:HDL but I am not aware of any positive interventional studies. HDL is more complicated than you think, and probably its function is more important than its level as shown by the work of Dan Rader. If you care to learn what HDL is, I recommend.”

            Good point about the function. I also refer to my earlier post on the issue of HDL & interventional studies.

            I’ll address a couple of points made by J_N while I’m at it:

            The meta-analyses I mentioned are of RCT evidence. See e.g.

            http://www.ncbi.nlm.nih.gov/pubmed/22889633

            As for LDL circulation time in blood, Marterjohn is missing the point. It’s not the circulation per se that is the problem – human body can get oxLDL particles out of the blood. It’s the amount of LDL & circulation time both of which increase the likelihood of LDL penetrating the arterial intima. The longer LDL particles are retained there, the more susceptible they are to e.g. oxidation there. Which is precisely the current understanding.

            Perhaps Masterjohn just cannot bring himself to admit that the evidence backing this up is solid & therefore he has to resort to grasping at whatever’s available and making silly adjustments of his own (and to hell with the evidence)?

            And the French paradox, please. What next? The Flat Earth society is right?

  56. WilliamLawrenceUtridge says:

    So corn oil, sunflower oil, safflower oil and rapeseed oil have never been eaten before their industrialization?

    Lots of things are part of a traditional diet that can be bad for you in small and large amounts, in general and specific cases. Witness PKU, alcoholism, favaism, tobacco, amino acid deficiency, goitre, etc. If traditional diets, whatever that meant, were so great, people eating them wouldn’t get sick. They do. Food isn’t medicine. Arguably, coconuts aren’t very “traditional”, since their range is only found on the periphery of Africa, where humans spent most of their time diverging from their common ancestor with chimps. “Traditional” is a meaningless term that varies according to which location and time period you are talking about. 1,000 years ago, brocolli wasn’t traditional because it didn’t exist, ditto cauliflower. Does that make it healthy or not? In 100 years, whatever we eat now will be “traditional”. The term is meaningless, ignores the evolution of humans, and ignores the evolution of plants and the animals we eat.

    Your claims of conspiracy (“so more people can be medicated”) are unconvincing. Conspiracy theories are used as a cheap cognitive trick to prevent people from doing the research or to defend a pre-existing conclusion from challenge. It’s lazy. If you’ve got evidence, link it.

    A diet is obesogenic when it’s higher than the calories expended. A guy ate nothing but twinkies and lost weight. Boom, your anecdote is disproven.

    1. Mike says:

      “So corn oil, sunflower oil, safflower oil and rapeseed oil have never been eaten before their industrialization?”

      Rapeseed oil was rarely eaten due to it high acid components and foul taste. It was used a lot during WWII to lubricate war ships from what I’ve heard.

      Most seed oils were extremely difficult to extract in any significant quantities before industrialization.

    2. J_N says:

      Yes, I don’t see any evidence of said vegetable oils being used as part of traditional diets, not least as cooking oils as they are marketed today. The industrialised methods to extract oils from seeds in any reasonable quantities simply did not exist. Rapeseed is different from canola by the way. The way canola oil is processed renders it completely different from rapeseed oil.

      The point is that foods consumed as part of traditional diets have stood the test of time. People got sick because of lack of hygiene, infections, deficiencies due to lack of food, poverty, etc. They did not develop diabetes and heart disease by sticking to their traditional diets and even the primitive tribes who are alive today and are less industrialised eating their traditional diets are in good health. Kitavans, Pacific Islanders, Tokeleau (sp?).

      Food is NOT medicince, that’s what I said. Food is nourishment. A well nourished person avoids the need for medicine far more than one who is not. What foods nourish us best is the point I’m making. Whole foods, not industrial ones.

      Alcoholism and food is not a comparison worth making. Many cultures have abhorred the use of alcohol and looked upon it as a sin for centuries. It is not something consumed as a food or as being health giving in general. It’s been considered an indulgence, as is tobacco.

      Coconuts have been part of the traditional diets of many people: Sri Lanka, Thailand, Philippines, India, etc. That’s quite a chunk of the world’s population right there. A food that has been consumed for centuries by a large amount of people and continues to be consumed is traditional.

      Broccoli and cauliflower not existing a thousand years ago alone does not prove if they are or are not healthy. Potatoes and rice also fall into this category. They may have a smaller history of consumption but it’s still much, much more than the industrial vegetable oils which have started to be produced in the mass quantities that they have only recently and have replaced the staple fats/oils in the human diet. There is no predence in any traditional diet of the PUFA consumption that exists in today’s developed society. PUFAs are highly unstable fats and are best consumed in small quantities and raw form, like in nuts, gently cooked fish, etc. Whoever came up with the idea that it was healthy to consume them in large quantities, that too after being processed industrially, needs to come up with some hard evidence to back this claim. The lipid hypothesis has not stood the test of time. It’s an oversimplified version of reality that has led people to become sicker and require more medication.

      For the claim of the cutoff value of 200, it isn’t a conspiracy.

      Here’s an inside look at how things sounded in the 1980s from Mary Enig, a world renowned expert on fats (lipids) and oils who researches and lectures extensively:

      “The 1984 Cholesterol Consensus Conference final report [contained] no mention of the large body of evidence that conflicted with the lipid hypothesis. One of the blanks was filled with the number 200. The document defined all those with cholesterol levels above 200 mg/dL as ‘at risk’ and called for mass cholesterol screening, even though the most ardent supporters of the lipid hypothesis had surmised in print that 240 should be the magic cutoff point. Such screening would, in fact, need to be carried out on a massive scale [because] the federal medical bureaucracy, by picking the number 200, had defined the vast majority of the American adult population as ‘at risk.’

      Your statement about a diet being obesogenic when the calories expended are less than calories consumed is pointless. It’s the same as saying a restaurant is crowded because more people are entering it than leaving. It doesn’t address the root cause. Why do people overeat on certain diets and not on others? Generally, when people don’t ‘overeat’, it’s because the foods are satiating and nourishing. The twinkie diet is an example of lack of palatability. Twinkies are processed, yes, but when all you have is twinkies, they don’t remain as palatable as they would be in a varied diet. You can only eat so many twinkies. You can do the same experiment by limiting yourself to just sugar and I bet you’ll see the same result. Stephan Guyenet has talked about Food Reward and Palatablitity in great detail. The point is, in general, a diet high in processed foods is not limited to twinkies. It has many options. Such diets result in the sort of obesity epidemic you see today. Eating traditional, unprocessed foods provides nourishment, satiety and prevents overeating even if one is not counting calories. Another major reason modern day diets are obesogenic is high PUFA consumption. Thyroid hormone is depressed on high PUFA diets and this directly effects metabolism. Refer to Ray Peat’s work for more details on the dangers of excess PUFA to thyroid.

      1. Mie says:

        “The point is that foods consumed as part of traditional diets have stood the test of time. People got sick because of lack of hygiene, infections, deficiencies due to lack of food, poverty, etc. They did not develop diabetes and heart disease by sticking to their traditional diets and even the primitive tribes who are alive today and are less industrialised eating their traditional diets are in good health. Kitavans, Pacific Islanders, Tokeleau (sp?).”

        Appeal to nature. These issues (what is healthy and what isn’t) are in no way solvable to shady and sketchy historical and ecological claims.

        As for Mary Enig’s claims: there’s quite a bit of observational data showing what happens on a population level in high-risk individuals with tot. chol. values exceeding 200 mg/dL. Since – when talking about atherosclerosis – we’re talking about a “life-long project”, it simply makes sense to aim lower. Especially when this value is easily reached via a multitude of diets and heatlhy lifestyle options, with no known adverse effects.

        1. J_N says:

          You can say I’m appealing to nature and opine that science is a better bet for deciding what’s healthy to consume and what’s not, but science’s track record as far as nutritional advice is concerned is poor when you consider the effects that this advice has had on general public health. The standard recommendations are based on insufficient evidence; observational studies from which causation cannot be derived and assumptions which can be easily debunked. I’ll take historical, ecological reasoning any day.

          Nature is there to be studied. Science is a tool to study it, understand it. If you start questioning elements of nature based on hypotheses of what is healthy, you might as well caution people against mother’s milk, which is high in SFAs and has a large proportion of lauric acid as well, just like coconut oil. The fact is, scienctific evidence is required to ascertain safety for drugs which are man-made, not foods occurring in nature. The onus is on people to prove that coconut oil is unhealthy, not the other way round. Science can be used to test hypotheses, make recommendations, change them, etc. It does not give us a perfect answer as far as nutrition is concerned, especially when researchers’ bias is inherently affecting the outcomes of the research. Also, coconut oil isn’t a drug which prevents too much research being carried out to ascertain it’s benefits, unlike drug trials which are sponsored by Big Pharma. Not saying there isn’t any coconut oil research, there is quite a bit, for example here:

          http://coconutoil.com/peer_reviewed/

          “As for Mary Enig’s claims: there’s quite a bit of observational data showing what happens on a population level in high-risk individuals with tot. chol. values exceeding 200 mg/dL. Since – when talking about atherosclerosis – we’re talking about a “life-long project”, it simply makes sense to aim lower. Especially when this value is easily reached via a multitude of diets and heatlhy lifestyle options, with no known adverse effects.”

          I am not sure which data you are referring to which definitively shows lowering cholesterol below 200 has any positive effect. It does not make sense to aim lower and I am not aware of a nutritionally complete diet which will give the majority of the population an ‘acceptable’ cholesterol level which is usually achieved only through extremely low fat dieting (which is not healthy since fat is required for production of many hormones, absorption of several vitamins & minerals, etc.) or statins. Refer to the following link for a discussion of cholesterol and mortality/heart disease. The ‘lower is better’ philosophy is unfounded:

          http://healthcorrelator.blogspot.com/2009/12/total-cholesterol-and-cardiovascular.html

          A further account of the political motivations behind the 200 cutoff is here:

          http://www.second-opinions.co.uk/enig_chol.html

          1. Mie says:

            “You can say I’m appealing to nature and opine that science is a better bet for deciding what’s healthy to consume and what’s not, but science’s track record as far as nutritional advice is concerned is poor when you consider the effects that this advice has had on general public health. The standard recommendations are based on insufficient evidence; observational studies from which causation cannot be derived and assumptions which can be easily debunked. I’ll take historical, ecological reasoning any day.”

            It is already evident you simply don’t know what you’re talking about, no need to prove it any further. 1st of all, “science’s track record” is by no means “poor”, but of course it progresses and changes. The same happens with nutritional recommendations, which BTW are not based solely on observational studies.

            As for h or e data – let alone “reasoning – it cannot simply prove anything about causation, which is why it’s way below prospective epidemiological studies in evidence hierarchy.

            “If you start questioning elements of nature based on hypotheses of what is healthy, you might as well caution people against mother’s milk, which is high in SFAs and has a large proportion of lauric acid as well, just like coconut oil.”

            Oh please. Mother’s milk is consumed only for a brief & very specific period of time, whereas we’re talking about something completely different. Your point makes no sense.

            “The fact is, scienctific evidence is required to ascertain safety for drugs which are man-made, not foods occurring in nature. The onus is on people to prove that coconut oil is unhealthy, not the other way round.”

            Repetition doesn’t make stupid claims any more reasonable.

            “It does not give us a perfect answer as far as nutrition is concerned, especially when researchers’ bias is inherently affecting the outcomes of the research.”

            Eh? What’s else is new? Has anyone claimed this?

            “Also, coconut oil isn’t a drug which prevents too much research being carried out to ascertain it’s benefits, unlike drug trials which are sponsored by Big Pharma. Not saying there isn’t any coconut oil research, there is quite a bit, for example here:

            http://coconutoil.com/peer_reviewed/

            “Refer to the following link for a discussion of cholesterol and mortality/heart disease.”

            This guy makes the same mistake as you did earlier: the J-curve reflects the fact that certain conditions and disease cause cholesterol levels to drop. This doesn’t mean that lowering cholesterol by diet (or by medication) causes problems with total or CVD mortality.

            “The ‘lower is better’ philosophy is unfounded:”

            Once again: Mary Enig’s conspiracy theories mean nothing in the light of what evidence tells us about lipid levels. Stop making the same unfounded claims and come up with new ones.

            1. J_N says:

              “It is already evident you simply don’t know what you’re talking about, no need to prove it any further. 1st of all, “science’s track record” is by no means “poor”, but of course it progresses and changes. The same happens with nutritional recommendations, which BTW are not based solely on observational studies.

              As for h or e data – let alone “reasoning – it cannot simply prove anything about causation, which is why it’s way below prospective epidemiological studies in evidence hierarchy.”

              Ahan! So I never knew what I was talking about in the first place. That explains everything. Progresses and changes, yes. First it says one thing based on a flawed set of studies, then says something completely different based on another set of flawed studies. A majority of nutritional recommendations are based on observational studies, meta-analyses of observations studies and trials which have inherent design flaws. The FFQ which is used to assess dietary habits is one the favourites of researchers. It tells us squat about actual diet. But what do I know, I’m actually stupid enough to believe that the foods we’ve been consuming for centuries and have thrived upon are good for us. But no way there is any causality there. Causality comes only from observational studies and those fantastic meta-analyses which do a great job of putting a lot of unreliable studies together so we can have one great, big unreliable study. The hierarchy is untouchable, so are the recommendations by the great researchers who are beyond reproach.

              “Oh please. Mother’s milk is consumed only for a brief & very specific period of time, whereas we’re talking about something completely different. Your point makes no sense.”

              Yes, we’re talking about how lauric acid in mother’s milk is so good for the development of the baby but suddenly when it’s in coconut oil, we should be very careful about consuming it because you never know what those pesky SFAs are upto. My point makes no sense whatsoever, I must seek mental help.

              “Repetition doesn’t make stupid claims any more reasonable.”

              Word.

              “Eh? What’s else is new? Has anyone claimed this?”

              Must be someone stupid.

              “This guy makes the same mistake as you did earlier: the J-curve reflects the fact that certain conditions and disease cause cholesterol levels to drop. This doesn’t mean that lowering cholesterol by diet (or by medication) causes problems with total or CVD mortality.”

              Oh, me and the mistakes I keep on making. Got to do something about it. It’s a U curve which shows that the best place to be cholesterol wise is 200-220 if you want the lowest risk of heart disease and 200-240 if you want the lowest all cause mortality. Cholesterol levels higher than 240 are as bad for overall mortality as those below 200. So let me get this straight. In case of lower cholesterol, it’s the disease which causes the levels to drop but in case of higher cholesterol, it causes heart disease. Very interesting. Them high cholesterol levels are a b*tch. But then they seem to be beneficial much beyond 200 even. Yet the statinators want to reduce them well below 200 because 200 is the magic number. Must be something wrong with the data then.

              “Once again: Mary Enig’s conspiracy theories mean nothing in the light of what evidence tells us about lipid levels. Stop making the same unfounded claims and come up with new ones.”

              Mary Enig and her conspiracy theories. She happened to be an eyewitness back in 1984 overhearing the committee members deciding on the 200 number in order to treat more patients, but we can disregard that, because we now know so much about lipids now. Much more than that old hag could ever know in her lifetime of research. The 200 number has proven to be the magic cutoff, beyond which people develop acute statin deficiency/SFA excess.

              Since all my claims are so unfounded, I guess I better stop before we find something.

  57. Thomas says:

    This appears to be a very, very shallow commentary on a deep subject. It doesn’t address the differences in fatty acid chain length, how different chain lengths are processed by the body (portal circulation, liver digestion and glucose output, mitochondrial transport, adipose disposition, etc). Also why are medium-chain fatty acids (MDFA) like those found in coconut oil also found naturally in mother’s milk and chosen for tube-feeding and baby forumulations? Because they’re easier to digest and healthier, that’s why. Fatty acids with more than 12 carbon atoms must be hydrolyzed in the intestines before absorption. They’re then re-synthesized into triacylglycerols and preferentially used for storage in the adipocytes (fat tissue) throughout the body. MCFA, in contrast, are directly absorbed without hydrolysis and preferentially transported through the portal venous system to the liver and metabolized there for energy, not to the periphery vascular system where they would otherwise increase blood tryglyceride levels. Carnitine acyltransferase, which is the enzyme system necessary for LCFA transport across the inner mitochondrial membrane, is not required for MCFA, which means that MCFA are more available for the mitochondrial beta-oxidation to produce energy (ATP) for cellular metabolism. MCFA also does not require the enzymes Enoyl CoA isomerase or 2,4 Dienoyl CoA reductase in beta-oxidation as unsaturated fats do. Moreover, it has been shown in multiple studies that dietary intervention with MCFA increased thermogenesis (metabolism) and endogenous oxidation of LCFA.

    Less supported by direct scientific studies, but logically consistent would be the role of MCFA in neural development and maintenance. Myelination of neurons, which is basically the encapsulation of neurons in a sheath of fat (why the brain is mostly composed of fat), is what causes the rapid development of children’s brains and nervous systems in their first year of life, which is why human milk contains so much fat, particularly MCFA. Demyelination is the hallmark of some neurodegenerative autoimmune diseases, including multiple sclerosis (MS), acute disseminated encephalomyelitis, Neuromyelitis Optica, transverse myelitis, chronic inflammatory demyelinating polyneuropathy, Guillain-Barré syndrome, central pontine myelinosis, inherited demyelinating diseases such as leukodystrophy, and Charcot-Marie-Tooth disease. When myelin degrades, conduction of signals along the nerve can be impaired or lost and the nerve eventually withers. While not all causes of demylenination can be solved by consuming MCFA, it would make sense that insufficient fat consumption, and especially insufficient MCFA consumption, could contribute to demyelination and other neurodegenerative diseases or at least impair the body’s ability to combat them. The causes of Alzheimer’s disease and other forms of dementia are not well understood, but age-related myelin breakdown is one hypothesis. Mental stimulation and balanced diet are often recommended as ways to delay symptoms of Alzheimer’s, and so to the extent that one is able to generate or preserve neurons, it would make sense to fuel that process with a dietary formulation similar to that of infants developing their brains initially, which would include copious amounts of MCFA, such as those found in coconut oil. So to say that there is no credible evidence that this is certainly the case is not to prove there is no reasonable cause to include coconut oil in your diet, especially if you’re suffering from a condition which may be helped by it.

    I think it’s more important to note that there is no credible evidence that consuming coconut oil in your diet is detrimental. And so there’s no harm in trying it. Whether it’s a miracle may be a case-by-case basis. But it’s probably reasonable to assume that most Americans do not get sufficient MCFA and over-consume LCFA, trans-fats, and omega-6 polyunsaturated fats. So to displace some of the overconsumption with some MCFA will almost certainly be a more balanced and healthy diet.

    1. Mie says:

      Thomas, you could’ve just stated that “there’s no reliable evidence of the heath effects of coconut oil but I like to hypothesize and extrapolate on whatever is handy”. The key points of your message in a much more reader-friendly form. :-)

  58. Mike says:

    “In a former life, when I was an Air Force doctor, one of my duties was to give “Healthy Heart” briefings with a script furnished by Air Force experts. It covered the scientific consensus of the time (the early 80s) about diet. It recommended a low fat diet, restricted cholesterol and saturated fat, and demonized tropical oils like palm oil and coconut oil. (Trans fats weren’t yet on the agenda.)”

    Fool me once, shame on you. Fool me twice, shame on me.

    Why should anyone trust ‘scientific consensus’ and/or the results of any current studies?

    From the 50′s until nutrition science is abysmal.
    http://www.heart.org/HEARTORG/GettingHealthy/FatsAndOils/MeettheFats/The-Bad-Fats-Brothers_UCM_305102_Article.jsp

  59. Thomas says:

    LOL @ “selling something that you recommend is a conflict of interest”. So you should sell things that you don’t recommend?

  60. Omega 6 is out of balance with Omega 3 in today’s diets, that’s because of the over use of PUFA in nearly every packaged food and also because the animals are fed shitty diets loaded with the stuff and then humans eat those animals. The NY Times had an article recently on the abundance of fake Olive Oil, so people thinking they are getting a MUFA fat are not getting that but some lousy oil instead. I believe the #1 cause of disease today is a combination many things: we stay out of the sun, we don’t walk outside much and run after our food, and we eat sugar separated from its fiber and trace nutrients. Sugar (fructose, not glucose) is the cause of bad LDL (the super sticky stuff that sticks to arteries). Fluoride is a Vit. D antagonist, not to mention we hardly get that much D being indoors a lot or outside, but covered with sun screen. And there’s crappy gut microbes due to sugar and HIGHLY likely inflammation from stress. Plus there’s dioxins found in animal sourced food, meat, eggs, dairy. The list goes on.

    I love Coconut fat. Use on my skin, hair, and eat it. I was very foggy one day, probably from not enough fat, and my brain woke up. It helps me feel satiated and eat less.

  61. WilliamLawrenceUtridge says:

    Most seed oils were extremely difficult to extract in any significant quantities before industrialization.

    Really…so the massive presses used in the Roman Empire to extract olive oil didn’t exist? And the Japanese noble expression “peasants are like sesame seeds, if you want more oil out of them you just have to squeeze harder” didn’t exist?

    It’s amazing that despite modern people doing everything wrong and eating the wrong diet and whatnot, we’re still living longer, in better health, than in generations past. Astonishing that we can do so many things wrong yet still see life expectancies climb (recent changes being the exception because calorie excesses of the superobese are finally starting to impact mortality rates).

    Eat food. Not too much. Select a variety. Cook it yourself. Don’t pretend it’s medicine. I personally find coconut oil is incredibly greasy and has an unpleasant mouthfeel.

    1. J_N says:

      I specifically mentioned olive oil as separate from the class of industrial vegetable oils. It has a rich history of consumption and I have no disagreement with you if you consider it healthy.

      Sesame oil is another one which has been consumed historically in not only Japan, but India as well. It was and is used predominantly as seasoning in Asian cuisine, in small amounts.

      Sesame Oil contains 42% oleic acid, 15% saturated fat, and 43% omega-6 linoleic acid. It can be used for frying because it contains unique antioxidants that are not destroyed by heat. However, the high percentage of omega-6 militates against exclusive use.

      My issue is with the industrially produced vegetable/seed oils which have no precedence of consumption in our history and are highly processed and refined. Even unrefined and cold pressed oils rich in PUFA should not be consumed as a major source of fat owing to the limited requirement for PUFA.

      It’s ok if you don’t like coconut oil. I personally use it liberally alongwith olive oil.

    2. WLU–Ah, but coconut milk, in a yummy curry and lots of fresh fruits/veggies and shrimp? or a variant of tom yum soup…the potential health benefits are just a nice addition.

      Matter of fact, what’s your take on the mentality behind such a near-obsession some people have with finding various breathless claims about a given food? why not just enjoy it with moderation (yeah, I know, some people have problems with the moderation part, but that’s not the issue here, I think.) Dr. Mark says food should not be just another treatment (and I agree) but WHY do people keep looking to make it so?

    3. Mike F says:

      Most olive oil comes from the fruit and not the seed. I also qualified my statement. I didn’t say it didn’t exist, I said seed oil wasn’t made in any significant quantity.

      Traditional forms of seed oil, sesame, grape, etc. were expensive and limited in quantity. And to this day good quality seed oil is still expensive.

      Any argument I’d make to further this discussion has already been said better already.

  62. Mie says:

    “First it says one thing based on a flawed set of studies, then says something completely different based on another set of flawed studies.”

    And here I was, thinking that the accumulation of evidence and novel insights into old data were PRECISELY progress. Silly me.

    “A majority of nutritional recommendations are based on observational studies, meta-analyses of observations studies and trials which have inherent design flaws. The FFQ which is used to assess dietary habits is one the favourites of researchers. It tells us squat about actual diet. But what do I know, I’m actually stupid enough to believe that the foods we’ve been consuming for centuries and have thrived upon are good for us. But no way there is any causality there. Causality comes only from observational studies and those fantastic meta-analyses which do a great job of putting a lot of unreliable studies together so we can have one great, big unreliable study. The hierarchy is untouchable, so are the recommendations by the great researchers who are beyond reproach.

    “Yes, we’re talking about how lauric acid in mother’s milk is so good for the development of the baby but suddenly when it’s in coconut oil, we should be very careful about consuming it because you never know what those pesky SFAs are upto.”

    Ever heard of dose and context? A simple analogue: is giving a drink heavy on sugar & intended to provide energy surplus detrimental to health? Depends. Not when we’re talking about a recovery drink consumed by an athlete. Most likely yes when we’re talking about a met.syndrome patient.

    “Oh, me and the mistakes I keep on making. Got to do something about it. It’s a U curve which shows that the best place to be cholesterol wise is 200-220 if you want the lowest risk of heart disease and 200-240 if you want the lowest all cause mortality.”

    Both names are used, U and J. Just like your OWN SOURCE mentions. Try reading them once, just once.

    Apart from that silly remark, you (once again) just repeated the same BS without addressing my points.

    So yes, I think we’re done here.

    P.S. Unless Enig can back up her claims with something concrete (memo, minutes etc. etc.), I’ll stick to my current stance.

    1. Mie says:

      Damn, forgot to delete that long part about different study protocols. It’s damn shame you can’t edit your comments.

  63. Mie says:

    “Point 1 clearly states that replacing animal and trans fats with seed oils rich in LA (n-6) resulted in an INCREASED incidence of heart attacks and overall mortality. That’s not making much of a case for n-6 rich oils, is it?”

    And just when I thought you couldn’t possibly display any greater ignorance … Do you understand the meaning of statistical signifigance? The point is precisely that since there’s none, we simply CANNOT tell anything reliable – whether n-6 fatty acids are detrimental to health or not, nada. Plus bearing in mind the fact that this was even when n-6 intake was much, much larger than nowadays.

    “Point 2 is basically saying that IF you are deficient in n-3, replacing animal and trans fat with a combination of LA and omega-3 fats reduces incidence of heart attacks and overall mortality. This shows the benefits of NOT being deficient in omega-3, that’s about it. It’s not a vindication of replacing SFA rich oils with PUFA.”

    … which is, once again, BS. This time from Guyenet, originally. We have ample proof of the independent health benefits of n-6 fatty acids, when consumed according to guidelines.

    http://www.ncbi.nlm.nih.gov/pubmed/19171857

    We also know of health benefits provided by n-3 fatty acids. However, both alone aren’t sufficient to account for the benefit found in Ramsden et al – and both alone cannot be found in PUFA rich foods.

    “The benefits of statins are not due to cholesterol lowering. They are because of their anti-inflammatory and pleotropic effects. Uffe Ravnskov has had a paper published where he shows that there is no dose-response effect of cholesterol lowering by statins on atherosceloric plaque, which would be expected if there was any causal link between LDL and heart disease.”

    Which, once again is BS. Ravnskov is about as reliable a reference here as David Icke would be if the discussion was about Mayan pyramids. The clinical benefits of statins are due mainly to their lipid lowering effect. See

    http://www.ncbi.nlm.nih.gov/pubmed/16214597

    As JUPITER and other trials indicate, lowering inflammation can provide additional benefits (there are currently two large trials addressing this going on).

    In addition, the regression of atheroclerotic plaques takes place too. See e.g. the SATURN trial

    http://www.ncbi.nlm.nih.gov/pubmed/16214597

    Uffe doesn’t have a clue.

    “Statins have a number of negative side effects including cognitive decline, muscle pain, CoQ10 depletion, etc.”

    Yep. Most of these can be addressed by switching from one statin to another. And if that doesn’t help, then something else (there is other medication available too). Ever heard of a drug with no adverse effects? I haven’t. The key is the clinical benefit gained after accounting for the adverse effects.

    “Emily Deans, a well-known Psychiatrist has blogged about the importance of cholesterol for the brain and the implication of cholesterol lowering on brain related illnesses.”

    I bet she had.

    “It is pertinent to note that there has been no causality established for high LDL and heart disease either.”

    BS. LDL is a causative risk factor. To deny this is to make a religious claim in scientific discourse.

    “If Lauric acid raises HDL by 10 and LDL by 20, that’s very good for the ratio. A LDL/HDL ratio of 2:1 is great. That’s why the authors state lauric acid has the best effect on TC/HDL ratio of ANY fatty acid.”

    J_t512 addressed this earlier in his post. It’s not an issue of foods rich in lauric acid vs carbs, it an issue of food rich in lauric acid vs foods rich in PUFA. Or why do you think coconut oil fares poorly whereas e.g. vegetable oils don’t when looking at beneficial changes in tot.chol:HDL ratio of whole foods, hmm?

    Next time (if there is a next time) try to address the points made earlier. Otherwise you’re not discussing, you’re preaching.

    “The following part of Masterjohn’s analysis (which I linked to earlier as well) is relevant before concluding health benefits based solely on the Total/HDL ratio findings of this study (which considered cholesterol levels to stabilize within 13 days by the way):”

    Good post, since it pretty much shows how much Masterjohn is talking out of his ass.

    1) The ol’ “correlation isn’t causation” claim. Yes, everybody knows that. And yes, Masterjohn himself chooses to ignore this when it suits his needs. Cherry, anyone?

    2) Speculating on this

    “Maybe cholesterol linoleate can accumulate in the liver for 13 days without adverse effects, but what happens over the long term when cholesterol esters progressively accumulate in that organ? Can that go on forever? Longer studies would be needed to find out.”

    as if it were likely to happen. If the effect of LA on LDL receptor activity would somehow become less relevant – or even detrimental – as time passes on, we would see this in observational evidence. But we don’t.

    3) Plain ignorance as in this

    “It isn’t quite clear how some saturated fats decrease the total-to-LDL cholesterol ratio. Perhaps they enhance LDL receptor function by decreasing oxidative stress, but there could be many possibilities.”

    Err, SAFA has been shown to decrease LDL receptor activity. And these SAFAs, like lauric acid, raise LDL a great deal more than HDL, so when foods containing them are compared to carbs, the tot.chol.:HDL ratio improves, yes. But when compared to PUFA, no.

    4) Good ol’ cherry-picking. Masterjohn claims that trials showing “that unsaturated fats reduce heart disease risk compared to saturated fats” were poorly conducted, whereas he neglects to mention that

    a) quite many of them are from the same era as e.g. Rose et al (1965) which he mentions – and with no large methodological differences –

    b) without mentioning in Rose et al (1965) the results weren’t statistically significant.

    c) And of course, Masterjohn doesn’t mention that meta-analysis by Hooper et al (2011) which showed that RCT evidence from fat modification trials shows reduction in CV events – a clear benefit.

  64. WilliamLawrenceUtridge says:

    @brewandferment

    Yeah, I have no idea where the obsession comes from. There is no reason to suspect that there is some magical food ingredient that will keep you in perfect youth and health for your entire life. Sadly, we will all die eventually, and in the years before our death we will almost certainly be in worse health than we were in our youth. I prepare for this by eating lots of fruits and vegetables, and getting lots of exercise. Putting all your eggs into one giant coconut seems like quite the gamble.

    My issue is with the industrially produced vegetable/seed oils which have no precedence of consumption in our history and are highly processed and refined. Even unrefined and cold pressed oils rich in PUFA should not be consumed as a major source of fat owing to the limited requirement for PUFA.

    Potatoes had no precedence in our consumption until a couple thousand years ago, dito tomatoes, turkeys, corn, peppers and most squashes. Bump that back to a couple hundred years ago for any non-South Americans. Distilled, high-potency alcohol also didn’t exist before a couple hundred years ago. In fact, most of the history of modern technology is the increasing purity and concentration of rare substances. Doesn’t mean it’s automatically bad for us. Further, mainstream medical advice isn’t “chug a bottle of Canola every day”, it’s to use it in moderation as part of a diet high in unrefined foods rich in fruits and vegetables. Use a small amount of oil in cooking. The serving size of high-oil foods like margerines is quite small, less than a tablespoon. In fact, the people who recommend highly-processed high-fat diets tend to be the fringe minority from what I can tell. Certainly the USDA guidelines don’t endorse it. Anybody who consumes large amounts of highly refined oils in the form of highly processed foods really isn’t eating healthy by any stretch of the imagination, according to conventional dietary advice.

    Eat food. Not too much. Mostly plants. Cook it yourself. Exercise. Still far better advice than “eat coconut oil in large quantities” in my mind.

    1. Chris says:

      In addition, grow some of it yourself. Learn what it takes to get edible stuff out of seeds, soil, fertilizer and water. Or maintaining fruit trees, especially with ravenous squirrels (that seem to love persimmons before they ripen!). It is not as easy as some think.

      By the way, on our vacation around our little but mountainous state, hubby and I would share a salad and an entree. We found that not only was the dinner bill cut in half, we ended up eating a much more reasonable (and healthy!) amount of food.

      (I thought being out of town for several days that the moderation issue would have been solved. Alas, no!: All of my comments still go into moderation. Le sigh.)

  65. Carmen says:

    It is a fad. The benefits of coconut oil are being broadcast everywhere you look. Whenever the next things comes to our attention, we’ll forget all about it. Remember the Atkins Diet? The Zone Diet? Hula hoops? I do like to use coconut oil in foods as it’s easy on my stomach. I’ve also read about benefits of coconut oil, and risks. I think it needs more time and research before we actually know. Eggs used to be extremely bad for us, and now, maybe not.

  66. Carlos Oliveira says:

    PART 1 – Some scientific articles that compare Extra Virgin Coconut Oil with others oils :

    As we can see in the reference and part of articlle published this month(february 2013) in the prestigeous medicine journal , the Britsh Medical Journal (BMJ) , I guess that things now will looks to be “upside down” to the researchers that in a old fashion , still believes (awry?) that extra virgin polyunsatured fats (as soy oil , etc) are better than extra virgin satured fats (as extra virgin coconut oil) .

    In the article of the BMJ ,”Use of dietary linoleic acid for
    secondary prevention of coronary heart disease and death: evaluation of
    recovered data from the Sydney Diet Heart Study and updated meta-analysis” , they concluded :

    From the article of BMJ:

    a) What is already known on this topic?·
    CIncreasing dietary omega-6 linoleic acid in the place of saturated fat lowers total cholesterol and low density lipoprotein cholesterol ·
    Advice to substitute linoleic acid for saturated fat is one component of dietary guidelines to reduce the risk of coronary heart disease; however, clinical benefits specific to linoleic acid have not been established.·
    A comprehensive analysis of the effects of linoleic acid on death from coronary heart disease and cardiovascular disease was previously not possible, owing to missing outcome data from the Sydney Diet Heart Study, a randomized controlled clinical trial” (part of the text of the scientific article of BMJ).

    And that :

    b) Still from the artile of BMJ :

    ” What this study adds:·

    In this cohort, SUBSTITUTING OMEGA 6 LINOLEIC ACID FOR SATURATED FAT DID NOT PROVIDE THE INTENDED BENEFITS, BUT INCREASED ALL CAUSE MORALITY, CARDIOVASCULAR DEATH, AND DEATH FROM CORONARY HEART DISEASE.
    An updated meta-analysis incorporating these missing data showed no evidence of benefit, and suggested a possible increased risk of cardiovascular disease from replacing saturated fat with omega-6 linoleic acid .( part of the text of the scientific article of BMJ).

  67. Carlos Oliveira says:

    PART 2 : scientific articles about. Extra virgin coconut oil:

    Continuing :

    According the United States Agricultural Research Service (National
    Nutrient Database- National agricultural Library) the percentual of the polyunsatured fatty acid called LINOLEIC ACID (or the so called Omega 6 ) in each 100 grams of vegetable oils are(approx.) :

    SAFFLOWER OIL – CONTAINS over 70% of linoleic acid (Omega 6)

    SUNFLOWER SEED OIL – CONTAINS 65% of linoleic acid (Omega 6)

    SOYBEAN OIL – CONTAINS 50% to 55% of linoleic acid (Omega 6)

    COTTON SEED OIL-CONTAINS 61% of linoleic acid (Omega 6)

    CORN OIL – CONTAINS 59% of linoleic acid (Omega 6)

    SESAME OIL- CONTAINS 41% of linoleic acid (Omega 6)

    OLIVE OIL – CONTAINS 9% of linoleic acid

    EXTRA VIRGIN COCONUT OIL – CONTAINS ONLY 1.8% OF LINOLEIC ACID (OMEGA 6)

    Based in the article of BMJ and in the percentuals of linoleic acid (Omega 6) in each vegetable oil , it looks that , for health, foods with high content off liinoleic acid (Omega 6) are ot so safe.

    As we can see above ,extra virgin coconut oil (E.V.C.O.) have a large advantage over the others vegetable oils , once E.V.C.O. have the lowest content of Omega 6 (only 1.8% of Omega 6),

  68. Carlos Oliveira says:

    Corrected:

    Based in the article of BMJ and in the percentuals of linoleic acid (Omega 6) in each vegetable oil , it looks that , for health, foods with high content off liinoleic acid (Omega 6) as soy oil, sunflower seed oil, córn oil, etc. , ARE NOT so safe .

    As we can see ,based too in the texts of articles above ,extra virgin coconut oil (E.V.C.O.) have a LARGE ADVANTAGE over the others vegetable oils , once E.V.C.O. have the lowest content of Omega 6 (only 1.8% of Omega 6),

    1. Carlos Oliveira says:

      Scientific articles about human trials with extra virgin coconut oil (EVCO) and others medium-chain triglycerides(MCT) :

      1) The Garvan Institute of Medical Research was founded in 1963. in Sydney, it is now one of Australia’s largest medical research institutions with nearly 500 scientists, students and support staff. Garvan’s main research programs are: Cancer, Diabetes & Obesity, Immunology and Inflammation, Osteoporosis and Bone Biology, and Neuroscience.

      I paste bellow sentences from the site of the Garvan Institute , and parts of the article made by researchers of the Garvan Institute , and published in the prestigeous american medical journal called DIABETES , about extra virgin coconut oil (EVCO) and others medium-chain triglycerides(MCT) as effective augmentation therapy as food supplement to diabetes type 2 patients .

      Some sentences from the site of the Garvan Institute and from the abstract of a research article shows that extra virgin coconut oil , in the small (and safest ) doses of only one tea spoon three times a day , enhances mitochondrial function and can lower the insulin resistance , helping in the prevention and treatment of diabetes type2 ( and maybe can helps in the so called diabetes type 3 too ?.)

      Maybe , can we make an empirical use of one tea spoon one time a day for prevention , and one tea spoon three times a day , using EVCO as an augmention therapy ?.

      FROM THE SITE OF GARVAN RESEARCH INSTITUTE OF AUSTRALIA :

      a) Title of a media release in 08 Sep 2009” : “ HOW EXTRAVIRGIN COCONUT OIL COULD HELP REDUCE THE SYMPTOMS OF TYPE 2 DIABETES” :

      “A new study in animals demonstrates that a diet rich in coconut oil protects against ‘insulin resistance’ (an impaired ability of cells to respond to insulin) in muscle and fat. The diet also avoids the accumulation of body fat caused by other high fat diets of similar calorie content. Together these findings are important because obesity and insulin resistance are major factors leading to the development of type 2 diabetes…”

      b) Title of the article of Garvan Institute of Australia published in the journal :

      DIABETES. 2009 November : “ ENHANCEMENT OF MUSCLE MITOCHONDRIAL OXIDATIVE CAPACITY AND ALTERATIONS IN INSULIN ACTION ARE LIPID SPECIES DEPENDENT “

      Part of the texto f the abstract : “ … MCFAs induce a substantially greater upregulation of mitochondrial oxidative capacity in muscle, and this appears to be at a sufficient level to prevent the deleterious effects of lipid oversupply on insulin action in this tissue… “ ( published in the journal : DIABETES. 2009 November)

      2) We can find in the abstract of a research article:from the Boston University about the total doses of 18 grams of extra virgin coconut oil (EVCO) as one of the SAFEST DOSES ( low doses) of extra virgin coconut oil (and others medicum-chain tryglicerydes too ).

      FROM THE JOURNAL METABOLISM 2007 JULY :

      Title of the article : EFFECTS OF DIETARY MEDIUM-CHAIN TRIGLYCERIDE ON WEIGHT LOSS AND INSULIN SENSITIVITY IN A GROUP OF MODERATELY OVERWEIGHT FREE-LIVING TYPE 2 DIABETIC CHINESE SUBJECTS. (from the Department of Medicine, Obesity Research Center, Boston University School of Medicine, Boston:

      Part of the text of the abstract : “ … The TEST OIL (18 G/D) was administered as part of daily food intake for 90 days. All subjects completed the study with self-reported full compliance.

      Body weight, waist circumference (WC), and serum samples were analyzed on days 0, 45, and 90. The MCT group showed an across-time reduction in body weight and WC, an increase in serum C-peptide concentration, a reduction in homeostasis model assessment of insulin resistance, and a decrease in serum cholesterol concentration (P < .05, repeated measures) …” (FROM THE JOURNAL METABOLISM 2007 JULY) .

      My note :The 18 mililiters by day, it is equivalente to one TEA SPOON (approx.six mililiters in each tea spoon) of extravirgin coconut oil (or MCT) THREE times a day.
      Doses of ONE table spoon TWICE a day can be so safe as that doses of 6 mililiters three times a day, but ONLY THE PHYSICIAN of the patient can gives permission to the patient takes extra virgin coconut oil and others MCT , or any food supplement or medicine drug.

      1. Carlos Oliveira says:

        As we can see in the article of Garvan Institute , EVCO and others MCTS , can works as mitochondrial function improvers :’ … MCFAs induce a substantially greater upregulation of mitochondrial oxidative capacity…’.

        As , between others biochemical , metabolical, molecular disorders , one of the main brain disorders in neurodegenerative diseases (Alzheimer disease, dementia by stroke sequelae , vascular dementia, Parkinson disease, etc) is the mitochondrial disorder , maybe we can hypothesize that the the improving of mitochondrial function that EVCO and others MCTs gives to muscles, can works to the neurons too , and together with the increased ‘offering’ of ketone bodies by EVCO and others MCTs as “alternative fuels” to the neurons , associated to the improving of mitochondrial function by that MCFAs , maybe it can leads to a synergistic double mechanism by EVCO and others MCTs to improve energy to the neurons in neurodegenerative diseases (?). (that is only a hypothesis)

  69. Carlos Oliveira says:

    - J Drugs Dermatol. 2007 October – title of the article – Novel antibacterial activity of monolaurin compared with conventional antibiotics against organisms from skin infections: an in vitro study.-authors : Carpo BG, Verallo-Rowell VM, Kabara J. – Department of Dermatology, Makati Medical Center, Makati City, Philippines.
    OBJECTIVE: A cross-sectional laboratory study to determine the in vitro sensitivity and resistance of organisms in culture isolates from skin infections and mechanisms of action of monolaurin, a coconut lauric acid derivative, compared with 6 common antibiotics: penicillin, oxacillin, fusidic acid, mupirocin, erythromycin, and vancomycin.
    CONCLUSIONS: Monolaurin has statistically significant in vitro broad-spectrum sensitivity against Gram-positive and Gram-negative bacterial isolates from superficial skin infections. Most of the bacteria did not exhibit resistance to it. Monolaurin needs further pharmacokinetic studies to better understand its novel mechanisms of action, toxicity, drug interactions, and proper dosing in order to proceed to in vivo clinical studies
    - J Invest Dermatol. 2009 October – antimicrobial property of lauric acid against propionibacterium acnes: its therapeutic potential for inflammatory acne vulgaris. –authors : Nakatsuji T, Kao MC, Fang JY, Zouboulis CC, Zhang L, Gallo RL, Huang CM.
    - FEMS Immunol Med Microbiol. 2003 May – Antibacterial actions of fatty acids and monoglycerides against helicobacter pylori – Sun CQ, O’Connor CJ, Roberton AM. – Department of Chemistry, The University of Auckland, Private Bag 92019, Auckland, New Zealand.

    1. Carlos Oliveira says:

      More scientific articles about the antimicrobial effects of the monoglycerides of extra virgin coconut oil (EVCO) , THE LAURIC ACID (forms 50% of EVCO) , and it derivative , the MONOLAURIN:

      - Bergsson G, Arnfinnsson J, Karlsson SM, Steingrimsson O, Thormar H. – In vitro inactivation of chlamydia trachomatis by fatty acids and monoglycerides. – Antimicrob Agents Chemother.1998

      - Bergsson G, Arnfinnsson J, Steingrimsson O, Thormar H. – In vitro killing of candida albicans by fatty acids and monoglycerides – Antimicrob Agents Chemother. 2001.

      - Schlievert PM, Deringer JR, Kim MH, Projan SJ, Novick RP. – Effect of glycerol monolaurate on bacterial growth and toxin production – Antimicrob Agents Chemother. 1992

      - Projan SJ, Brown-Skrobot S, Schlievert PM, et al. -Gglycerol monolaurate inhibits the production of blactamase, toxic shock syndrome toxin-1, and other staphylococcal exoproteins by interfering with signal transduction. – J Bacteriology. 1994

      1. WilliamLawrenceUtridge says:

        A couple points:
        a) I’m not sure who you are posting these for anymore, I don’t really think anyone cares about this page anymore
        b) weblinks are always preferable to lengthy copy-pastes, which might even be copyright violations
        c) recent articles are always preferable to older ones, very few people here would find a 19-year-old primary source to be particularly convincing
        d) why are you bothering to post this in the comments section on a website? Why not take this basic research and test it in real-life scenarios? I’m always reluctant to trust test tubes and rat studies, since people are not test tubes or rats.

        1. Carlos Oliveira says:

          a) “… I’m not sure who you are posting these for anymore, I don’t really think anyone cares about this page anymore..”

          Thank you very much , once it is a honor to me , that you as a prestigeous researcher that you are , you spent your time to read my comments
          But I guess that as me (note : I’m not a researcher) , there are others readers here, that are not researchers too , and that want to read a little more about extra virgin coconut oil and it derivatives, the lauric acid and monolaurin . Then I pasted that little information about that so controverse issue.

          b)” … weblinks are always preferable to lengthy copy-pastes, which might even be copyright violations…”

          Once not all readers here, as me too, are not scientific researchers , some of us , the readers , can find to be easier and faster to read small parts of the texts of scientfic articles , than to read all the article to take our conclusions . I only pasted that part of articles here, trying to make things easier to non researchers like me.
          As a prestigeous researcher that you are, you know better than me , that to paste some sentences from an article , do not violate none copyright , and I guess that the authors of the articles above, that wants to gives access to most people as they can , about the benefits of very small doses of extra virgin coconut oil , they never will see my comments as a “ copyright violation” , once I put the name of the authors , and once they are enough clever to understand that it is to propagate the important information of their articles.

          1. Carlos Oliveira says:

            Continuing :

            c) “… recent articles are always preferable to older ones, very few people here would find a 19-year-old primary source to be particularly convincing…”
            If you give me again the honor to read some of my comments above, you will see that there are references of scientific articles from 1978 to 2013 , as the article published this year, in february 2013 , in the British Medical Journal with the title : “Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis “ (BMJ – february 2013)

            d) “ … why are you bothering to post this in the comments section on a website? Why not take this basic research and test it in real-life scenarios? I’m always reluctant to trust test tubes and rat studies, since people are not test tubes or rats…”
            If you take a look again in my comments above , you will see that I pasted the title of an article (and part of it) , that researchers fromn BOSTON UNIVERSITY made a scientific TRIAL WITH HUMAN BEINGS (“in real –life scenarios) , with médium chain triglycerides :
            Title of the article : Effects of dietary medium-chain triglyceride on weight loss and insulin sensitivity in a group of moderately overweight free-living type 2 diabetic chinese subjects. (from the Department of Medicine, Obesity Research Center, Boston University School of Medicine, Boston)

            About to be “bored” , we have always the choice to do not read the comments that do not have none interest to us . It is a question of choose it or not .
            Anyway , thank you very much to give me the chance to clarify that my targets with my comments are only to change more information with persons that see this issue about extra vigin coconut oil as something that desserves deeper studies and comments by scientists , and by non scientists.

  70. WilliamLawrenceUtridge says:

    “médium chain triglycerides” do not equal “coconut oil” or “virgin coconut oil”. If actual experts have reviewed this august body of knowledge and none came back to recommend coconut oil, it just seems like it’s not worth recommending the purchasing and consumption of this expensive and obesogenic food. Perhaps this is a temporary feature and in the future coconut oil (or its purified extracts) will be viewed as a nigh-miraculous treatment. In the meantime, promoting your views would seem to be much more fruitfully undertaken somewhere that a researcher in the area might take notice. But, please yourself.

    1. Carlos Oliveira says:

      Thanks

      Extra virgin coconut oil is a food supplement that I guess that the patients have to talk to his/her physician before to use it,

      If the physician of the patient gives permission to use EVCO , the better maybe it is ,to use very small doses as 1 to 3 tea spoons by day , but always as part of a health style of life with moderate physical exercises, and meals with lots of vegetables, fruits, water (as the meals that you use to recommend).

      Only to clarify : medium chain-triglycerides are some of the main components of extra virgin coconut oil , but not all medium-chain triglycerides are made from extra virgin coconut oil .
      .

      .

    2. That’s about as sensible an argument as saying that “protein” does not equal “turkey breast” therefore it’s not worth recommending the purchasing and consumption of this expensive and obesogenic food. How about the proper argument that coconut oil (like turkey breast) contains healthful properties and should be included as a part of a balanced diet? The main problem with the “American diet” is that U.S. government recommendation has been to reduce fat to below 30% of calories and to consume mostly omega-6 polyunsaturated oils. That has directly lead to the explosion of obesity and metabolic syndrome. A plethora of evidence now points to the need to balance omega-3 and omega-6, which cannot be done when over-consuming omega-6 to the level the average American does, even with taking an omega-3 supplement. The only logical course is to replace those soy and corn oils with other fats, including monounsaturated (olive, peanut, canola) and medium-chain saturated (coconut, palm) primarily, and long-chain saturated (cream, butter, lard) too in moderation. Coconut oil certainly contains MCFA and is a part of a healthy balance of fats. Trying to paint it as a fringe supplement is ludicrous. It has always been a staple food throughout human history. It’s not some kind of artificially derived chemical that has to be purified. The fact of the matter is that a paltry few studies on hydrogenated coconut oil decades ago along with an irrational fear of saturated fats besmirched coconut oil’s good name. Countless studies in the interim have vindicated it as a healthy food.

  71. WilliamLawrenceUtridge says:

    That’s about as sensible an argument as saying that “protein” does not equal “turkey breast” therefore it’s not worth recommending the purchasing and consumption of this expensive and obesogenic food. How about the proper argument that coconut oil (like turkey breast) contains healthful properties and should be included as a part of a balanced diet?

    The last part of your statement is true – coconut oil and turkey are both foods. By corollary, neither are medicine. Claims that turkey, and coconut oil, have medicinal properties unique to them, that transforms them from food into medicine, is one that must be tested rather than asserted. Certain components of both may be purified and distilled into medicines (which must be tested for safety and efficacy). Turkey and coconut oil may contain healthful properties the same way all foods contain healthful properties – but these healthful properties no more render them medicines than the healthful properties of an apple.

    Also, turkey breast is rather low in fat but high in protein, which has many advantages. Coconut oil, gram for gram, is far more fattening, and obesity has known health risks. Recommending people consume an extra serving of any high-fat food (1 tbsp = 120 calories or so) in the absence of clear, obvious health benefits identified in randomized, controlled trials, is irresponsible. Coconut oil may be healthier than transfats, beef tallow or olive oil – but can you show me a RCT that identifies this fact? I doubt you can, and until you can you’re recommending people consume a high-fat food as medicine with no good reason.

    That has directly lead to the explosion of obesity and metabolic syndrome. A plethora of evidence now points to the need to balance omega-3 and omega-6, which cannot be done when over-consuming omega-6 to the level the average American does, even with taking an omega-3 supplement.

    I’m pretty sure the scientific consensus is that the explosion of obesity and metabolic syndrome is due to eating too much and in particular too many refined foods and exercising too little. I’ve seen the “omega fatty acid” balance argument before. I’ll believe it when it’s endorsed by several major medical societies. However, I will also note that your recommendations are borderline identical to the USDA’s – a broad diet of mixed foods, including reasonable servings of lean meats, fruits, vegetables, and vegetable fats.

    The only logical course is to replace those soy and corn oils with other fats

    The only logical thing to do is to treat it like a food until proven otherwise, and consume it in moderation if you like the taste.

    Trying to paint it as a fringe supplement is ludicrous.

    Can you point to any major medical bodies that recommend its consumption? But Joe Mercola says it’s a miracle. That’s my definition of fringe, that man is a loon, but perhaps you have a different one.

    It has always been a staple food throughout human history.

    So has sausage, raw seal meat, whale blubber, beer and fava beans. Being a staple food doesn’t mean it’s healthy, and particularly doesn’t mean it’s medicinal.

    It’s not some kind of artificially derived chemical that has to be purified.

    First, “artificial” is not the same as “healthy”, any more than “natural” equals “healthy”. Lots of natural things will kill you, and if appropriately concentrated, will also heal you – and same for artificial things. Purification and standardization increases the safety of drugs, but can also concentrate harmless substances to the point that they are harmful. Vitamins are an example – polar bear liver will kill you, and chronically high doses of some vitamins will do so as well over the longer term.

    Countless studies in the interim have vindicated it as a healthy food.

    Apparently not enough for any major medical body to recommend it. I’m going with them, thanks.

    1. Thomas says:

      If by medicine, you’re referring to a “drug”, and not the wider practice of diagnosing and treating disease, then by definition, food is not a drug. A drug is a substance, other than food, that has a physiological effect when ingested or otherwise introduced into the body. Obviously food has the same definition as a drug — in that it has a physiological effect when ingested — other than that food is excluded from the definition of a drug. In other words, food and drugs are identical, except that drugs are non-food, i.e. have no nutrient value. But while food is not a drug, it is certainly medicine. It is the primary form of medicine, as you yourself alluded to the idiom: an apple a day keeps the doctor away. Proper diet should in most cases avert any need for additional medical care. Furthermore, as you yourself admitted, drugs can be synthesized from food by “purifying” away the nutritive value of the food such that only the non-nutritive elements of the food remain. This being the case, it is then logical to conclude that while food is not a drug, foods do absolutely contain drugs. And therefore, supplementing your diet with foods containing drugs is a perfectly reasonable way to achieve desired physiological effects without resorting to non-food drugs. Your distinction between food and drugs is irrelevant. Furthermore, the nutritive parts of food are arguably the more important ones as far as their medicinal applications are concerned in regards to metabolic syndrome.

      Coconut oil, calorie for calorie, is no more fattening than turkey breast. And calorie for calorie, it is arguably much *less* fattening than sugar and perhaps even less than turkey breast due to its satiating feedbacks. I.e. after eating 500 calories of coconut oil, you’ll be less likely to consume more calories than after eating 500 calories of turkey breast. Neither MCFA nor proteins are particularly harmful to metabolize, whereas other nutrients such as alcohol and fructose and excessive amounts of omega-6 polyunsaturated fats are harmful, cause inflammation, and lead to adipogenesis. To the extent that coconut oil displaces harmful foods, it is a boon to health, independent of any positive physiological effects of its own. There is no evidence that a high-fat diet is in the least bit dangerous whereas a high sugar diet is certainly dangerous. In general, the more calories we consume as fat, the less we consume as sugar. That is why the primal/paleo diet, glycemic index diet, and Atkins diet are successful.

      In addition to coconut oil, you site “sausage, raw seal meat, whale blubber, beer and fava beans” as traditional staple foods. And I agree. All are healthy as evidenced by the low instance of disease in the populations who consume them in the proportion that they consume them. The burden of proof for decrying a traditional food to be unhealthy is on those making the claim. If coconut oil were some novel invention of chemists, skepticism would be justified in adopting it. But as a traditional food consumed by much of the world much healthier than we Americans, the skepticism must be on excluding it from your diet.

      As far as where research is directed, it generally goes to where companies can make money and to where lobbyists direct government interests. That’s why most dietary research is directed at vindicating the corn and soy industries. The last thing they want is for us to recognize that the most profitable crops in America are making us sick. But by all means, continue following the recommendations which have caused Americans to become the most diseased country on the planet despite having the best access to food and medicine.

      1. WilliamLawrenceUtridge says:

        Proper diet should in most cases avert any need for additional medical care

        Congenital disorders. Infectious diseases.

        And therefore, supplementing your diet with foods containing drugs is a perfectly reasonable way to achieve desired physiological effects without resorting to non-food drugs.

        That assumes that the compounds within foods are of adequate volume and concentration to have a meaningful physiological effect, particularly for treatment of acute conditions. This is rarely the case. In the rare cases where you do achieve these concentrations, such as with say, menthol, they also have adverse effects, just like drugs do. If it can have an effect, it can have a side effect, because the body is poorly designed to segregate molecular actions, and reuses the receptors in multiple parts of the body – it’s why SSRIs will affect your brain and your gut.

        Coconut oil, calorie for calorie, is no more fattening than turkey breast. And calorie for calorie, it is arguably much *less* fattening than sugar and perhaps even less than turkey breast due to its satiating feedbacks. I.e. after eating 500 calories of coconut oil, you’ll be less likely to consume more calories than after eating 500 calories of turkey breast.

        Calorie for calorie, yes. Gram for gram, no – coconut oil is far more concentrated because it lacks water, while meat has lots of it (and protein, which also has a satiating effect). At no point have I ever said “eating a tablespoon of sugar is equivalent to a tablespoon of coconut oil”, nor would I. Most of the studies I’ve seen and heard of regarding weight loss and gain indicate that it is calories-in, calories-out that matter, irrespective their source. Nor did I suggest the wholesale consumption of alcohol was a good thing, but I will point out that lots of fructose, in the form of fruit, is well-supported as healthy. Rarely are any diets successful over the long-term, particularly fringe and fad diets like paleo and atkins. The populations that consume large amounts of whale blubber and seal meat also expend huge amounts of calories to get them, an enormous confound making any conclusions premature, and irrespective, groups for whom these were traditional foods still experience significant increases in life expectancy upon the advent of modern medicine. Hunter-gatherers still died younger than obese middle class North Americans.

        As far as where research is directed, it generally goes to where companies can make money and to where lobbyists direct government interests…continue following the recommendations which have caused Americans to become the most diseased country on the planet despite having the best access to food and medicine.

        Mmmmm…baseless conspiracy-mongering…ignoring the fact that the problem is Americans not following mainstream medical recommendations regarding diet and exercise…that’s some tasty straw man…

        1. Thomas says:

          Like I said, proper diet should *in most cases* avert any need for additional medical care. What’s rare is the acute cases of severe infectious disease or congenital disorders. Most of our health care system is involved in the slow laborious decline of health due to poor diet and the various acute problems such as tumors and heart attacks which result. It is the rare case that, following a proper diet, an individual needs acute care involving concentrated drugs. E.g. one case in which I needed acute care, it was antibiotics for a case of diverticulitis. This could have been avoided if I’d been better educated about the need for eating sufficient fiber, which I thought was only for old people, not for a 20-something. My doctors (and teachers) failed me because they did not ensure I was getting adequate nutrition, or to even know what that was, i.e. well care, but only checking for signs of sickness. When you get sick, often as a result of poor diet as either the primary or contributing cause, then you need drugs. The institution and practice of medicine should prevent you from getting sick, not only give you drugs afterward. That’s when you should be focusing on diet, which provides meaningful physiological effects over the course of time, not in response to an acute condition.

          Calories-in/calories-out is not a sufficient view of diet and weight loss/gain. Obviously there is a difference between consuming 2000 calories of beer and 2000 calories of salad. They are NOT metabolized even remotely the same. Fructose is in fact metabolized almost identically to alcohol — in your liver, causing fatty liver disease and metabolic syndrome in excess. So if you don’t think that 2000 calories of beer is a good idea, then neither is 2000 calories of orange juice. Whole fruit is healthy because it contains so much fiber that it would be very difficult to eat 2000 calories of fruit. 2000 calories is equivalent to about 40 whole oranges. Good luck managing that. But it’s only 4.5 32-oz (large soda sized) cups of orange juice. You can go through that without even thinking about it (say, while watching TV or working on your computer) and you’d still be quite hungry afterward. So, yes, fruit is good because the amount of fructose you can consume in whole fruit is relatively small, but fructose itself is bad in quantities larger than you can get from whole fruit. It’s similar to a single glass of wine being good, but the whole bottle not so much. Our bodies are meant to metabolize fat, protein, and glucose, and we function well when doing so. Fructose and alcohol are treated basically like toxins. Although we can get some calories from them, in excess they cause side-effects including cirrhosis, adipogenesis, insulin resistance, etc. Just because fructose is naturally occurring in fruits — and fruits in general are good for you — doesn’t mean fructose is good for you. Arsenic is also naturally occurring in fruits, but I don’t suggest you drink a glass of it.

          The *fact* of where research is directed does not have to be the result of a conspiracy, but just the emergent property of our current agricultural-medical-industrial-political system. The fact of the matter is that it is convenient and cheap to engage in an agricultural system that rotates corn and soybeans because it makes the best use of the soil with the least amount of energy. As such, our country produces a huge surplus of corn and soybeans, and research has been directed for decades at finding both dietary and other uses for these resources in order to best monetize them. That is where the invention of high-fructose corn syrup, soy-based meat substitutes, corn oil, biodiesel, ethanol, soy-based foam insulation, and other products came from. The market did not demand that corn and soy be made into these things; the producers of corn and soy funded research to try to fit their particular products into other niches. And they likewise have a strong lobby in DC ensuring that their products are not in any way besmirched with regard to the health recommendations of consuming them.

          Americans HAVE been following the recommendations regarding diet and exercise for the past 40 years or so since the food pyramid was published and fats (especially saturated fats) were demonized. Americans in aggregate brought their fat consumption down from 40% of calories to under 30% and significantly reduced saturated fat. As a result, they have replaced those fats with sugar (including fructose), which has caused overall calorie consumption to increase and metabolic syndrome to become an issue. It is the government-recommended diet that is the problem, not the solution. The solution is to go back to 40% of calories from fat and reducing fructose to what you can get from whole fruits only.

  72. WilliamLawrenceUtridge says:

    Like I said, proper diet should *in most cases* avert any need for additional medical care…Most of our health care system is involved in the slow laborious decline of health due to poor diet and the various acute problems such as tumors and heart attacks which result.

    At best, proper diet, whatever that means, might avert some chronic health complaints for some people. There are some genetic predispositions for late-life problems that no diet or exercise will ever eliminate. Further, heart attacks and tumors are consequences of aging, the fact that we are now living long enough to die of cancer and heart attacks rather than spear through the belly, starvation and infection. It’s no fault of the medical system or the USDA dietary recommendations that we can’t do much for an 89-year-old man with a tumor in his gut, the human body did not evolve to live into a long and healthy old age.

    This could have been avoided if I’d been better educated about the need for eating sufficient fiber, which I thought was only for old people, not for a 20-something. My doctors (and teachers) failed me because they did not ensure I was getting adequate nutrition, or to even know what that was

    I’m sorry, it’s your doctor’s fault that you didn’t follow the standard dietary recommendations of high-fiber grain products and lots of fruits and vegetables?

    The institution and practice of medicine should prevent you from getting sick, not only give you drugs afterward.

    What do you want doctors to do, follow you around and nag you to eat your vegetables? Force you at gunpoint to put down the Big Mac? Patients have a responsibility to take care of their own health, and it’s unfortunate that the invulnerability of youth is often challenged only when we experience a serious health complaint.
    Calories-in/calories-out is not a sufficient view of diet and weight loss/gain [snip] Our bodies are meant to metabolize fat, protein, and glucose, and we function well when doing so.That doesn’t obviate calories-in/calories out. If you consume more calories than you expend, you gain weight. The fact that it is easier to consume more calories in the form of refined foods (like, say, coconut oil) doesn’t change that balance. CICO is quite sufficient for explaining why we gain weight, it’s not, and it’s not meant to be, an explanation of why we eat. Can you show me any USDA recommendation that says “consume fruits in the form of drinking 2,000 calories worth of oranges”? But certainly there are juice fast diets that would recommend this.

    Fructose and alcohol are treated basically like toxins. Although we can get some calories from them, in excess they cause side-effects including cirrhosis, adipogenesis, insulin resistance, etc. Just because fructose is naturally occurring in fruits — and fruits in general are good for you — doesn’t mean fructose is good for you. Arsenic is also naturally occurring in fruits, but I don’t suggest you drink a glass of it.

    So, you’re saying the dose makes the poison, a recognized principle in toxicology. No argument there. You also seem to be implying that fruit is good, but high-fructose corn syrup, in pulls taken directly from the bottle are bad. Again, no argument. A bowl of powdered fructose, also a bad thing, as is a bottle of whiskey. Yup, agreed. But where can you ever find mainstream advice that implies any of this is a good thing? Mainstream advice is – unprocessed foods, whole grains, moderate intake of lean meats, low-fat cheese. Nowhere does the USDA recommend the consumption of processed foods.

    The *fact* of where research is directed does not have to be the result of a conspiracy, but just the emergent property of our current agricultural-medical-industrial-political system.

    You can also see it as the search for, and failure to find, magic ingredients that guarantee a lifetime of good health without any consequences. Unsurprisingly, this doesn’t exist, though quacks, organic farmers and supplement companies are happy to try to sell them to you by the bottle (such as the ability to buy fresh, cold-processed, first pressing virgin coconut oil gathered by nubile maidens riding free-range unicorns at your local Whole Foods). Don’t pretend McCain’s is the only company willing to sell you a crappy, unproven product – whoever is selling you that lovely bottle of coconut oil is not doing so out of the goodness of their hearts, it’s because they can make a profit.

    The market did not demand that corn and soy be made into these things; the producers of corn and soy funded research to try to fit their particular products into other niches. And they likewise have a strong lobby in DC ensuring that their products are not in any way besmirched with regard to the health recommendations of consuming them.

    And what’s your insight here, that agricultural subsidies in the US are profoundly irrational? Yup, I completely agree. They also contribute to the enormous food security the US has – to the point that obesity is a greater problem than starvation.

    Americans HAVE been following the recommendations regarding diet and exercise for the past 40 years or so since the food pyramid was published and fats (especially saturated fats) were demonized. Americans in aggregate brought their fat consumption down from 40% of calories to under 30% and significantly reduced saturated fat. As a result, they have replaced those fats with sugar (including fructose), which has caused overall calorie consumption to increase and metabolic syndrome to become an issue. It is the government-recommended diet that is the problem, not the solution. The solution is to go back to 40% of calories from fat and reducing fructose to what you can get from whole fruits only.

    Actually, no. The problem is the substitution of saturated fats with highly processed foods containing substantial amounts of highly processed sugars. The USDA does not recommend replacing butter with fruit roll-ups, the USDA recommends replacing butter with fruit. American consumers are the ones reaching for pop, junk food and fast food in spite of the USDA recommendations. It’s a frequent lie promulgated by the purveyors and pushers of fad diets that the USDA is fine with replacing fats with high fructose corn syrup. Here are three generations of food guidelines. Show me where it says “replace fat with soda” or “eat more white bread”. That looks an awful lot like 50% fruits and vegetables. In fact, the latest recommendations includes a table of empty calories. Notice soda is 100% empty calories.

    There is a substantial difference between “the USDA has a set of reasonable, healthy dietary recommendations” and “the American people follow the USDA’s reasonable, healthy dietary recommendations”.

    Also, back when processed foods didn’t exist, but high-fat diets did, did people still die of heart attacks?

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