If you carefully read the patent application, they state repeatedly that the only ingredient tested was MCT oil. The triglyceride of Caprylic acid is a medium chain triglyceride, and they say in their application that other combinations of MCTs would be expected to have the same effect. It was administered in whipped cream, which is not the same as emulsifying the product. They do say the emulsification may improve absorption and talk at length about having some products that are emulsified. Also, you may want to research coconut oil and cholesterol before making blanket statements that is will surely increase it. There are several studies out there showing that this is not the case if non-hydrogenated coconut oil is used. Nearly all of the saturated fats in coconut oil are the short and medium chain fatty acids, C6 through C12, which behave differently than the long chain saturated fatty acids. It is not difficult to find the nutrient composition on line.
You have had almost daily discussion about coconut oil and MCT oil for several months now and I understand that a number of people are improving using coconut oil and/or MCT oil and yet I still haven't seen any marketing about the Accera product. Even the adult physicians I work with have not heard a thing about it. My understanding in writing from a representative of the national Alzheimer's Association is that Accera withdrew their product from further clinical trials and will simply have GRAS status, which MCT oil has had for many years. How will they be able to promote it specifically as a treatment for Alzhiemer's disease? And how long will it take for them to provide the public with information that it may be beneficial for the many other diseases that have a problem with decreased glucose uptake? Should those people not be told that this could help while waiting for years for clinical trials that will never result in a stamp of approval from the FDA for those entities? There probably is more to ketones that simply providing alternative fuel, but it is a simple concept that ketones may allow neurons that cannot transport glucose to make energy by bypassing the problem; it is still unknown why these cells can't use glucose. There are three ketone bodies, beta-hydroxybutyrate, acetoacetate, and acetone (which is exhaled and doesn't hang around long.) No matter which medium chain triglycerides are metabolized, these same three types of ketones bodies are the end product. Therefore the ketones produced by eating coconut oil are one and the same as those produced by caprylic acid, or a a mixture of capric and caprylic acid (the OTC MCTs oil). Coconut oil has other fatty acids including some lauric acid, and all chain lengths from C6 through C 24, some monounsaturated and polyunsaturated fatty acids, including omega-6. Since the healthy brain is about 60-70% lipid, and every cell membrane and organelle require lipids, and the myelin sheaths around every nerve require lipids, I kind of like the idea of using coconut oil, since it makes every chain length of lipid available. There is still a lot that is unknown about lipids and biochemistry as a whole, how these substrates are utilized in our bodies. Steve improved when we were only using coconut oil. Was it simply the ketones or something else also? No one knows the answer at present. So while we are also using MCT we will keep using coconut oil.
My husband was quickly going down the tubes and since coming upon the information about MCT by chance and starting coconut oil, he has turned around and our life has changed. I suppose I could have kept this information to myself - I must say that I resent being vilified for telling people about it. Coconut oil is a food used by millions of people elsewhere in the world. It will never reach the status of a "drug" - what drug company will spend the money to do clinical trials when they won't be able to make it an expensive prescription drug after they put the money into it? To me it seems Dr. Henderson's studies were published in relatively obcsure journals that the majority of physicians don't even know exist and when there were a couple of press releases, they called Ketasyn (now Axona) a "novel therapy" that improved the memories of people with Alzheimer's and never divulged that it is simply MCT oil (at this point in time it is simply MCT oil that they obtained from Stepan Company - the very same product Dr. Veech has been using for years to make his ketones.) The website also does not readily disclose that it is MCT oil that produces the ketones. You only find this out if you download and can understand the paper written by Dr. Henderson.
guitarguy - I am giving 1 T. of coconut oil on toast and 1 T. MCT oil or almost that much daily. I have noticed improvement and I don't think that small amount of the coconut oil will hurt him as much as not giving it to him. I am going to order a bottle of the MCT fuel and incorporate some of that also. I agree with the Dr. about the fact that by the time trials are done it will be too late for my dh and I choose to bite the bullet and try about anything that even hints at progress. His quality of life is small now and I hope I can keep it at this level for a longer time.
If he had not shown improvement by this time I would have stopped the dosages.
marynewport and sunshyne - I really appreciate the work you are both doing regarding the viability of the MCT oil and coconut oil and posting things here on this board. However, I must admit most of your reports are way over my lowly head. I continue to skim over your writings and try to make my own decisions over how to dose to my dh. The way I look at it is, his future is pretty dim and anytime I see a glimmer of "hope" I am going to grasp it and pray for some answers to this terrible disease. I realize it is going to be quite a while before we have something available as a proven cure or preventative. Right now, until something better comes along, I am doing my own thing with the coconut oil and MCT oil. Thank you both again and I hope you continue with your postings and others report their experiences with both.
sunshyne keeps bringing up the fact coconut oil has saturated fat. I did a search for MCT Oil to find where to buy it and all the nutrition info says it is 100% saturated fat which would be logical since it comes from coconut oil. The only difference I can see is that coconut also has a little bit of poly and mono fats. marynewport - if it will help/delay my hb from going from MCI to AD, then we are for trying it. If it helps those who are way further along than him, then maybe it will help stop it for longer or maybe forever. Only time will tell for any of us.
We take Red Yeast Rice for cholesterol - tried statin drugs but his memory went on him. We have been on the Red Yeast Rice, which my naturopath says works just as well without the side effects, and the last check was after 6 weeks it had brought his cholesterol down from 220 to 210.
I am a big supporter of natural supplements when possible. I found it interesting that of all the AD drugs, galantamine which my hb is on, is the only one derived from a natural source vs a synthetic drug. Anyway, if right now MCT Oil and Coconut Oil are offering hope, then why not? My hb doctor's keeps bugging him about doing stool screening (he did do it in Nevada last fall but the results have not caught up to us I guess), but he forgets and I won't force it. Who cares if he is going to die from AD if cancer should come first?
I also appreciate the indepth info I have recieved here. I also went to the Dr. site and found the coconut oil at walmart that she spoke of. We are delaying dx as we are early stage and are noticing marked improvements. As far as I'm concerned and DH agrees its a " mind over matter" thing. If they don't have their "mind" does the rest really "matter"?
We are a family here at Joan's place. We come from many different backgrounds, but we have a very close bond -- we are all caregivers for our husbands and wives who are suffering from dementia, and we have come together here to help each other. Many of us are professionals -- doctors, nurses, scientists, engineers, educators. Many of us have other skills and knowledge bases. Some of us are brand-new to dementia, others have been all the way through the journey to the end and beyond. Each of us shares whatever we have to offer, to make the journey easier for all of us.
Me, I'm a scientist and businesswoman. Among other things, I founded and ran my own biotech company for 15 years, funding our research with many millions of dollars in grants and contracts that I received from more than a dozen Government agencies, including NIH, NSF, NASA, and DARPA. (DARPA may not mean anything to you, but it does to Dr Veech.) I've collaborated with leading scientists around the world. I have quite a few patents of my own, I've published in peer-reviewed journals and authoritative books, I sit on Scientific Review Groups at NIH and other agencies, and I review papers for a number of journals.
So one of the things I have to offer my dear family here is the ability to look into claims that various treatments can help AD patients. I report on what I find so that the others can make informed decisions for their loved ones.
I have read all of Dr Henderson's papers, issued patents, and published patent applications relevant to this subject. I've also read Dr Veech's, and Dr VanItallie's.
In fact, to contribute to this thread, I read papers that ranged from those published in the 1950's (I had to go back that far to find some of the ones most frequently cited by coconut oil enthusiasts) to some so new they are still in press -- their authors kindly sent me editor's proofs.
I am sure that everyone here is interested in your personal experience with your husband. All of us are trying to help our spouses in any way we can.
But please do not try telling my family here that coconut oil is "good for you" without checking your facts. I have, and from everything I've read, it's not. Don't try to tell my family here that coconut oil has been shown to be a safe and effective treatment for AD patients. It hasn't.
And I will not sit idly by if someone spreads misinformation on this site, because it could hurt someone I care about.
Thank you, Sunshyne, for your concern, research and knowledgeable reporting. Coconut oil may well fall in the category of "if you drink coffee..." If you work crosswords....If you keep your mind active.... Subjective observations aren't the same as controlled studies; and, for me anyway, my hb's dementia changes from day to day--sometimes hour to hour from good, better, worse and up and down the scale no matter what, it seems.
I want to relate a recent experience that I think will illustrate the difficulty of assessing whether anything helps with this disease. I've been reading this thread for a while, debating whether to start giving S. coconut oil, one of the MCT products, or waiting and giving Axona a try. For about the last month, S. has been remarkably happier, more affectionate, silly and playful, less grouchy, touchy, or dare I say, borderline nasty. I have wracked my brain but cannot think of a change that would have caused it, but there has been absolutely no change in his medications, daily routine, the weather has been even worse and more depressing, I haven't changed my approach in how I deal with him--in other words--nothing I can attribute this positive change to. However, if I had started one of the oils, etc., in December, I would certainly think that there was a cause and effect going on here. I realize that improvement in mood is different than in memory (no change there), but my point is that the unpredictability of this disease makes extremely difficult to say whether a particular treatment is working. That said, I really appreciate Sunshyne's postings too and am still pondering the choices.
We've all learned that what affects one spouse one way may not give another the same results at all. I haven't gone with any coconut oil or the like (though I agree it sounds promising), and we haven't joined any studies. That said, I did notice how my husband behaved about the time everyone started the oils. And mine, too, has been being more cheerful, less grumbly, in recent weeks. Maybe it's the daylight coming back... in spite of the snow I heard a cardinal calling this morning..
I think most of us would resent someone sitting on what appeared to be a harmless treatment because not enough double-blind studies have been run, and yet understand why scientists have to do them. I think most of us have encountered people who've been in studies which supplied treatment (or placebo) and then had it withdrawn at the end of the study. Joan herself encountered this when the treatment showed some signs of being harmful. We're all frustrated or disdainful of the black-box warnings or their equivalents when it comes to AZ.
So Mary, I think I would have acted exactly as you did, and tried to spread the word, but Sunshyne, I understand and appreciate very much your careful research and wouldn't have YOU change for the world.
I need to step in here. Marynewport and Sunshyne are doctors and scientists respectively, who have done extensive research in their fields, and as scientists are entitled to differing opinions. We are extremely appreciative of you sharing your knowledge with us. I have two requests. First, being completely scientifically illiterate, I cannot follow most of what you are writing, and would ask that one or both of you explain in the simplest of non-scientific terms what these oils are supposed to do for the mood and memory. What they're supposed to do; whether they are approved by some appropriate agency; if it is purely "anectdotal" evidence. That's it. That's all this brain can handle.
MCT Coconut Accerra
Secondly, if you wish to debate and disagree on scientific principles, protocols, methods, please do so via private e-mail.
If all else fails, I have a dear friend who happens to have a Ph.D in biochemistry, and she "dummies down" information for me so I understand it.
Sunshyne, your work is wonderful and I am tremendously grateful that you do it. I wish you put it on a web site I could send people to, like the diabetes one at http://www.phlaunt.com/diabetes/
My own way of thinking about this is to want different kinds of information. I want to know what information is scientifically validated. But I'm also happy to try something that is not (if I think it safe) and take the approach "my body, my science experiment." If it has a beneficial effect that is just placebo effect that is great in my book--I've gotten benefit without messing with my body (assuming what I am trying is ineffective but harmless).
My husband (early stages Lewy Body Dementia) and I are both using about 1 T a day MCT oil and may go back to mixing it with coconut oil. I'm not worried about cholesterol issues for me because I have very high HDL. For him, we will reconsider if his cholesterol numbers get worse when he next has blood work. We both eat a fairly low carb diet to control diabetes/prediabetes.
Keep up what you are doing! I hope this can be a community where we can value and use all kinds of knowledge-- scientific, experiential and alternative, in whatever balance is comfortable for each one of us.
(1) Patent applications , if well written, are crafted to enable the broadest possible claims.
They are NOT intended to convey research data for critical evaluation by other scientists. The inventor only has to reveal enough about the invention that others "skilled in the art" could practice it. No inventor who understands the process is going to reveal any more of his valuable proprietary information than is absolutely necessary to make the patent defensible.
Nor are patent applications required to be limited to statements that have been "proven" in the laboratory, or that are even particularly sound from a scientific standpoint. The inventor can simply let his imagination take flight. (The resulting patent, if any, may not end up having any value, of course.) Vague statements about emulsification, for example, are all that is needed for Accera to claim products that contain emulsified MCTs (provided that the claims are structured to cover this particular aspect). They don't have to provide details on how they emulsified anything. In fact, they aren't required to have actually gone ahead and worked with an emulsified formulation. Mentioning it is all that's necessary.
Also, the text of a patent application is not changed after it is submitted -- only the claims are changed. The text, if well written, contains a lot of pure speculation, on many different concepts. Once the application is submitted, there is a lot of discussion and argument between the inventor and the patent examiner about what is "known" from the "prior art" and open literature, which becomes a part of the record and may be used to defend the patent, but is never published. (It may, however, have a huge impact if there is ever an infringement lawsuit.)
This interaction between inventor and examiner will usually narrow the initial set of claims. It may, sometimes, result in the inventor realizing that some claims might be expanded ... but a claim can never be broadened if the text did not lay the foundation for doing so. Hence the reason for including speculation and flights of fancy in the text.
Ultimately, the final wording of the claims is hashed out, and those claims define what the patent actually protects. In some patents, the claims bear very little resemblance to the text. For example, the examiner will usually insist on splitting a broad application into several different patents, covering what the patent office considers to be different inventions, which are then covered by different sets of claims. The text remains the same in all of them.
Bottom line, a patent or patent application can give one clues as to what the inventors have done or are thinking about doing, but are rarely a good source of precise, valuable details on scientific experiments.
(2) With regard to Charlotte's comments about saturated fats: there are several different definitions involved here, which are confusing the issue.
From a purely chemical standpoint, all of the fatty acids and triglycerides we've been talking about are "saturated" in that they don't have any carbon-carbon double bonds.
However, the FDA has evaluated the potential health impacts of a number of broad categories of food/nutrient constituents, and requires certain information about them to be put on food/nutrient labels.
By the FDA's definition, the saturated fats that must be disclosed on those labels are supposed to be the sum of lauric, myristic, palmitic, and stearic acids. These are the fatty acids and triglycerides the FDA considers to pose a significant health risk.
"MCT oil", as the term is commonly defined, is primarily a mixture of caprylic and capric triglyerides (with minor amounts of a few others, depending on how the product was made.)
I hadn't really bothered looking at the FDA nutritional labels on MCT oil products, because they don't provide enough information to make an informed decision -- the different saturated fats (FDA definition) pose different degrees of cardiovascular health risk, via different mechanisms. And the FDA does not require any information about caprylic or capric acids on the labels, since these are considered to be "neutral" fats.
Instead, I had looked for products which reveal the analysis of the average sample -- I wanted to know whether the MCT oil is relatively pure, and whether it is heavier on caprylic than capric acids.
(Quite a few of the products I found don't reveal the analysis of the MCT constituents, which may be a sign that the manufacturer doesn't make a particularly pure product. I wouldn't consider buying one of those.)
So, just to be sure of my facts in responding to Charlotte, I looked at the FDA nutritional labels on the MCT oil products in my kitchen. The label on the MCT oil by Sci-Fit (which has the highest concentration of caprylic acid of any of the products I've found) states, as it should, that it contains "0 g" of saturated fat. It also has a section of its label listing the amounts of each of the MCTs it contains -- something that the FDA does not require, but something Sci-Fit is proud of.
"Premium MCT Gold" made by Ultimate Nutrition doesn't bother with the standard FDA nutritional label, since one would enter "0" under everything but "total fat". Instead, it has a label that shows it contains "100% MCTs", and also lists a typical analysis of those MCTs.
"MCT Fuel" by Twinlabs turned out to be pretty amusing. The label indicates that all of the "total fat" is "saturated fat". It *should* show "0 g" just like the Sci-Fit product, because Twinlabs does provide its analytical results, and the triglycerides in Fuel are almost entirely caprylic/capric. I gather that scientists who know the chemical definition of "saturated fat" prepared the label, rather than nutritionists. <grin>
(3) Warning re FDA labels: A product that contains less than 0.5 g trans fats can legally state that it contains "0 g" trans fats. So you may want to delve a little more deeply into that "0" for any products you buy that contain very many hydrogenated fats. 0.49 g trans fat per serving strikes me as a pretty hefty amount.
(4) Charlotte, I hate to burst your bubble about your husband's cholesterol levels, but you can get that much variability in the results just by jumping up and down for a while between blood collections, or by collecting blood with or without that tight band that is sometimes used to make blood pool in the lower arm (forget what it's called, caregiver dementia at work.)
Also, it is very well established now that total cholesterol levels are not an effective way to predict cardiovascular disease risk. Bare minimum, you should look at the ratio of total cholesterol to HDL. The higher the HDL fraction, the better. If that change in the total cholesterol level was due to a decrease in HDL, then the lipid profile is worse, not better.
Now, I have heard that red yeast rice may be helpful in controlling cholesterol -- talking to a fellow scientist about that just the other day -- and I'm going to look into that possibility. Certain types of fiber can help lower unhealthy serum cholesterol fractions by helping to prevent the body from taking up dietary cholesterol in the gut. Maybe red yeast rice works that way, don't know, haven't had a chance to check into it yet.
Like you, I am a big fan of natural supplements ... provided I know what sort of evidence exists that the supplements do what I need.
(5) Medical foods (1) are comprised of constituents which have GRAS status *and* (2) have undergone testing to demonstrate efficacy against a specific disorder. Axona has medical food status as a treatment for AD, not GRAS status.
Accera has not "withdrawn from further clinical trials". They did not need any additional trials to gain "medical food" status for Axona. But they do have additional trials planned, which are designed to more fully elucidate the underlying mechanisms that cause the improvement that has been seen in AD patients, to help them further improve their product. They also have some ideas on how to modify the current Axona formulation to make it more effective for patients with the APOE4 allele, and once they've started working on that, I'm sure they'll be conducting more trials to get approval of that.
(6) Accera closed on their most recent round of venture funding some two months ago. This round was intended for setting up the initial sales force and preparing to launch Axona -- establishing vendors, manufacturing facilities, compliance with regulatory issues, marketing, sales, distribution, and customer support, issues like that. Such things take time.
However, the last I heard, Axona is now expected to launch in February, rather that their previous projection of March.
Their initial sales force is expected to comprise something like 25 reps, if I recall correctly, to target 25 key market regions. (A fledgling company can hardly blanket the entire country within a few of months of venture funding.) And I would imagine that we won't hear much about their marketing efforts. Since Axona is being sold by prescription, it would make sense for Accera to focus the bulk of their marketing resources on physicians who specialize in treating AD patients, not on general practitioners, let alone on the general public.
(7) Dr Henderson published his research papers where research scientists would see them. A journal is hardly "obscure" just because an MD who is a practicing physician (rather than a researcher) would not typically subscribe to it. I strongly suspect that most practice-only physicians have never heard of many of the most prestigious research journals.
(8) With regard to Dr Newport's impassioned plea: "And how long will it take for them to provide the public with information that it may be beneficial for the many other diseases that have a problem with decreased glucose uptake? Should those people not be told that this could help while waiting for years for clinical trials that will never result in a stamp of approval from the FDA for those entities?"
Are we to infer that you recommend we do away with clinical trials and FDA regulatory oversight altogether? That you feel if someone suggests a given product MIGHT help treat a disease, they should be allowed to make claims to the general public that it will, and sell it to them for that purpose -- without valid, scientifically sound evidence to support their speculations and show that the product will be safe as well as effective?
Clinical trials take time. That can be very frustrating and upsetting for those of us who don't have time.
But how many investigational new drugs have looked extremely promising for treating AD, on the basis of theory and pre-clinical studies and even Phase I and Phase II clinical trials ... and then failed in Phase III?
And how many INDs are discovered to actually be harmful, during clinical trials?
Some of our members are enrolled in the Bapineuzumab trials, for example. A precursor to Bap looked wonderful ... until clinical trial participants started dying. By your rationalization, we should all have been free to start giving our spouses the precursor years ago.
I have no problem whatsoever with you telling the world that you're giving your husband coconut oil *and* MCT oil. I have no problem whatsoever with you telling the world your impressions of his response.
I do, however, have a serious problem with anyone misrepresenting what is and is not known about the health effects of coconut oil -- especially someone who uses her status as an MD to bolster her qualifications to tout its purported benefits.
I have a really serious problem with someone misrepresenting perceived benefits in one patient with one disease as being virtually guaranteed benefits for all patients with that same disease ... let alone claiming that it is evidence that significant benefits will be realized by other patients with many other disorders.
And, for that matter, I also have a very serious problem with what appear to be deliberate attempts to vilify Accera, its scientists, and its product, which are based on misinformation, misinterpretation, and/or ignorance.
How, exactly, does it help all those people who have dementia to badmouth a product that has exceptional potential -- demonstrated in clinical trials -- to be beneficial to them?
Joan, I hadn't seen your post, I was busy writing the above (and trying to get this durned site to accept what I wrote without repeatedly protesting it was too long...!)
I will respond to your request asap ... but right now, I have a hungry husband prowling around and protesting about THAT in no uncertain terms. <grin>
Tip for lenghty posts: When you write lengthy posts, write them in a Word Document first. Sometimes when you are writing too much for one post, it gets lost. Once you have finished the Word document, you can transfer it in sections to the post.
Joan, I know you just requested that this debate be continued privately by e-mail; however, I really feel like I am getting an education and appreciate reading what both parties understand to be the correct way of thinking about this. The more knowledge we have, the better we are equipped to make up our own minds.
I agree. Sharing knowledge is fine. It is when I feel that discussions are escalating into personal arguments that I prefer they not take place on the boards. And for those of you who can decipher the technical scientific information - go for it. I just want someone to explain it to me simply.
As a physician, I like reading the posts by Sunshyne, Dr. Newport, and others regarding their experience and research into this topic. I feel I should get CME's (Continuing Medical Education) credits for reading Sunshyne's posts. I agree with Lori2 - keep the posts here where we all can read them and get the information we need to take care of our LO's. As with all scientific research, I expect that there will be disagreements. My only plea is that you disagree without being disagreable.
Maybe its just me but I see irony in the situation of the coconut oil vs. cholesterol. where my DH is in AD i seriously doubt 1 tsp of coconut oil is going to up the colesterol levels to where i would be concerned in his AD journey-mid-late 6.. its seems that with all the other black boxed drugs i am also giving for dementia and the potential side effects that they can incur, this seems rather trivial. i also dont monitor his sugar intake anymore as well just to give him some pleasures at this point. i have seen some mild cognitive improvements with just the min 1tsp of coconut oil since giving it a few months ago so within the scheme of things i will continue for now unless some dire consequences occur. i also appreciate all the scientific debate with regards to the issues at hand, its beneficial to weigh all sides -Divvi
Not only are we being educated about the medical issues but also about the economic issues involved in bringing products to market. The difficulties of being the “small” guy with an unusual approach—who gets heard—who gets funding—the testing—the need for a profit--all the issues involved that we seldom think about.
One really quick point in regard to divvi's comment: my concern about cholesterol levels in dementia patients isn't their long-term cardiovascular health per se. High cholesterol levels have been closely linked to the development of AD and the rate at which it develops. And high cholesterol levels can be expected to exacerbate cardiovascular disease that is contributing to VaD (vascular dementia.) So I'd be concerned that the bad might outweigh the good.
OK, then I did also want to say a word or two about clinical trials, if you'll humor me -- who funds them, and why. (This won't take as long to prepare as the analysis Joan requested, and may help everyone understand where that analysis comes from. It also addresses one of Dr Newport's big concerns.)
There are many different organizations who might fund a clinical trial -- for example, the company that owns rights to a patent on a drug or formulation or drug delivery technology; a Government agency (typically one of the National Institutes of Health, but not always), a charitable organization, or a venture capital (VC) firm.
Let's stick with three of these, for simplicity's sake: the company, NIH, and VC. (Of these, the VC world has far and away the most money to invest.)
If the company is large and profitable, NIH will frown upon attempts to get Government support -- and the company wouldn't want to give up any of its rights, anyway. So the company typically funds the clinical trials, by itself.
If the company is small and struggling, it might get support from from NIH, especially in the pre-clinical and early clinical stages, to demonstrate "proof of principle". Promising results will get the VC world and the Big Pharma world interested, they'll invest in the small company, the drug will get developed, and everyone benefits.
When a small company gets to the point it attracts VC investment at any level, it becomes much harder to get money from NIH. So then, the company typically has to fund its clinical trials, often with the help of Big Pharma partners.
Now, what about potential treatments where the patent rights have expired, or the treatment cannot be patented for some reason. Does it languish, untested and unproven forever?
Not at all. Someone at a university might be interested in conducting studies, or someone in a Government laboratory may want to, or there are companies whose business is to conduct research under grants and contracts without ever intending to commercialize their results.
So let's look at an example ... let's say that it appears that wine may benefit AD patients, because people in France have a lower level of AD and they drink a lot of wine. This is quite intriguing, since it might be counter-intuitive that wine would be beneficial -- one might expect alcohol to be harmful, not helpful. So some scientists start looking at the effects of alcohol on the dementia patient, others start looking for other constituents in the wine that might have some sort of beneficial effect.
Someone suspects that resveratrol may be the active component responsible for the purported benefits to AD patients. Maybe some scientists in academia or Government labs start studying its properties, and they present their findings in papers and symposia. Preliminary studies appear promising.
Caregivers catch wind of it, and start to buy different nutritional supplements that contain resveratrol, and give them to their ADLOs. Some of them think they see improvement, the word spreads, and the excitement grows.
Now, who would fund a clinical trial to see whether resveratrol may indeed be of widespread benefit to AD patients? It can't be "patented" per se, and various nutritional supplements that contain resveratrol are widely available, and cost very little.
Well, the anecdotal and/or scientific evidence developed to date appear to indicate that the purported benefits are coming from a particular source of resveratrol, or a more complicated formulation that contains other things besides plain, old resveratrol. Maybe resveratrol needs to be isolated from a particular source, or prepared in a certain way. Some company may have a lock on a promising source; another may have a proprietary (or even patented) technique for preparing a resveratrol supplement; a third might have ideas on how to administer resveratrol so that it performs better. Any one of these may decide to fund clinical trials, because they're much more likely to profit than the average bear if they can show their "special" reservatrol actually does benefit the patient.
That's what happened with huperzine A.
But maybe there isn't a company that fits any of those descriptions. Maybe none of the resveratrol preparations appears, anecdotally, to be superior to any of the others. Or maybe none of the companies can afford to fund a trial.
Well, a scientist at an academic institution or a Government lab or a CRO or a research institute may want to conduct a clinical trial. How do they get money? By writing a grant application to a Government agency such as NIH, or a charitable research foundation.
Grant applications are competitive. There are many scientists out there who think they have a handle on something that might treat AD. And the amount of money available from NIH and other Government and private, non-profit organizations is limited. Only the most convincing grant applications -- those with the best supportive evidence, the best clinical trial designs, and the most qualified research teams -- get funding.
This is why the Alzheimer's Association is lobbying Congress to increase the funding allocated to AD research -- so that more of these potentially promising products which can't be patented or otherwise "protected" will still get adequate attention.
But it doesn't help to badmouth the pharmaceutical industry -- they're not the enemy. Their stockholders expect profits. (How many of you own stock in pharmaceutical companies, directly or indirecty???) Pharmaceutical companies target the approaches that are the most promising AND the most likely to generate profits.
And it is silly to say that a promising treatment will never be properly tested just because it can't be patented. If there is enough compelling evidence, it will be tested. Someone over on the Alz Assoc recently said the same thing about resveratrol that is being said about coconut oil -- there will never be any clinical trials on resveratrol.
Actually, there is one trial already under way on resveratrol, and a second trial preparing to recruit.
Do I think coconut oil will ever undergo clinical trials as a treatment for AD? No. Not because of profit issues, but because the cardiovascular health risks of coconut oil are too well established.
Do I think there might be some benefits from coconut oil? Well, it contains caprylic and capric acids; caprylic acid has been shown to be beneficial in clinical trials, and capric is likely to be, based on everything else that is known about it. But, ultimately, I don't think that they will outweigh the risks. After all, you don't have to consume all of the unhealthy saturated fats in coconut oil to consume caprylic acid -- you can buy MCT oil by the quart, or caprylic acid by the barrel, or Axona when it becomes available.
Maybe coconut oil contains something else that is beneficial, either by itself, or in combination with caprylic acid, or that even makes caprylic acid more effective. After all, we know now that certain trace constituents in vegetable oils, such as phytosterols, can have a big impact on the ways in which the fats in those oils are processed in the human body.
But right now, nobody knows that coconut oil really is beneficial to AD patients -- there is only anecdotal evidence, and only a teeny tiny bit of that. And if coconut oil is beneficial, nobody has a clue whether it's simply due to the caprylic and capric acids.
I'd be more inclined to do a more in-depth analysis of coconut oil constituents -- not the fats, but the trace constituents, such as the antioxidant gallic acid esters -- see which of those are most likely to prove beneficial, and study them in combination with caprylic acid, rather than push for studies in human beings.
I think we'd be likely to shoot ourselves in our collective feet, because of the well-known health risks, and never get past that to discover another promising constituent in the coconut oil (if there is one.)
Thank you Sunshyne, thats quite some info to absorb. i was thinking that in the john travola's sons death --son was on depakote to help with his seizure episodes, then due to side effects of the depakote affecting liver functions over 'long term', the drs (or parents) took him off of it. the irony of all this of course, is the liver function was the lesser of the two evils, the poor boy died of seizures and hitting his head in the bathroom way before the anticonvulsant did long term damage to liver-. so in effect i can relate this tragedy to our use of the coconut oil. long term use may elevate cholesterol counts which in return could escalate cardiovascular disease and lessen our AD spouses life span due to coronary issues or like sunshyne suggests could possibly accelerate the AD. the choice seems to be, chose improved quality of life now over longevity. with AD i think none of us really want to consider the longevity factor with what awaits our loved ones in end stages. i speak for myself whose DH is in late 6ish stage now. if he were recently dx'd maybe i would be more hesitant about the cardiovascular issues long term. for now if we can improve the quality of life even a tad at this point, then the risk is worth it in our case. but with all considerations mentioned here, we do have blood work done twice/yr so we will factor the results and see where we are-Divvi
With cholesterol as with everything else, everyone’s body reacts differently. Dr. Newport states that her husband’s cholesterol levels did not go up with his use of coconut oil. My experience was different. For about 5 years, I have been using coconut oil for cooking. Several years ago, for what reason I don’t remember (maybe I’m the one with memory problems) I added, orally, a tbsp of coconut oil a day. My cholesterol shot up by about a hundred points. It took a while for it to come back down to where it was. So if you are using coconut oil instead of the MCT oils be sure to keep an eye on cholesterol levels.
I found some very intersting reading on coconut oil and cholesterol at the westonaprice.org website. Dr Mary Enig, PhD. this is a non profit foundation that explores nutrition worldwide and there are many intersting articles under coconut oil if you do the search. they dispute the same topics that we are posting about -maybe sunshyne can check it out too - divvi
Thank you for the chewing out, criticism, dumbing down, lording over, whatever you want to call it. I did not appreciate it.
1) I do know that the ratio of HDL vs LDL is more important total cholesterol.
2) I research things before I try them. I don't even take a prescription without researching it first. Just cause a doctor says to take it, I don't. I made the mistake when the dr gave my hb zocor. Three days later he couldn't remember the person he had worked with all day. So i don't blindly take things. The supplements I take that are recommended by my naturopath, I don't just take her word for it - I research them too.
3) You stated high cholesterol is a risk factor to AD. So are a lot of other things. But, I don't put a lot of value in what they say. I remember back when they said that the highly educated, those that read a lot, do puzzles, crosswords, exercise and eat broccoli will have a lower risk. Right after they said that it was announced that Ronald Reagan had AD. When we were visiting my husband's dad in the Alzheimer unit, one of the wives pointed out the former occupations of all the men there - 75% were highly educated: doctors, scientist, researchers, teachers, high ranking officers - the list goes on - all proving everything they have listed as lowering your risk is only guess work. The only area they are closer to being right is the gene factor or EOAD. I don't put much value in these guesses anymore.
4) There has to be something in coconut oil that lowers the risk if areas where they use it all the time have a lower occurrences. Maybe it isn't the coconut at all. Maybe it isn't he resveratrol at all. They don't know.
5) I do not, I repeat - do not own stocks in any pharmaceutical company. I am just a one of those lower income people that our politicians seem to forget. We live on hb's meager unemployment check that many of you cannot even imagine living on. And if I don't find a job soon, all the supplements will stop - then won't have to worry about the fats in coconut oil.
6) I asked a simple question about the saturated fats in MCT oil - I checked at least 10 different brands I found in a google search and everyone listed the same amount of saturated fat as coconut oil. IMO - you could have answered that question much nicer than attacking me and making me sound like an idiot. But you answered like a doctor who likes to tells you that there is no way he could be wrong.
I realize you are under stress but so are the rest of us. You may not have meant it that way, but since you were replying to my post I felt it was a personal attack on me. You put so much information out there like you were trying to prove I was dumb and then rubbing it in. Reminds me of when a football team has won a game by a huge margin but continue to pile the points on to rub it in.
This will be my last post in this section, so don't hesitate posting in this section.
Charlotte, I do apologize if my posts offended you in any way. They certainly weren't intended to. Communicating in writing can be difficult, and things can sound quite different from the way they are intended. I was, actually, agreeing with you about natural supplements. And about the MCT oil labels sometimes being wrong, too -- I hadn't looked at that part of the label before and was quite surprised to find that one of the products I had in my kitchen was labeled wrong, that's all.
Please don't stop posting here because I inadvertently hurt your feelings. I promise not to say anything about your posts at all, to make sure I don't upset you again.
divvi, I had noticed Dr Enig's name while doing my coconut oil search. However, Google Scholar only pulled up a half-dozen papers published in journals, going all the way back to 1983, and the journals tend to have names like "Indian Coconut Journal" and "Philippine Journal of Coconut Studies". (These are not really top-tier publications in the science world.)
Enig appears to be a lady on a mission.
She is reportedly a founder and vice president of the foundation, which is dedicated to "restoring nutrient-dense foods to the American diet through education, research and activism." Foundation sponsors include health product companies, and meat and fish producers. Most of the articles that I looked at on their web site weren't published anywhere.
I believe I saw something which indicated that she is a consultant to the coconut oil industry and receives funding from them. I stopped reading her papers when it became clear she preaches an international conspiracy on the part of the main-stream oil industry to vilify coconut oil so it can't compete with other products.
I have a theory that if you have science on your side, you don't have to rely on conspiracies to explain why the FDA (and every equivalent organization in every other developed country) has concluded that saturated fat is unhealthy.
Wikipedia notes, among other things, "Enig argues that cholesterol does not contribute to heart disease and calls it a 'phony issue.' "
Enig claims to be Director of the Nutritional Sciences Division of Enig Associates, Inc. However, that company's web site says, "Our firm is principally conducting theoretical modeling research in the following areas: electrodynamics; radiation transport; radio frequency signatures; electromagnetic pulse device design; high power microwave design; magnetohydrodynamics; computational magnetohydrodynamics and electromagnetics; and advanced warhead design." It is a tiny company with a handful of employees, from what I can find about it on the web. I suspect that the President, Eric Enig, may be related. And that the Nutritional Sciences Division has an employee roster of one.
You are asking for a simple explanation and here it is: People with Alzheimer's have a problem that some call "diabetes of the brain" in which the neurons are unable to take up glucose, which is the usual fuel for neurons and so they die off gradually, beginning at least 10-20 years before symptoms become noticeable. Neurons can also use one other fuel - ketones - which are not normally circulating in someone eating the normal American diet, unless someone is starving for at least two days or eating a very low carbohydrate diet (they go into "ketosis".) When circulating, ketones increase blood flow to the brain and readily cross into the brain cirulation, where they can be taken up and used by neurons, potentially keeping them alive and functioning. I think of it as an alternative fuel - some cars runs on gasoline and others on diesel - for some people, their neurons need "diesel" (ketones) and won't function on "gasoline" (glucose). Medium chain triglycerides when eaten are converted by the liver to ketones, which may then become available to cells and are used by the mitochondria in the cells to produce energy (ATP.) Ketones do not require insulin to enter the cell and can by pass the problem of decreased glucose uptake completely. Foods that contain a significant amount of medium chain triglycerides include coconut oil, palm kernel oil, both about 60% MCT, MCT Oil (derived from coconut oil or palm kernel oil,) human breast milk (about 10-17% of the fat is MCT), goat's milk (about 10% of fat is MCT, and a small amount in cow's milk fat/butterfat. There probably is more to it than this, but at the very least, ketones may provide a source of energy for cells that cannot use glucose. When the cells have energy available, they are able to perform their other functions better.
Regarding the cholesterol issue, these are my husband's results after months of taking at least 6 tablespoons of coconut oil per day: total 192 (< 200 normal), HDL 77 (at least 40 is ideal), LDL 99 (< 130 ideal), triglycerides 79 (< 150 ideal)CRP < 0.1 (< 0.8 ideal). He has taken Zocor for at least five years after having a total cholesterol of 278. Until taking coconut oil, his LDL was always > 130 even on Zocor and his HDL was just barely over 40. His cholesterol is responding in the way that Mary Enig, Ph.D. (Know Your Fats) says it would. I am well aware that he is one person. I just want to make one more point about the cholesterol issue. Our spouses are deteriorating and ultimately will die of this disease without something to turn that around. I would rather have Steve in his happy, more confident, "new and improved condition," in which he currently feels that he has gotten his life back, as opposed to his former, "I am dying, so why bother" mode, and take some risk that a higher cholesterol level might produce cardiac disease at some years down the road. I know that if I do nothing, and stop providing him with medium chain triglycerides, he will surely die of A.D., and in all likelihood that would happen in the next 3-4 years or sooner, if he were to stay on the path he was on last spring. It has been 8 months, he has retained his improvement and continues to improve. He likes coconut oil, as do millions of people in other parts of the world, and we plan to continue to use it until something better comes along.
For Sunshyne, another paper to read: "D,L-3-hydroxybutyrate treatment of multiple acyl-CoA dehydrogenase deficiency (MADD)," Johan L.K. Hove, et. al., The Lancet, Vol. 361, April 26, 2003. This is about treatment with "ketones" that Dr. Van Hove says were obtained from the UK, in three young children with an enzyme defect involved in glucose uptake, who had remarkable gradual "turn arounds" to a virtually normal state after prolonged treatment. One of these children was actually quadriplegic (spastic) and had also lost the ability to talk and after 19 months was walking independently. The MRI on this child showed areas that were previously atrophied that had actually "filled in." The levels on these chldren were very similar to the levels obtained by Dr. Henderson (and on my husband.) These are children and may be more likely to grow new neurons, but we do know now that adults can sprout new neurons.
marynewport Thank you for the "layman's" description of ketones. I like many appreciate ALL the input on this subject, but in all honesty I'm a little dizzy from all the technical issues.Is there a brand(s) of cocconut oil that you have found to be the best for your DH to take? DickS
Accera is trying to find it. The company is enrolling 100 patients in a more definitive, 90-day IIb safety trial at sites in Florida and California. If that trial shows significant benefits, the company will need another $16 million to $20 million for phase III trials.
If not, the drug might work as a dietary supplement, Clark said.
"I don't care which way it goes," Henderson said. "It has to work first."
While he keeps a scientific distance from the research, Henderson fervently believes his theories. And lives them.
He is not only convinced that Alzheimer's is caused by faulty glucose metabolism, but he also is certain a high-carb diet caused the problem.
Turns out, the APOE4 allele has survived best in populations that live as hunter-gatherers. That includes Inuits and Papua New Guineans, cultures that eat few grains.
The APOE4 allele hasn't done well in cultures with a long historic exposure to agriculture, such as those in the Middle East.
Evolution shows that grains and APOE4 don't mix, Henderson argued in a paper published in Medical Hypothesis, and dedicated to his mother.
APOE4s can stave off the disease by eating like our Paleolithic ancestors - lots of meat and vegetables. No carbs, he concludes.
"It's majorly in my view an environmental disease," he said, champing on a salad of chicken, shrimp and beef at Wahoo's Fish Tacos.
"Everyone in our office observes some sort of carbohydrate restriction," said Orndorff, whose office bookshelf includes The Paleo Diet.
But if everyone ate right, and the disease vanished, wouldn't that ruin the market for Accera's drug?
"If it turned out that everyone ate a low-carb diet, and nobody got Alzheimer's, and I never made a cent?" Henderson shrugged. "I'd be OK with that."
This just gets more interesting by the minute. I'm soaking up this information like a sponge. Since I'm a carb lover, though, it's downright disturbing. Thank you, Sunshyne, Dr. Newport, Lori2 and others for all the valuable information. Also, Sunshyne, the patent and clinical trials information was very interesting. Never dreamed it was so complicated.
Hey, GuitarGuy, I could not find your email in your profile - it says n/a. If you email me at ketones08.com, I will send that and a few other articles to you.
I am in a conversation with a friend who contends that coconut oil is good for you, not bad. He follows the Enig/Fallon/Fife line of thinking. He feels that the error comes in because (to quote him) most of the studies of saturated fats are based on Ancel Keys research which included trans-fats along with the saturated fat. I think we can all agree that trans-fats are bad.
I am hunting for studies that relate to just saturated fat. So far I’m not having much luck. Admittedly I am a novice but I am trying. Can anyone give me some help?
I am still on the fence as to whether to try coconut oil. My husband has FTD not Alzheimer's, I am interested in others experiences with coconut oil and FTD. Have any caregivers of FTD tried with their spouses?
Kadee, Just my opinion—I have no idea if it will help FTD but it wouldn’t hurt to try. The MCT oils, on the internet, are marketed and used by bodybuilders. From what I have read, I don’t think there is any down-side to taking it. On the other hand, I’m not totally convinced that coconut oil is safe. I would certainly try the MCT oils if I were you—you never know what will work until you try.
Per Joan's request, a comparison of Axona, MCT oil, and coconut oil for treating AD. (Joan, please let me know if your PhD friend would like any papers or additional details re my literature searches.)
The bottom line, with regard to the argument that it's better to take the risk associated with consuming the high levels of saturated fats in coconut oil, rather than suffer helplessly with AD ... this is not an either/or choice. Use MCT oil now, and Axona when it becomes available.
Notes:
(i) Triglycerides and fatty acids are divided into short-, medium-, and long-chained molecules, based in part on the length of the carbon chain and, more recently, on the way they are metabolized. Currently accepted definitions: - Short-chain: C4 (butyric) and C6 (caproic) - Medium-chain: C8 (caprylic) and C10 (capric) - Long-chain: C12 (lauric), C14 (myristic), C16 (palmitic) and C18 (stearic) - C12 (lauric) is sometimes lumped in with the MCTs, especially in older papers, since animal model studies showed that, under the right conditions, it can be partially processed into ketone bodies. However, most of the recent papers on fat metabolism lump C12 (lauric) in with the long-chain triglycerides (LCTs), since the majority of C12 (lauric) is processed into fat and stored in adipose tissue, and since lauric fatty acids are known to pose a significant cardiovascular health risk.
(ii) Some triglycerides (and fatty acids) can be metabolized into ketone bodies. However, the amount of that is actually turned into ketone bodies depends on carbon chain length, and bioavailability - The shorter the carbon chain, the more of the triglyceride that is turned into ketone bodies. C8 is turned into ketone bodies very efficiently; C10 rates are similar but slightly lower; but most of C12 is processed by the lymph system and turned into fat. General rule: C8 ≥ C10 >>> C12 - The triglyceride must be in a form that is readily absorbed and digested for it to be metabolized. Triglycerides are not soluble in water. For maximum absorption/digestion, therefore, the triglyceride must be emulsified. (Emulsification maximizes the surface area of the oil droplets, making more of the triglycerides available to enzymes.)
(iii) In analyzing the health risks of saturated fats, I ignored most, if not all, studies done with cells, tissues, and animal models. I considered controlled studies in humans to be far more compelling evidence. And since it was easy to find dozens of studies done in humans, there was no need to rely on more questionable, non-human models.
Comparison of the products proposed for treating AD symptoms:
Status: - Medical food, FDA-approved for treating AD
Evidence of efficacy in treating AD: - Clinical trials (double-blind, placebo-controlled) in AD patients, both patients who are taking AD meds, and those who are not. AD patients who did not carry the APOE4 allele improved throughout the clinical trials; those who did carry the allele held steady; placebo controls of patients with or without APOE4 declined significantly.
Potential health impact: - Constituents all have FDA GRAS (Generally Recognized As Safe) status - Substantial body of evidence in humans that C8 is a "neutral" fat with no negative effects on cardiovascular disease risk factors, including cholesterol levels/ratios.
Other notes: - If the only mechanism of action was the use of ketone bodies as "fuel" in brain cells, AD patients would not improve over the course of many months; nor would the presence or absence of the APOE4 allele make any difference. - The mechanisms underlying the efficacy of Axona for treating AD are still being elucidated. Since Axona has been shown to raise blood levels of ketone bodies, it is thought that at least some of the mechanisms involved are related to ketone bodies. My earlier thread on MCT oil for Parkinson's summarized what is known about the impact of raising blood ketone body levels on brain cells. I have an excellent review article on the neuroprotective properties of methods that increase ketone body concentrations, by Maalouf, Rho and Mattson, if anyone is interested. It is not available via the web since it is still in press ... Dr Maalouf sent me an editor's proof. - C8 (caprylic) has antiviral activity. Unknown whether this has any relevance regarding the treatment of AD patients.
Primary ingredients: - ~65% C8 (caprylic) - ~35% C10 (capric) - "MCT Fuel" by Twinlabs is emulsified for improved bioavailability / transformation into ketone bodies
Status: - FDA GRAS (Generally Recognized As Safe) status
Evidence of efficacy in treating AD: - Anecdotal only - Might be expected to have some efficacy, since MCT oil is typically 65% C8 (caprylic), which has been shown to be effective against AD in Axona clinical trials
Potential health impact: - Substantial body of evidence in human studies that C8 and C10 are "neutral" fats, with no negative effects on cardiovascular disease risk factors. - Growing body of evidence in humans that moderate consumption of MCT oil (5 g) can lower cholesterol and triglyceride levels. MCT oil reduces fat mass, through down-regulation of adipogenic genes as well as peroxisome proliferator activated receptor-γ; recent studies confirmed that reduction of body fat was not transient. MCT oil reduces lipoprotein secretion and attenuates postprandial triglyceride response.
Other notes: - C8 (caprylic) and C10 (capric) have antiviral activity. Unknown whether this has any relevance regarding the treatment of AD patients.
Status: - ~80-90% of coconut oil is saturated fats that are considered by the FDA to pose significant cardiovascular health risks
Evidence of efficacy in treating AD: - Anecdotal only - Might be expected to have some efficacy, since coconut oil is ~5-10% C8 (caprylic), which has been shown to be effective against AD in Axona clinical trials
Potential health impact: - Substantial body of evidence from studies with coconut oil on humans that coconut oil poses a significant cardiovascular health risk, including raising cholesterol levels - Substantial body of evidence from studies on humans that C12-C18 saturated fats pose significant cardiovascular disease risks via multiple mechanisms (see below) - High cholesterol levels have been closely linked to the development of AD and the rate at which it progresses. Also, high cholesterol levels can be expected to exacerbate cardiovascular disease that is contributing to VaD (vascular dementia.) - Anti-inflammatories are expected to be helpful in treating AD. Saturated fats can have an adverse effect on some anti-inflammatory agents. See, e.g., Nicholls SJ, Lundman P, Harmer JA, Cutri B, Griffiths KA, Rye KA, Barter PJ, Celermajer DS. Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. J Am Coll Cardiol. 2006 Aug 15;48(4):715-20. - Recent studies have showed that saturated fats can affect the immune system, which was unexpected. This is something that we're just beginning to understand. This is one reason that playing around with the saturated fat intake of an AD patient is inadvisable, in my opinion.
Other notes: - Substantial body of evidence, using biopsies of human fat (adipose) tissue samples from around the world, that C12 (lauric) is primarily processed via the lymph system and stored in fat (rather than transformed into ketone bodies for use as "fuel.") - Certain trace constituents (e.g., antioxidants) found in vegetable oils are thought to be very beneficial to human health, and especially to AD patients. Coconut oil has, by far, the lowest amounts of any tocopherols and tocotrienols of any of the vegetable oils. - C8 (caprylic), C10 (capric), and C12 (lauric) have antiviral activity. Unknown whether this has any relevance regarding the treatment of AD patients.
More details on the caardiovascular health risks of C12-C18 saturated fats:
- The C12-C18 saturated fats are all considered by the FDA to pose health risks, based on a huge body of evidence from epidemiological studies done on humans, many of which used coconut oil as the source of the saturated fats. For example, the Seven Countries Study found strong positive associations between 25-year death rates from coronary heart disease and average intake of lauric, myristic, palmitic, and stearic acids. (Each of these saturated fats, individually, was linked to coronary heart disease death rates.)
- The mechanisms whereby C12-C18 saturated fats pose health risks depend on the saturated fat involved. * All four saturated fats (C12-C18) increase total blood cholesterol and LDL, promote post-prandial lipaemia, and, through their action on platelet adhesion, encourage thrombosis. * Several studies showed that increasing the intake of C12 (lauric) was associated with a significant increase in risk of new atherosclerotic lesions. * A recent meta-analysis of 60 controlled human trials found that C12 (lauric) had the largest cholesterol-raising effect of all four saturated fats; it raised the LDL levels the most of all four, but it decreased the ratio of total to HDL cholesterol due to an even greater increase in HDL. Both C14 (myristic) and C16 (palmitic) raised total serum cholesterol, but had little effect on the ratio due to similar increases on both total cholesterol and HDL. * C18 (stearic) had minimal effect on total cholesterol, LDL, or HDL. However, in addition to the adverse activities it has in common with C12-C16 (above), C18 (stearic) has been shown to increase Lp(a) concentration and may activate Factor VII and impair fibrinolysis, all of which are considered to be risk factors.
My earlier posts on the potential health impacts of coconut oil and the C12 - C18 saturated fats contained a number of links to excellent review articles. I would be happy to provide more information, including many other articles, to anyone who wants it.
Lori2, I'm not sure anyone can help you. People who persist in claims like that simply won't be bothered to go to the literature to see whether they're true, and won't listen to you when you do.
Certainly, Keys had an influence -- his "Seven Countries" study was a classic epidemiologic study that was, I believe, among the first to report a strong positive correlation between saturated fatty acid intake and coronary heart disease mortality rates, as well as a significant association between total saturated fatty acid intake and total cholesterol.
But to claim that "most" of the studies are based on his work is ridiculous.
If you want to give it a try ...
Review articles with many citations:
http://www.jlr.org/cgi/content/full/46/2/179 (e.g., this review says: "...The definitive demonstration that saturated fats tend to raise while polyunsaturated fats tend to lower blood cholesterol in humans came first from the laboratories of L. W. Kinsell in California and soon after from the laboratories of E. H. Ahrens, Jr., in New York (49, 50). These investigators carried out metabolic ward studies in hospitalized subjects under close surveillance. They did single-variable studies, i.e., they kept all the elements in the diet constant, except that a saturated fat was substituted for a polyunsaturated fat (or vice versa). The total fat content was not changed, and there was no change in body weight. Both Kinsell (51) and Ahrens (52) utilized the elegant tool of the liquid formula diet in their studies, i.e., the subjects took all their diet in the form of a "milk shake" of precisely known composition given orally several times daily. When the formula contained an unsaturated fat (corn oil, safflower oil), the blood cholesterol level fell from the level on an ad lib diet; when the unsaturated fat was replaced by a calorically equivalent amount of a saturated fat (butter, lard, coconut oil), changing nothing else in the formula, the blood cholesterol rose. Each subject served as his or her own control, so there was no confusion resulting from individual idiosyncrasies in response. The results were highly reproducible in any given individual. The magnitude of the effect varied from individual to individual, but on average, the cholesterol level was about 35 mg/dl lower on the unsaturated oil formula. Similar results were obtained by Beveridge, Connell, and Mayer (53), by Bronte-Stewart et al. (54), and by Keys, Anderson, and Grande (55), using different methods but all arriving at the same basic conclusion: substitution of polyunsaturated fats for saturated fats, other factors being held constant, including total fat intake, reduces blood cholesterol levels. Keys stated the case nicely in 1957: "It is clear that it is unnecessary to prescribe a diet extremely low in total fats to lower the serum cholesterol; exclusion of the saturated fats (in butterfat and meat fats) has the greatest effect, and this effect may be enhanced by substitution of such oils as corn oil and cottonseed oil"(56)....")
A handful of the many individual studies which showed C12-C18 saturated fats pose a health risk over the years, and were done with coconut oil itself: * Reiser R, Probstfield JL, Silvers A, Scott LW, Shorney ML, Wood RD, O'Brien BC, Gotto AM Jr, Insull W Jr. Plasma lipid and lipoprotein response of humans to beef fat, coconut oil and safflower oil. Am J Clin Nutr. 1985 Aug;42(2):190-7. * Mendis S, Kumarasunderam R. The effect of daily consumption of coconut fat and soya-bean fat on plasma lipids and lipoproteins of young normolipidaemic men. Br J Nutr. 1990 May;63(3):547-52. * Ng TK, Hassan K, Lim JB, Lye MS, Ishak R. 1991. Nonhypercholesterolemic effects of a palm-oil diet in Malaysian volunteers. Am J Clin Nutr 53:1015S-1020S. * Beegom R, Singh RB. Association of higher saturated fat intake with higher risk of hypertension in an urban population of Trivandrum in south India. Int J Cardiol. 1997 Jan 3;58(1):63-70. * Kumar PD. The role of coconut and coconut oil in coronary heart disease in Kerala, South India. Trop Doct. 1999 April;29(2):122 * Mendis S, Samarajeewa U, Thattil RO. Coconut fat and serum lipoproteins: effects of partial replacement with unsaturated fats. Br J Nutr. 2001 May;85(5):583-9. * Zhang J, Kesteloot H. Differences in all-cause, cardiovascular and cancer mortality between Hong Kong and Singapore: role of nutrition. Eur J Epidemiol. 2001;17:469-477. * Jain AC, Mehta MC. Racial differences in coronary artery disease-risk factors. In "Antioxidants and Cardiovascular Disease", Nath R, Khullar M, Pawan K, eds. 2004.