I have nothing to do with statins but I DID get your attention.

I have nothing to do with statins but I DID get your attention.


First, before you start taking a drug for which proven efficacy in decreasing cardiac mortality is but an illusion for nearly all those taking them, you should be aware that these drugs may be the most toxic chemicals ever prescribed outside of cancer chemotherapeutics. Many quite serious side effects have come to light which are virtually ignored by medical journals and the prescriber. For example, how many of you know that the statins carry the same FDA warning as thalidomide regarding the risk of causing birth defects?

The FDA classifies Mevacor and other statins as pregnancy category X, which means they are not supposed to be taken by pregnant women. Not only have category X drugs been linked to fetal abnormalities in animal or human studies, but the FDA also has declared that the benefits of taking them do not outweigh potential risks.[1]

As bad as that is women of child bearing age are taking them in increasing numbers. Every day more and more studies reveal just how toxic these drugs really are. Most doctors seem completely unaware of their hidden dangers like the rare but catastrophic global amnesia, massive increases in the risk of polyneuropathy (painful decreases in sensory input from the feet usually), increased incidence of diabetes, increased incidence of neurodegenerative diseases like Parkinson’s and Alzheimer’s disease, compelling evidence of causing heart failure and most recently the acceleration of atherosclerosis. Only to fixate on the terrible twos: the potential rise in liver enzymes or increases in muscle aches and pains which are the least important of the drug reactions. I know the title of this blog is on statin toxicity but that’s a huge topic and there’s a few other things I need to get off my chest in this blog first. Later on, in a separate blog, I will go over how vital cholesterol is and why it should never be lowered and several dozen of the most disturbing adverse drug effects. Make sure you are sitting down when you read them. They are truly frightening.


Furthermore, they are inappropriately prescribed to entire populations of patients such as the elderly in whom high levels of cholesterol are proven to be protective in reducing the chances of a heart attack and all-cause mortality. The Framingham study told us that after the age of about 50, a low cholesterol level is associated with a significantly greater overall mortality. The older you get, the more dangerous it is to have a low cholesterol level.[2] Basically if your total cholesterol (TC) is about 190 mg/dl and above good, if it’s below 142 mg/dl watch out.

Women are another group for which statin therapy is contraindicated. For women cholesterol is protective across the board, the higher the TC the lower all-cause mortality.

The strongest data show that men who have had a heart attack, in what we call secondary prevention, benefit the most from statins up to their late 60’s only. If you have a heart attack after that age it’s better to have a higher level of cholesterol post heart attack. Studies show that the higher your cholesterol is the lower your chances of dying from all causes including heart attack.


If I make a good case against the statins and later (separately) the SSRI’s (which is easy to make) it is my hope that you will realize that Big Pharma isn’t this wonderful, altruistic, industry hell-bent on helping humanity. Instead Big Pharma is like any other corporation beholden to its stock holders for high profits in the exact same way Big Tobacco was. It has co-opted medical education, research and publication for its own purposes of profiteering. As such one can no longer simply read “the sum totality of the evidence” as an irrefutable argument for or against the use of a particular medication because that sum totality may have been completely funded by conflict-of-interest money. Drug companies have more money than entire countries so don’t think they can’t produce volumes of junk science. Later I’ll prove to you that they do just that.

In other words we must view all studies funded by the pharmaceutical industry as suspect and never conclude anything without following the money. In modern times I do not think it prudent for a doctor to change his or her treatments based on a single or multiple drug company funded studies. I recommend reading Dr Marcia Angell’s book The Truth About Drug Companies. Dr Angell is a modern day heroine of mythological proportion who has taught me much of what I know about this sordid industry. She was the editor-in-chief of the prestigious New England Journal of Medicine for 15 years before finally quitting out of frustration I suppose. On a daily basis she could see the conflict of interest (COI) and the routing of medical subspecialties that Big Pharma was in the process of doing. It seemed to her that the professional journals were becoming nothing more than slick, Madison Avenue promotional materials for luring doctors into using their dubious, expensive, new drugs. She is not alone as you will see when you read my chapter on vaccines and the Commercial Sick Care System (CSCS). I quote no less than four former editors: one from the Lancet, one hails from the highly respected BMJ, and two from the NEJM along with the investigations from several prominent physicians.

Research into the ethical problems of industry-sponsored studies demonstrated that they often withheld study data from the chief investigators, made the decision to publish-or not-based on back room corporate dealings, employed ghost writers whose results were more often painted in a favorable light without the input of the physicians who ran the investigation. Whereas non-industry funded studies were more often found to have negative results or contradictory conclusions regarding the drug under investigation. Furthermore, the revolving door policy between FDA and Big Pharma is endemic threatening to throttle the entire industry and poison the well if it hasn’t already.

We find most of the research doctors, if not all of them, are tied to industry either as grant receivers, paid consultants or on some other payroll option. When I read the disclosures for example on just one cardiologist on the panel of experts who brought us the new statin guidelines, I found that he was on the payroll of 7 drug companies each at an income of over $10,000 per annum. They are not required to stipulate exact incomes from each but the highest category is the over $10,000 category. He also owns stock in drug companies.

What’s the big deal if a doctor is on the payroll of a pharmaceutical firm? You’ll hear that comment frequently from paid consultants. Set down your glass of flouride for a minute and think: isn’t it obvious that if your doctor is being paid, sometimes hundreds of thousands of dollars, he or she just might have a slight bias? Seriously (I’m asking the doctor now), can you look at me with a straight face and tell me you are impartial when it comes to recommending a drug for a company that’s allowing you to buy a vineyard in Napa Valley? These are all symptoms of a failing medical model the Commercial Sick Care System (CSCS).

Keep that in mind as I delve deeper down the rabbit hole. If there wasn’t some truth to the claim that statins are bogus you would not be seeing scores of books written regarding their false claims and fraudulent findings. Some that I have read are: Curtis The Cholesterol Delusion, Colpo The Great Cholesterol Con, Kendrick The Great Cholesterol Con, and Ravenskov Ignore The Awkward. Don’t forget the great article on Saturated fat by Taubes as well as dozens of web sites. I especially like Ravenskov’s site. The latest book is by Dr Sinatra who makes yet another case against the statins and the high-cholesterol hypothesis in The Great Cholesterol Myth. Then there is the research of Dr Stephanie Seneff of MIT whom I also quote along with many others.

Take Anthony Colpo’s tome The Great Cholesterol Con. With over 400 pages of insightful information, Colpo meticulously proves to us that there is a con job at work. He shows that the very studies our institutional thought leaders quote from-providing the foundation for which our current cholesterol lowering guidelines are based-have conclusions that often do not correlate with the data, are transparently weak or outright fraudulent. The very theory that high cholesterol causes heart disease may be the biggest con in the history of medical science. (The second biggest con will end up being the newer classes of antidepressants and the atypical antipsychotics, closely followed by vaccines). In Colpo’s and Kendrick’s books, and modern studies (Duke University) we come across trials that show eating saturated fat and cholesterol improve cardiovascular status, (as was also demonstrated with the Framingham Study but downplayed). They meticulously take study after study and show no correlation between cholesterol levels in the blood and coronary heart disease (CHD) or heart attacks. In fact, higher cholesterol levels in the elderly are cardioprotective. The higher the cholesterol is in a person over the age of about 70 leads to a decrease in heart attacks, all-cause mortality and a longer life.

OK, if this is a con job of colossal magnitude prove it. If I can prove to you that “native” LDL cholesterol, the so called bad cholesterol, is harmless then you will feel confident when tossing out your statin prescription. Heart disease has to do with things that cause blood vessel inflammation (injury). From Anthony Colpo’s excellent paper published in the Journal of American Physicians and Surgeons, LDL Cholesterol: “Bad” Cholesterol or Bad Science? I am including all of his original references so that your doctor can look them up if so inclined.

The Composition of Atherosclerotic Plaques.

Despite popular perception, atherosclerotic plaques are not simply big wads of fat and cholesterol that have stuck to the walls of arteries like mud inside a pipe. The growth of atherosclerotic plaques takes place primarily inside the artery wall, between the inner and outer layers (N Engl J Med 1999;340:115-126). The plaques are complex entities with numerous components, including smooth muscle cells, calcium, connective tissue, white blood cells, cholesterol, and fatty acids. Proliferation of plaques may occur, not because of simple elevations in blood cholesterol, but because of unfavorable physiological conditions that damage or weaken the structure of the arterial wall. These factors include nutrient deficiencies (Cell Mol Biol 2004;50:877-884), poor glycemic control [elevated blood sugar and elevated fasting insulin level] (Arterioscler Thromb Vasc Biol 2004;24:816-823),cigarette smoking (J Am Coll Cardiol 2004;43:1731-1737),  homocysteine [this is the nasty one doctor’s never check and is a proven cause of atherosclerosis] (J Thromb Thrombolysis 2004;18:75-87),  psychological stress [I call if the great destroyer] (Circulation 1999;99:2192-2217),  nitric oxide depletion [often times high blood pressure is the first sign of NO depletion] (Curr Diabetes Rep 2005;5:17-23), high iron levels (Shah SV, Alam MG. Role of iron in atherosclerosis. Am J Kidney Dis 2003;41(3 Suppl 1):S80-S83),  microbial infection (Cardiol Clin 2003;21:333-362;Cell Microbiol 2004;6:117-127),  dietary trans fatty acids (Am J Clin Nutr 1999;70:832-838), excessive refined carbohydrate intake (Eur J Clin Invest 1998;28:329-333), and excessiveomega-6 fatty acid intake and/or deficient omega-3 fat intake (Prostaglandins Leukot Essent Fatty Acids 1998;59:229-233). All of these factors have been shown to exert an atherogenic effect unrelated to serum cholesterol elevation.

Damage to the arterial wall triggers an inflammatory state in which the body recognizes injury and sets about to repair it (Ross R. Atherosclerosis—an inflammatory disease. N Engl J Med 1999;340:115-126). This response-to-injury scenario is well accepted by the vast majority of cardiovascular researchers, although many of them continue to promote the hypothesis that LDL cholesterol is involved in triggering or aggravating the inflammatory state that eventually leads to heart disease or stroke. There is little evidence to support such a contention. In fact, cholesterol, like other components, may be present in atherosclerotic plaque as part of the repair mechanism.

As you can see from the above there are many factors at play in this complicated disease. It is anything but the toddler’s version patients typically receive on Junk Food TV or in their doctor’s office. In fact, do you see any mention of LDL cholesterol as a causative factor in the above listing? (Inconsistent font? Thank WordPress)


I think I can convince you of this in one sentence. Heart disease is responsible for 50% of all deaths in America. That is, endothelial inflammation is an underlying theme in most disease states not just heart disease. Everyone has it and what does everyone eat? Processed convenience foods rich in Ω6PUFA, trans fats, sugar and refined carbohydrate. It turns out that consuming the so called heart healthy omega 6 polyunsaturated fatty acids (Ω6PUFA), hydrogenated oils, cereal grains and sugars are the real promoters of heart disease because they cause endothelial inflammation-they injure the lining of your blood vessels.Note the major change in fat consumption that occurred from the turn of the century, where heart disease was a novelty it was so rare, to 1950 where CHD became as common as dandelions in the spring.

Butter consumption was declining while the use of vegetable oils, especially oils that had been hardened to resemble butter by a process called hydrogenation, was increasing—dramatically increasing. By 1950 butter consumption had dropped from eighteen pounds per person per year to just over ten. Margarine filled in the gap, rising from about two pounds per person at the turn of the century to about eight. Consumption of vegetable shortening—used in crackers and baked goods—remained relatively steady at about twelve pounds per person per year but vegetable oil consumption had more than tripled—from just under three pounds per person per year to more than ten.[3]

My own research on heart disease got me started on pharmaceutical grade fish oil while tossing out the omega 6 oils back when the only person talking about it was Barry Sears: The Omega Zone & The Anti-inflammation Zone. I used the book Protein Power by Eades to lose the fat. The Protein Power/Zone diet approach, before the Commercial Sick Care System had a chance to cripple me, led to a 60+ pound weight loss which helped relieve all sorts of problems including some but not all of my angina. I had this great barometer: when I ate something particularly bad my chest pain was amplified. Likewise, eating really healthy foods and taking fish oil partially relieved it. This certainly is not the case for most patients but it served me well in my decade’s long search for the proper nutrients and lifestyle. And of course thank God once again for giving me the intelligence and stubbornness to avoid cardiologists and treat all prescriptions with suspicion.


[2] Kendrick. The Great Cholesterol Con. p. 96

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Category: STATINS

About the Author ()

Dr. Christopher Rasmussen (aka Reality Renegade) is the author of his upcoming book, "InflaNATION: Industrial Diners & A Doc In The Box." By deliberately avoiding harmful industrial foods and the Commercial Sick Care System with its Pills and Procedures paradigm, Dr Rasmussen cured himself of a deadly disease-which became the reason for writing this book. In the book, he provides the facts you must know and the solutions to regain your health, maintain wellness, and outlive your parents' generation in an extraordinarily toxic world.

Comments (16)

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  1. Danny Lyons says:

    Thank you Christopher for another excellent informative article.
    While my comment is off topic it may be of interest.
    I have spent the last 2 years educating myself as best I can on,heart disease,cholesterol, statins and diet in that order unfortunately. Like you I suffered a MI mine in (2010) age 44. I had several of the precursors for metabolic syndrome central obesity, impaired fasting glucose, and hypertension. I was a heavy smoker and largest part of my diet was refined carbohydrates. Having no medical background, mine was engineering I was totally compliant to the letter with the medical advice, medication and dietary recommendations I received on leaving hospital.

    Fast forward one year (sept 2011)and the standard recommended food pyramid had greatly assisted in my already heavy body weight of 255 pounds extending to 290 plus pound.(my height is 5 feet 10inches). My initial statin medication of Lipitor 80mm was decreased to 40mm at the end of year one because I could no longer tolerate the pain I was suffering in my joints. The reduction didn’t cure the problem it did make it more bearable.

    2012 was a continuous succession of different diets and training regimes, willpower was strong although wrongly starving myself by having a maximum daily intake of no more than 1300 calories( still believing a calorie was a calorie was a calorie) the weight started to come off and off and off. I spent the first 10 months of 2012 eating low fat exercising more and more and been constantly hungry, ignorance can be bliss, especially as the weight kept dropping.

    The first six months of 2013 I now refer to as my questioning period, From Yourself to Dr Eades to Dr Kendrick to Dr Curtis to the Yosephs etc etc I was really uncomfortable with the statin medication, I raised my concerns on several occasions with my doctor and with my cardiologist but despite knowing I was right and blatantly seeing on several occasions they couldn’t discredit or argue with the information I put in front of them with regards the damaging effects and uselessness of statins they refused to concede, after all who was I to question them.

    Alas in March of 2013 I stopped all Statin medication, within three weeks I had no more joint pains and felt generally sharper. In July of this year I cut out sugars and dropped carb intake to 80 grams per day and increased calories to about2,500 approx not exactly sure I don’t count calories any more. I stopped taking glucose intolerant meds (glucophage) in September of this year and also stopped taking Plavix75mg as well. Despite now weighting 161 pound with blood glucose normal levels both pre prandial and post prandial with regular blood pressure readings of 105/70 and feeling fantastic my doctors still refuse to accept turning the food pyramid on its head was the way to go and there still horrified I won’t take statins. Now since start of November 2013 I dropped carb intake to 0 and eat just proteins both dairy and meats fish etc and healthy fats. Unfortunately I had to get bloods done last week and everything was perfect liver kidneys etc etc but of course because of my sudden complete drop in carbs at the start of November my total cholesterol number has gone way up. CHol 332 mg/dl HDL 80 Trig 63 LDL 251. I swear the doctor is only delighted with himself and no amount of explaining to him about LDL particle size or Trig/HDL ratio etc will convince him of anything other than I need to be statin induced immediately. I know a return to approx 5o gram of carb and probably 40 gram of resistant starch per day will cure the issue of the high LDL number regardless of the fact I don’t see Cholesterol as a precursor for CVD. I suppose asking my Doctor did he believe in Santa was a fair question seen as he believed in good and bad cholesterol and failed to be able to distinguish between a Sterol/alcohol and a lipoprotein.
    Anyways Christopher please keep up the good work and continue educating folk like myself, you sure are making a difference. The tide is turning slowly.

    • Christopher Rasmussen MD, MS (aka "Reality Renegade") says:

      Hello Danny,
      I have a long-winded response for you. Quite by coincidence all of the below discussion will be featured on the next three blogs!!

      First of all let me compliment you your amazing body fat loss. That extra weight was on its way to killing you. That and the smoking. Do you still smoke? If so stop. You did the fat loss you can stop the cigs too. Very important that you quit or all of your efforts may be in vain. Also start an exercise program.

      Now as far as low carb goes feel free to eat anything from the fruit and vegetable (FAV) kingdom with a few exceptions with the non-fibrous starchy carbs like potatoes and bananas. However you can eat apples and the like. I eat tons of fruits and berries.They are a great source of safe carbs as long as they stay in the whole form when eaten. Or did you mean zero starchy (non-fibrous) carbs when you dropped down to zero?

      CHol 332 mg/dl HDL 80 Trig 63 LDL 251 As you can see, that is a marvelous HDL and your TG/HDL ratio is perfect. It tells me that you no longer have any visceral fat and hence a much lower level of inflammation too. I do not even check LDL anymore it’s nearly worthless because it has no predictive power. There was a Harvard study that came out I think about 2 years ago that demonstrated very clearly how the TG/HDL ratio is a vastly superior predictor of cardiac risk. Over about 7 and risk goes up by a factor of about 16 if I remember it correctly. Under about 3 and you are safe even if you smoke, are overweight and deconditioned (never exercise). That’s pretty powerful but I’m not surprised because LDL and CHD are not related. Also at an HDL of 80 or higher you are virtually protected from a cardiac event-across the board of LDL values. That comes from a slide I use in class.

      Another thing your doctor missed was that your LDL is the large, fluffy type and THAT’S THE TYPE THAT’S HARMLESS TO YOU. How do I know you have the large fluffy type? Because of your very healthy TG/HDL ratio-it tells me that’s what you have. You can verify that by getting a LipoScience NMR lipid profile if you wish. This type of increase in HDL, LDL and TC is common when you eat more fat and cholesterol (and fish oil). The super low TG is carb related, the high HDL shares a carb component too. Lower the carbs and the HDL goes way up while the TG’s drop (Westman Duke University).

      Here’s what wellness looks like: Fasting insulin < 5; TG/HDL unity or < 1; hsCRP 0.5 or less; AA/EPA ratio 1.5-3 with 1.5 being the very best. Have you heard of the AA/EPA ratio? This can be ordered from, the Life Extension Foundation's lab section. Look under Omega Score. Are you taking pharmaceutically pure fish oil? Let me know about that it's very important that you do. Go to select products or fish oil and choose the OmegaRx type. I have been taking this same product for almost 17 years. If you have heart disease you need to take at least 8 capsules per day (or 2 tsp of the liquid-store in the freezer BTW). Be careful if you are on prednisone or the like or blood thinners. In general it's usually no problem even with these others but proceed with caution and inform your doctor. I take the equivalent of 12 caps per day. Did you see the mentioning of cholesterol in this (besides the HDL)? This is what I'd recommend so that we can all sleep at night. Get a heart scan if you haven't yet. A heart scan is the best predictor of all. It beats all good markers combined. You can then follow your calcium score to assess how you are doing. If everything's going well and you have very little inflammation the score will decrease over time. The 2-D needs no doctor's order, the 3-D with contrast dye needs an order. Either one but the 3-D is very cool I must admit. Next check the labs I mentioned above like a fasting insulin level and CRP. If your CRP is very low you are doing well. Third check your homocysteine level and oxLDL level. After all it's oxLDL that is the nasty particle that CAN cause damage, not native LDL. SEE MY UPCOMING BLOGS FOR THIS INFORMATION. Homocysteine is dangerous and needs to be checked. Most docs don't know anything about it. This is a perfect example of how ingrained the cholesterol theory is in all of us. How old are you know? This lipid profile could have much to do with your thyroid status too. A TSH is worthless. Check your freeT3 to reverseT3 ratio. Go to site. Lastly your doctors act as if a statin will save you from everything. At your age (I'm assuming late 40's) a statin can help by reducing a second heart attack by 30%. However, here's the trick: it is the relative risk reduction only. In real numbers you doc will need to treat 49 more patients-all like you-for 5 years in order to prevent ONE HEART ATTACK. ONE. That's called The Number Needed To Treat concept (Abramson Overdosed America). At the same time you will hurt, become increasingly feeble, age more rapidly and possibly give you diabetes, dementia, mental-emotional illness (see my first & second statin blogs). If lowered too low (LDL) you climb up the U-shaped curve on the left side increasing your chances of hemorrhagic stroke, accidents including homicide, and cancers.... I think you are doing very well. Thanks for sharing and keep in touch. Chris

  2. Danny Lyons says:

    No I don’t smoke stopped on the morning of April 12th 2010 the day I had my MI.I meant zero starchy non fibrous carbs. Also I reduced fibrous carbs down to 30grams from the start of November, it was part of a 6week n=1 experiment I was doing (trying to shift subcutaneous fat left from stretched skin). Fruit intake is mostly berries sometimes an apple. Regards the vegetables I normally stick with veg that grows above ground. I do need to increase my intake of fruit and vegetables. I Exercise for 1 hour 4 times a week cardio (stationary exercise bike) every alternate day and walk a fair bit as well weather permitting. No to be honest I have not heard of AA/EPA ratio, I will look into it and see if it’s available here in Ireland. I take Pharmaceutical omega 3 called Omacor, 2 x 1000mg capsules a day, each capsule contains EPA 460mg and DHA 380mg, and should I increase?
    Medication I am currently on is Aspirin 75mg, ACE inhibitor called Ramapril 7.5 mg and a beta blocker called cardicor 7.5mg. I supplement with Ubiqinol CoQ10 100mg daily, magnesium taurate 750mg, Vitamin K2 120mcg (menaquinone-7) Liv 52 and 5000 IU of vitamin D3. I would like to be able to come off all medical medication if possible. I will look into all your recommendations with regards the tests. Most importantly have you released your book yet

    • Christopher Rasmussen MD, MS (aka "Reality Renegade") says:

      Good Morning Danny,
      If I recall it’s about 7 hours ahead in Ireland (from the Midwest)? With your huge weight loss I’m surprised that you still need the BP meds. That’s yet one more reason why your thyroid may be involved since hypothyroidism (it can be very subtle) always causes hypertension and a big increase in serum lipids: TC, LDL. Does your country fluoridate their water? Here fluoridation is huge affecting about 200 million people and most of the fluoride levels are high enough to inhibit thyroid function. So there is a lot of hypothyroidism here. Many of them are mistakenly placed on statins, blood pressure medication and sometimes an SSRI for depression that comes with low thyroid because docs only check the TSH, never listen to symptoms like cold hands and feet or sudden weight gain, swells up after a night on the town, etc. Just a thought. At your age if you correct your thyroid now you can often prevent atherosclerosis from getting worse. Yes, believe it or not. At least that’s what some compelling studies have shown. The thyroid is key for endothelial health. (Mark Starr MD Hypothyroidism type II the Epidemic).
      I remember Omacor here in the States. They changed the name to Lavaza or something like that.The Zone Labs brand that I take is just slightly less concentrated than yours and it’s as pure (5 star IFOS rating). Omacor is great and it’s the most concentrated on the market (and the most expensive). In Barry Sears books he recommends all those with heart disease to be taking at least 8 caps of his brand which is also very concentrated. For you that would probably translate to 6 caps. That will hopefully place you in the wellness category (1.5-3) for AA/EPA ratio. I like the fact that you are well-read enough to be adding in Vit K with your Vit D. As far as cardio prevention with Vit D you may wish to consider bumping up the dose. However, that only depends on your serum level. For cancer and cardioprotection you want to be sure the level is at least 50 nanograms/ml or as high as 100 for the upper limit. I quote no less than a dozen world experts on Vit D and they all agree that 100 is the upper limit and that around 50 is the minimal level to achieve the anti-cancer and anti-atherosclerosis benefits. It may help your hypertension too. There is an established model showing Vitamin D’s effects on the renin–>angiotensin–>aldosterone axis. This recommendation clashes with the IOM recommendations which are far too low. They suggest that you have an upper limit level that defines hypovitaminosis D (<30ng/ml). Mine is about 80 ng/ml the last time I checked taking 10,000 IU per day.
      Magnesium is essential. Some scholars have claimed that all of the benefits seen with aspirin for protection against heart attack may be due to the buffering component which contains a therapeutic level of magnesium-close to 50mg if I am not mistaken. Good choice. I would consider the other standard antioxidants too. Vitamin C and E as the succinate (dry) form and it must contain gamma tocopherol. The synthetic alpha tocopherol is worthless.
      The book is not out yet. It will probably be 4 smaller ones since most (not counting you and I) will not read a thousand page book unfortunately. I am shopping around for a publisher now. I'll tell you one thing. Writing a book is a lot of fun. For me my find of knowledge increased by an order of magnitude-all in the area of preventive medicine.

  3. Danny Lyons says:

    Yes in the Republic of Ireland our water is fluorinated its government policy. Having said that my Thyroid function result from 9-12-2013 was FT4 15.2 PMOL/L reference range is (9 -20) and my TSH was .98 mlU/L reference range (.35 -4.94) unfortunately FT3 was not measured.
    My understanding (hope I’m correct) is that higher-than-normal TSH levels are most often due to an underactive thyroid gland so according to my result that would not be my case (I hope). I have a 100% blockage, no operation or stenting, just medication, in the region of 30% heart muscle damage, would that explain the BP medication? I must do a n=1 on my BP increase with no meds.
    That’s very interesting about the omega 3; I will now increase my dose to 6 per day although I may look into the omega 3 you mentioned because the Omacor are expensive particularly at a high dose. I will take your recommendation on the vitamin C. I had previously looked at supplementing with vitamin E but I read it had an unfavorable interaction with vitamin K (bleeding), but obviously you wouldn’t be supplementing with it if that was the case. Is there a specific dosage of vitamin K you recommend? I’m now intrigued that a correction in thyroid can often prevent atherosclerosis from getting worse. Once again you have given me a good direction in which to move forward. Do you have an opinion on supplementing with resistant starch?
    I would be of the opinion that because of your qualifications and the fact that you survived a MI all those years ago would defiantly increase the chances of quite a large number of people relishing the prospect of reading a 1000 page plus book written by yourself.
    Once again thank you for the words of experience and knowledge.

    • Christopher Rasmussen MD, MS (aka "Reality Renegade") says:

      Hello Danny,
      Yes, I remember now that Ireland is one of the only countries in all of Europe that fluoridates their water-I’ll bet you are thrilled about that! The problem with checking a TSH is that it is unreliable. Yours is normal but you could still have “tissue hypothyroidism.” That’s where the cells that need thyroid hormone cannot utilize it because they cannot convert T4 (inactive) into T3 (the active material). It is dependent on the deiodinase enzymes I and III at the tissue level. Scores of conditions can render those enzymes dysfunctional-virtually any disease state will do it including obesity. That’s why it’s a good idea to check your free T3 and reverse T3 and check for antithyroid antibodies too while you’re at it. With heart disease at such an early age like me we need to make sure all the i’s are dotted and T’s crossed right? The website will help make sense of these tests.

      Another big one is your homocysteine level. In spite of the fact that it has been proven to be a powerful risk factor in atherosclerosis (Kilmer McCully MD) no cardiologists I know of pays any attention to it. But it’s deadly and responsible for untold misery because when the level is high it can cause dementia, heart disease, broken bones, stroke, silent stroke and many other conditions. You will want to keep your level under 6.

      As far as vit K goes you’ll want to get at least 200 ug (micrograms) of MK7. That seems to do the trick for helping to prevent calcification where it’s not supposed to be along with vit D3. Micronutrients are absolute key as well so you should look into a good multimineral (WITHOUT IRON). Or you can take SeaHealth Plus which is what I take every day with 70 micronutrients per dose and potent polyphenols to boot. That can be ordered from the same place that you can get cheaper and just as good fish oil. Order the OmegaRx type it’s cheaper than the EicoRx and is the best one for you. The EicoRx is altogether different don’t take it. I get the bottle of liquid fish oil and take a T per day-the equivalent of 12 capsules per day. If you got the liquid you would have to take 2 teaspoons (equivalent to 8 capsules) per day. Keep the cap on tight and store in the FREEZER-it won’t freeze solid don’t worry.
      Do you recall what your ejection fraction is? With 30% muscle damage I am curious if it compromised your cardiac output at all.
      Perhaps a publisher will agree on the 1,000 pages. I suspect that we “readers” are in the minority however. I know the NY Times best sellers are usually under 400 pages. Even readers seem to have shorter attention spans. As for me the bigger the better. Oh one last thing Denise Minger has a book out which I plan on buying called Death by Food Pyramid. I quote her in several places in my book. She’s fun to read and smart. Might be pretty worthwhile.

      • Danny Lyons says:

        Absolutely agree with you about the importance of all the i’s dotted and T’s crossed.
        Results of echo transthoracic 16-4-2010 were as follows Chris:
        Impaired LV systolic function with ejection fraction estimated at 40 to 45%. Extensive inferior and posterior wall hypokinesis also involving the inferobasal segments. The mitrial valve is largely spared and functions normally. The wall segments are all of normal thickness consistent with recent infraction. The anterior wall is normal with some subtle bundle branch block pattern morphology. The aortic valve is unremarkable. The RV systolic function is also mildly impaired suggesting some minor RV involvement. Tricuspid function is normal. RV systolic pressures are also normal measuring less than 15mmHg. No pericardial effusion seen.
        Conclusion: impaired LV systolic function in the setting of a recent infraction with inferior posterior and inferobasal wall hypokinesis. Some minor RV involvement seen as well.
        Results of echo transthoracic 6-2-2012 were as follows:
        Left ventricle is structurally normal with well preserved systolic function regional wall motion abnormalities evident. I am in sinus rhythm and transmittal Doppler study suggests normal relaxation. Right ventricle is structurally normal with well preserved systolic function. Both atria are normal. Aortic root is normal. Mitral valve is normal. There is trace tricuspid incompetence. RVSP 20-25mmHg which is normal . No effusion or mass evident. Pericardium is normal.
        I have taken your advice and ordered a good multi vit.
        As always thank you for your very valued input.

        • Christopher Rasmussen MD, MS (aka "Reality Renegade") says:

          Hi Danny,
          Looks like you improved remarkably in your EF in two years! Sure beats the usual downward course that we expect when told to keep eating unhealthy “heart smart” foods. So it’s about a 20% decrease from normal currently. I had a little apical hypokinesis and I often wonder if that’s the reason why I never feel as if I can ever be in the peak of fitness I used to feel back in my residency years.
          I am curious if one can actually continue to increase EF and cardiac output if one continues on a very healthy lifestyle approach. Presumably the compromised myocardium post MI stays in a sort-of suspended animation-not dead, not really alive. I don’t know much more about that phenomenon but it fascinates me. I suspect that one can always continue to improve perhaps with the correct supplements like L-carnitine and alpha lipoic acid combo which is supposed to improve mitochondrial activity. This info comes from Berkeley professor Dr Bruce Ames.

  4. Jack Cameron says:

    It makes sense that hypothyroidism leads to atherosclerosis and increased risk of CHD. Hyothyroidism causes a reduction in energy expenditure which results in decreased utilization of glucose for energy, particularly on a standard high carbohydrate diet. The body responds by increasing liver de novo lipogenesis (conversion of carbohydrates to lipids) in order to prevent elevation of blood glucose. The increase in lipid synthesis by the liver results in increased synthesis of TG and TC. The increased lipids are preferentially directed to adipose tissue (belly fat).

    You noted that there has been a huge increase in consumption of n-6 linoleic acid (LA)during the past century. It has been estimated that between 1909 and 1999 intake of LA has increased from 2% to 7% of calories. The increase in LA intake has caused a significant increase in hypothyroidism.

    During the 1940s, cattle producers learned that feeding cattle grains high in LA resulted in more rapid weight gain caused by impairment of thyroid function that in turn reduced energy expenditure. Just how increased LA intake causes impaired thyroid function has only been determined fairly recently.

    N-6 LA is the precursor to n-6 arachidonic acid (AA) which is the backbone of n-6 eicosenoids which are signalling molecules that regulate many physiological functions. Increased n-6 LA intake results in decreased tissue n-3 fatty acids and excessive n-6 eicosenoids that alter many physiologic processes including metabolism. To date ten types of eicosenoids have been identified each with many subtypes. The most recently identified eicosienoids are endocannabinoids that that activate the same receptors (CB1 and CB2) activated by marijuana. Excessive LA intake elevates endocannabinoids which induces obesity by impairing thyroid function. (hypothyroidism) “that leads to “ectopic lipid storage and hepatic insulin resistance by promoting centrally mediated hypothyroidism”.(Pubmed 22912404). Elevated endocannabinoids also also offsets the appetite reducing ability of leptin thereby increasing appetite. Like excess marijuana, excess LA intake causes reduced energy expenditure and increased appetite that leads to obesity.

    An ecological study examined the correlation increased intake of 273 different food commodities between 1909 and 1999 and the increase in obesity during that time. It was found that only increased intake of foods high in LA (soybean oil, poultry and shortening) were strongly associated with increased obesity.Increased intake of sugar was weakly associated with increased obesity. Faulty government dietary guidelines that advocate substituting vegetable fats for animal fats have greatly contributed to increased LA intake.

    It has been found that cholesterol lowering statins increase serum n-6 AA.

    The hypothyroidism, increased appetite and obesity causes by LA-induced elevation of endocannabinoids is but one of a half dozen or more ways that increased LA intake causes increased risk of coronary heart disease.

    • Christopher Rasmussen MD, MS (aka "Reality Renegade") says:

      Hi Jack,
      Nice piece. Have you read Dr Mark Starr’s book Hypothyroidism Type II? I fist became aware of the role that thyroid plays in protecting us from cancers and atherosclerosis from an interview with Dr Starr on Coast to Coast Radio years ago. There is compelling evidence that normal thyroid function will prevent atherosclerosis from developing-as long as you catch it by the 5th decade of the patient’s life (or earlier). It still helps after that but by the 70’s with advance disease it doesn’t help much. Of course our “experts” suggest that docs only check a TSH as an accurate screening tool. But there is plenty of research showing that the TSH is the worst test and is the least reliable for assessment of thyroid function.

      How is it that excessive LA intake impairs thyroid function? Is it a direct receptor effect on the thyroid, does it decrease I uptake, peripheral effect (tissue level) or what?

      I recall Dr Barry Sears discussing the role of fish oil in blocking the endocannabinoid system thus reducing the desire to binge eat in the middle of the night-if you take the oil at bedtime. Do you know anything about taking fish oil to prevent night sweats? I had a patient with that condition that swears by it.

      I was not aware of the role of Omega 6 FA’s in reducing thyroid function. That is truly fascinating. I have a chapter devoted to ALL the causes of our current obesity pandemic-at least all of the causes that I can think of which is about 18. I’ll have to research this new one and add it in. If this is true it’s effects are global and scary.

  5. Jack Cameron says:

    I am not familiar with Dr. Mark Starr’s book Hypothyroidism Type II. I will check it out today.

    The hypothyroidism induced by elevated endocannabinoids caused by excessive intake of omega-6 linoleic acid (LA) is but one of a half dozen or more mechanisms by which excessive LA intake increases risk of atherosclerosis and coronary heart disease. (I will get into that later) The primary way to reduce the problems associated with too much LA is to eliminate intake of all sources of polyunsaturated fats from vegetable oils.That is not too difficult for those on a low carb diet as a much of the LA comes from foods such as potato chips, french fries, commercial baked goods and snacks. LA is present to varying degrees in all animal fats and in “good” fats such as olive oil and coconut oils, so aiming for a target intake of 2% of calories, compared to the present average US intake of 7%, is a reasonable goal. Poultry and pork can also be a major source of LA, particularly when the animals are fed grains as most are.

    I have become quite familiar with the scientific shorthand used in abstacts about endocannabionids so I will try to elaborate on the reference I gave on the subject; The first sentence of the abstract reads;

    Fatty acid amide hydrolase (FAAH) knockout mice are prone to excess energy storage and adiposity whereas mutations in FAAH are associated with obesity in humans.

    The two major endocannabioids are anandamide and 2-AG. Anandamide is degraded by the enzyme “fatty acid amide hydrolase”, or FAAH, while 2-AG is degraded by MAGL.

    The degrading enzymes prevent endocannabinoids from becoming excessive and consequently the effects are normally far less than the effects of marijuana. In a study with mice where both degrading enzymes were blocked., the endocannabinoids rose unchecked and resulted in loss of short term memory to the same extent as caused by marijuana.

    In the subject study mice lacking the ability to synthsize FAAH were used which resulted in elevated anandamide that caused impairment of the thyroid. It was noted that humans who have mutations in FAAH often are obese because of elevated anandamide.

    It is of note that the activity of FAAH, the enzyme that degrades anandamide, increases with increasing obesity, but the acitivity of MAGL that degrades 2-AG does not increase with obesity. As a consequence, those who are obese often have elevated levels of the endocannabinoid 2-AG, but not elevated anandamide. Consequently the obese will tend to have reduced metabolism, together with increased appetite cause by 2-AG, which makes it difficult to lose weight.

    The cause of the hypothyroidsm is described in the abstract as follows:

    “Here we show that reduced energy expenditure in FAAH(-/-) mice could be attributed to decreased circulating triiodothyronine and thyroxine concentrations secondary to reduced mRNA expression of both pituitary thyroid-stimulating hormone and hypothalamic thyrotropin-releasing hormone. These reductions in the hypothalamic-pituitary-thyroid axis were associated with activation of hypothalamic peroxisome proliferating-activated receptor γ (PPARγ), and increased hypothalamic deiodinase 2 expression. Infusion of NAEs (anandamide and palmitoylethanolamide) recapitulated increases in PPARγ-mediated decreases in EE. FAAH(-/-) mice were also prone to diet-induced hepatic insulin resistance, which could be attributed to increased hepatic diacylglycerol content and protein kinase Cε activation. Our data indicate that FAAH deletion, and the resulting increases in NAEs, predispose mice to ectopic lipid storage and hepatic insulin resistance by promoting centrally mediated hypothyroidism.”

    It is my understanding the the term “centrally mediated hypothyroidism” indicates that the hypothyroidism is mediated via the hypothalmus part of the brain.

    I will address the importance of omega-3 fatty acids on endocannabinoids in a later comment.

    • Christopher Rasmussen MD, MS (aka "Reality Renegade") says:

      Hello Jack,
      It’s interesting to see another mechanism by which our “heart healthy” polyunsaturated omega 6’s are destroying our health. I try to hit that point home often and how important it is to avoid the cheap seed oils and stick with EVOO.
      Any thoughts as to pot smoking affecting thyroid function being that it is a weak endocannabinoid agonist?

  6. Jack Cameron says:

    Hi Chris,

    I read some of reviews of Dr. Starr’s book but hypothyroidism. Neither my wife or I have ever had any thyroid problems so I am not compelled to buy the book right now. It does make sense that hypothyroidism would cause atherosclerosis as lipogenesis resulting from hypothyroidism increases production of cholesterol and TG.

    I am not familiar with use of fish oil for preventing night sweats.

    I have a chapter devoted to ALL the causes of our current obesity pandemic-at least all of the causes that I can think of which is about 18. – See more at: linoleic acid mediates obesity through a number of mechanisms and would be a good candidate for the to be at the top of the list of causes of obesity. Elevated endocannabinoids induces obesity by causing hypothyroidism and by stimulating appetite.

    The degree of hypothyroidism that results from excessive dietary LA has not yet been clearly determined. Scientists have developed a lot of ways to manipulate endocannabinoid (EC) levels by means other than food.. ECs can be elevated by blocking the enzymes that degrade the ECs, or by using mice that do not synthesize the degrading enzymes. The EC receptors can be blocked or mice lacking EC receptors can be used. Few studies have been done using food alone (excess LA) to increase ECs so the extent to which dietary LA alters thyroid function is not clear. The study discussed in my earlier comment and in a second study discussed below both manipulated EC levels by means other than food.

    Two other studies that attempted to evaluate the effect rodent of dietary LA on obesity and “energy efficiency” (IE hypothyroidism) are subsequently discussed. The latter two studies had a couple of fundamental errors to start with, came to some erroneous conslusions and were confounded somewhat by the effect of prostacyclins on adipocytes in the mice during lactation and nursing, but they provide a lot of data of interest. Further, they are the only studies I know of that use dietary LA to try to sort out the effect of ECs on metabolism and appetite.
    I have a chapter devoted to ALL the causes of our current obesity pandemic-at least all of the causes that I can think of which is about 18. – See more at: link to the study on endocannaabinoid induced hypothyroidism discussed in my previous comment is

    the link to a second study on the same subject, “Acute effects of –anandamide and the CB1 receptor antagonist AM251 in the regulation of thyrotropin secretion,” is Both studies have free full text available. The abstract to the second study reads in part:

    “We examined the acute effects of endocannabinoid, anandamide, and of synthetic cannabinoid receptor antagonist, AM251—- on TSH, thyroxine (T(4)), and triiodothyronine (T(3)) secretions. Euthyroid male rats showed a 42% decrease in serum TSH, 2 h after a single i.p. injection of 0.02, but not 0.2 mg/kg body weight (BW), anandamide, accompanied by a 39% reduction in serum T(4), without alteration in serum T(3). At 0.5 and 1 h, these serum hormones showed no significant change. Hypothyroid rats showed a 35% reduction in serum TSH (P<0.01), 2 h after anandamide injection, which had no effect on hyperthyroid rats. In both thyroid states, no modification of serum thyroid hormones was observed. Intraperitoneal injection of 0.17 or 1.7 mg/kg BW AM251 in euthyroid rats caused, 1.5 h later, 1.7-fold or 4.3-fold increase in serum TSH respectively, without changing thyroid hormones. Stimulatory effect of 0.17 mg/kg BW AM251 and inhibitory effect of anandamide was abolished in the group injected with AM251 followed by an anandamide injection, 30 min later. Intracerebroventricular injection of 20 ng (but not 200 ng) anandamide induced a decrease in serum TSH at 60 min after injection, which tended to disappear at 120 min. Anterior pituitary explants presented significant reduction in TSH release in the presence of 10(-7) M anandamide in incubation medium, which was blocked by 10(-7) M AM251. In conclusion, anandamide has the ability to acutely inhibit TSH release in eu- and hypothyroid rats, acting at the hypothalamus-pituitary axis. Since, in addition, the cannabinoid receptor antagonist AM251 increased TSH release, we suggest that endocannabinoid system has a role as negative regulator of TSH secretion."

    In brief, the study showed that injection of the EC anandamide resulted in decreased secretion of thyroid hormones. Blocking the EC receptor prevent the decrease in thyroid hormones demonstrating that the decrease in thyroid hormone that occurred after injection of anandamide was due to activation of the CB-1 receptor by anandamide.
    Like most studies on endocannabinoids, the two studies used means other than food to manipulate the endocannabinoids. The studies therefore do not provide insight into the extent of hypothyroidism that may result from dietary n-6 LA.

    Effect of dietary LA on metabolism and appetite:

    A study published in 2012, Dietary Linoleic acid elevates endogenous 2-AG and anandamide and Induces Obesity. attempted to quantify the effects of the increase in dietary LA that occurred in the US during the 20th century on metabolism and appetite. Participants in the study, as shown on a copy of the abstract on October 12, 2012, included the University of Bergen, Bergen, Norway and National Institutes of Health, Bethesda, Maryland.Oddly, the name of the NIH no longer appears on the abstract.

    The polyunsaturated fats of the diets included only the rudimentary essential fatty acids, n-6 LA and n-3 ALA (No HUFA) Groups of mice were fed (1) a low LA diet that ostensibly represented LA intake around 1900, (2) a high LA diet representative LA intake around year 2000 and (3) a high LA diet to which was added enough long chain n-3 (DHA and EPA) to restore the omega-3 index to the level found in the low LA (1900) diet. The three diets were fed with both a medium fat diet (35% of calories) and a high fat diet (60% of calories). The fats in the diets consistent of many different oil but were mostly coconut oil.

    The low LA diet included 1% n-6 LA and 1% n-3 ALA (1 to 1 ratio) as% of calories which is not even close the the estimated average US essential fatty acid (EFA) intakes in 1909 of 2.23% n-6 LA and 0.35% n-3 ALA (6 to 1 ratio). (The use of the n-6 to n-3 ratio of 1 to 1 is based on an erroneous statement "humans evolved on a diet with equal amounts of n-6 and n-3 fatty acids made years ago that has become widely accepted as truth. I got an e-mail from Cornucopia recently that included that same erroneous statement. Evidence indicates that humans evolved over a couple of million years on a diet comprised mainly of wild ruminants that have an n-6 to n-3 ratio of about 2.3,. Humans incorporated fresh water fish in their diet about 40,000 years ago according to analysis of bones, and fish became the source of 10 to 50% of dietary protein in different areas of Europe) It is unlikely that LA intake was ever as low as 1% of calories in human history, nor has the n-6/n-3 ratio ever been as low as 1 to 1. The goal of approximating changes in EFA intakes in the US during the 19th century was therefor a failure from start.

    The High LA diet included 8% LA and 1% ALA which compares favorably with the estimated 1999 US intake of 7.23% LA and 0.72% ALA..The relative omega-3 indexes of the high LA and low LA diets does approximate those of current EFA intakes in the US and Japan.

    Some results of interest are as follows:

    (1) Mice on the medium fat (35%) and high fat (60%) low LA diet did not become obese whereas mice on the high fat (60%) diet became very obese. It is concluded that a high saturated fat diet does not cause obesity as is often claimed, and that the obesity resulting fro a "high fat diet" is due to high LA content of the standard research high fat diets..

    (2) In rodents fed the medium fat (35%) diet, increasing rodent LA intake from 1% to 8%of calories diet resulted in a 75% increase in endocannabinoids, a 2% increase in food intake and a in a 13% increase in feed efficiency, or weight gain per calorie of food intake which indicates reduced energy expenditure,due to hypothyroidism. Weight increased by 10% and the obesity index increased by 20%.

    In mice on the medium fat, high carbohydrate diet, the increase in weight and obesity resulting from the high LA diet.was due mainly to decreased energy expenditure, not increased food intake. In contrast, mice on the high fat had only a 3% increase in feed efficiency but a 165% increase in endocannabinoids and a 20% increase in food intake and adiposity index. It was concluded that the higher increase in feed efficiency of mice on the medium fat diet was due to the higher carbohydrate content of the diet. (When energy expenditure is reduced and carbohydrate intake is high, the body increases de novo lipogenesis to reduce the elevation of circulating glucose)

    (3) For both medium and high fat diets, when mice on on the 8% LA diet were given 1% DHA and EPA, their omega-3 index and tissue n-6 AA was about equal to the levels of mice on the 1% LA diet, but body weight was about the same as on the 8% LA diets while feed efficiency, adiposity index and endocannabinoid levels were about halfway between those of the 1% and 8% LA diets. In other words, reducing AA and the omega-3 index with n-3 HUFA but only partially reduced the obesigenic effects of high LA intake.

    Inexplicably the study concludes ". Reducing AA PL by adding 1% energy long chain fatty acids to 8% energy LA diets resulted in metabolic patterns resembling 1% LA diets" which is obviously inconsistent with the results,

    The "omega-3 index", which is the percentage of total fatty acids that is n-3 HUFA has long been thought of as a magic number which is indicative of heart health. It appears that the obesigenic effects of excessive dietary LA correlate closely with the total n-6 content of total fatty acids (LA and AA) and are not correlated with the omega-3 index or with the n-6 AA tissue content as a percent of HUFA. It is apparent that the adverse effects of excessive LA intake can not be fully corrected simply by taking n-3 HUFA supplements to reduce the omega-3 index. Reducing n-6 LA intake is essential to resolving the problems..caused by excessive dietary LA. Of course, getting enough n-3 HUFA is also important

    While the study began with a faulty premise and ended with a faulty conclusion, the large amount of data provided does includes information that is helpful, but it takes some digging to find it..

    A second study by the same folks reveals a confounding factor in the first study.

    In September of 2013, almost a year after the aforementioned study was published, the same group of folks came out with a second study entitled "Dietary Linoleic Acid Elevates the Endocannabinoids 2-AG and Anandamide and Promotes Weight Gain in Mice Fed a Low Fat Diet". I can not provide a link to the study because the study has disappeared from Pubmed and from the entire internet! (I made a copy of the full study so I can prove I am not imaging things). The second study noted that in the first study, rodents on the low and high LA diets were fed the low and high LA diets from the start of gestation which apparently confounded the study results.due to the effect of the ecosenoid prostacyclin on the number and size of adipocytes.

    Excessive LA intake during gestation and nursing can cause obesity in infants by elevation of the eicosenoid prostacyclin. Both in rodents and humans, long-chain fatty acids act at the preadipocyte stage and trigger the formation of adipocytes. Fatty acids as well as eicosanoïds arising in from the metabolism of linoleic acid (LA) play a role as precursor of the eicosenoid prostacyclin, and the adipogenic effect of prostacyclin takes place only at the preadipocyte stage. Pups from mice fed a diet high in LA are 40% heavier one week after weaning than those from mothers fed a standard diet The LA-induced enhancement of fat mass is abolished in mice bred to have no prostacyclin receptors demonstrating the critical role of the prostacyclin receptor in excessive adipose tissue development. The effect of LA diet is confined to the gestation/lactation period. Importantly, the weight difference between mice fed LA and LA/LNA diet is maintained at the adult age. In other words, PUFAs of the n-6 and n-3 series are NOT equipotent in promoting adipose tissue development. Adipocytes once formed exhibit little or no turnover in the body. Therefore the high increase in LA with slight or no change in LNA observed in breast milk and formula milk over the decades may be responsible, at least in part, of the dramatic increase in the prevalence of childhood overweight and obesity.

    In short, a high LA diet during digestion and nursing results in hyperplasia and hyperphasia, or more and bigger adipocytes, which causes excessive weight which can carry through to adulthood. Exactly how this effected the results in not clear..

    The second study included a low fat and a medium fat diet but no high fat diet and no use of n-3 HUFA in any diet. The second study differed from the first study in two respects: first, all the mice were fed a standard research diet containing 7% LA during gestation and nursing through the rist six weeks of life: second, mice on the Low LA diet the mice were fed 1% LA and 0.3% ALA which increased the n-6 to n-3 ratio to 3.3 to 1 compared to 1 to one in the first study. .

    In the second study, when on the medium fat diet, the mice on the 1% LA and 8% LA diets ate the same amount of food and gained the same amount of weight so there was no difference in food efficiency, food intake, weight or adiposity index. Mice on the 8% LA diet did have substantially higher (about 50%) endocannabinoid levels than mice on the 1% LA diet, but no indication of hypothyroidism based on food efficiency.

    Mice on the low fat diet had a 44% increase in energy efficiency when LA was increased from 1% to 8% indicating decreased energy expenditure which indicates hypothyroidism.

    The authors speculated that the lack of any apparent effect of increased LA on metabolism in the medium fat diet may have been due to the fact that both groups of rodents had been fed a high (7%) LA diet from the beginning of gestation.

    Increased LA intake elevates endocannabinoids and causes non-alchoholic fatty liver (NAFLD) :

    The increased lipogenesis caused by excessive intake of LA causes fatty liver.. Increased lipogenesis results in increased TG and cholesterol as well as increased belly fat. The primary lipid product of lipogenesis is palmitic acid which is not a particularly beneficial saturated fat. Excessive intake of fructose can cause fatty liver by impairing the enzymes that degrade endocannabinoids.

    While the average LA intake in the US is on the order of 7 to 8% of calories, many people consume a lot more and are more at risk for fatty liver and hypothyroidism.In my opinion, the increasing prevalence of NAFLD is evidence of the hypothyroidism induced by excessive LA intake.

    There are dozens of studies regarding treatment of fatty liver with supplemental omega-3 HUFA. Decreasing LA intake would be a logical first step to treating fatty liver.

    • Christopher Rasmussen MD, MS (aka "Reality Renegade") says:

      Hi Jack,
      People make note of this! Jack has provided another powerful reason why we need to steer clear of these FA’s. Of course most Industrial Dinners are laced with them.

      Also if you still drink tap water look into getting a RO filter that traps fluoride. Subclinical hypothyroidism, I think, is at epidemic levels in the US. To wit Synthroid is one of the most prescribed medications in the US. Fluoride inhibits thyroid function among other things. I should get a posting out on this one of these days. I have one or two more on statins yet to go.

  7. I do trust all of the concepts you’ve presented to your post.
    They’re really convincing and can definitely work. Still,
    the posts are too short for starters. May just you please prolong
    them a little from next time? Thank you for the post.

    • Christopher Rasmussen MD, MS (aka "Reality Renegade") says:

      I do indeed wish that I could but sadly I think you are the exception. I would prefer to post 6 or 7 pages but those in the know inform me that if you make them too long, say over 4-5 pages, nobody reads them. I will be adding in some blogs for another site and they tell me no more than 3 pages! Soon I suppose it will have to be me doing videos. I hope not. I appreciate the fact that you must love to read as I do.

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