My problem with Volek's study is that it's analogous to putting someone on a LC diet and then doing a GTT.

They kept people on a low-fat high-carb diet and put others on a high-fat, low-carb diet and then did a lipid tolerance test.

In both cases, your response to the nutrient (carbs in GTT and fat in lipid test) will be impaired because you stop producing enzymes you don't need.

The people on the low-fat diet didn't tolerate fat as well as people who had been on a high-fat diet when suddenly challenged with a tremendous amount of fat.

What I'd want to know would be the lipid responses *during* the 6 weeks on the two diets.

What his results show me is that eating a high-fat diet makes your body adapt to burning fats. This is what I would expect.

While these results are interesting, I wonder how relevant they are in a real life setting. The fat load that generated these results was 123 grams, which would be like eating 1.3 sticks of butter in a single meal, or like sitting down and drinking nearly 3 cups of heavy whipping cream all at once. Who does that?

Dr. Davis, I know you are encouraging 3 hour postprandial TG checks in the TYP program via CardioChek. Are you seeing these types of postprandial results (viz. results similar to Volek's) following meals with less exaggerated (i.e. normal) fat intake?

Here is prospective study done in Sweden with a follow up period of 12 years that shows a higher consumption of dairy fat like butter and cream is associated with a 45% reduction in risk for heart disease. "Nothing in biology must make sense except in the light of evolution"
http://www.mdpi.com/1660-4601/6/10/2626/pdf

After eating low-carb for over a year, my post-prandial triglycerides never go above 100.

I do agree with Gretchen on the adaptation process.  I shudder to think what an OGTT test would show.  Maybe some day, I'll drop $70 to find out if I can get someone to take me.  I'll be in no shape to drive after consuming that much sugar.

I agree Gretchen. There can be a long adaptation period. Dr. Davis's patients are blessed to have him as their doctor, but I suspect he can't quite kick the lipid hypothesis!

At least for me, I think Dr Ron Rosedale's diet is best.  Low carb, protein at 50 to 70 gms. No grain, mostly no dairy.  He says if you want to lose weight you need to avoid saturated fat because saturated fat keeps you insulin and leptin resistant.   Unless you drink olive oil, the diet winds up being low calorie.
Hmmmm.  Maybe that is the answer.

I have to wonder what the mechanism is for high triglycerides causing heart disease? High triglycerides in a high carb diet usually means high insulin, high glucose vs fat metabolism,and low hdl. Aren't high triglycerides in a low carb diet a slightly different picture?

Right or wrong, I admire your willingness to go against the tide (any tide) for what you see as right.

Absolutely!  What amazes me is, in spite of their adaptation to a high fat low carb metabolism, the patients still saw their OGTT triglyceride results improve over time!  This is my experience too.

There is no doubts, on a high animal fat diet or on a high fat diet of any kind, our tolerance to glucose is indeed reduced.  50g in one does is OK for me (I weigh ~65kg) but 100g in one go as sugar would still be too much and would make me feel sick (but the same amount of carbs in vegetables spread over a day would be ok).

It took a good few years to improve my tolerance.  Right after (2 weeks after) I went on a high animal fat LC nutrition (in 1999) I could not tolerate even a 50g of sugar in one shot! Even one bottle of beer (~20g of carbs) would make me feel stomach sick + give me a headache.   It took me more than 2 years to reach this tolerance to carbs, and I even noticed some steady improvement from year 2 to year 7 into this.

It is indeed totally illogical, although unsurprising given the present standards of medical science, to use big glucose shots to assert patients response under  predominantly ketogenic metabolism.

It is a curious lack of curiosity on behalf of the mainstream medicine that no nutrition research group seem interested in studying the exact effects (all beneficial for me), vitamin and nutrient requirements (very different!) and adaptation issues on the high fat low carb diets.

Stan

The last few posts have generated quite a few comments!!!


Anonymous said...
"The last sentence made me cry."


Alfred E. said...
"This is becoming more confusing by the minute. First, no carbs, only fats and protein. Now, no butter, no dairy, no, carbs, just a few drops of fat and protein. I am going to cry, like the previous poster."


Dana Law said...
"I've learned a lot but need some direct guidance. I find that making daily decisions on what to eat difficult. I want to eat healthy and have some variety. Here's the question. What do you eat? What did you have for breakfast this morning? What did you eat last night? What do you keep in the fridge and on the counter to make following your dictates easier. I don't want to over-think it but all this information is overwhelming."


Helen said...
"Again, with so many cautions of what not to eat, I'd love to see a Dr. Davis-approved diet plan. If I were just following all the Don'ts, I'd go crazy (and hungry)."


The bottom line is that Jimmy Moore, William Davis, Matt Stone, Kurt Harris, Stephan Guyenet, Don Matesz, Art Ayers, Billy E., B.G., T., Mark Sisson, Richard Nikoley, Michael Eades, Matt Metzger, Peter, Arthur De Vany, Chris, Ryan Koch, Chris Masterjohn, Jenny Ruhl, Richard Bernstein, Fred Hahn, Jonny Bowden, Larry McCleary, Mary Vernon, Dave Dixon, Mike O'Donnell, Scott Kustes, Gary Taubes, Rob Wolf, Seth Roberts, Loren Cordain, Sally Fallon, Mary Egin, Keith Thomas, Tom Naughton, PaleoDoc, Nora Gedgaudes, Barry Groves, John Briffa, Laura Dobson, Dana Carpender, Keith Norris, Rusty Moore, Doug McGuff, Martin Berkhan, Bryce Lane, Erwen Le Corre, Dan, Drew Baye, Uffe Ravnskov, Eric Westman, Lierre Keith, Brian Peskin, Steve Parker, Jeff Volek, Stephen Phinney, Diana Schwarzbien, Barry Sears, Nina Planck, Lyle McDonald, T.S. Wiley, James Carlson, Steven Gundry, Keith Berkowitz, Richard Feinmann, Jan Kwasniewski, Konstantin Monastyrsky, etc., etc., etc. cannot come to a cohesive way of eating that is workable for everyone. My guess is there are not two of these people whose diet is identical!!

Is it any wonder we are confused? Many folks are looking to emulate the diets of others - a method that will never provide personal optimal health.

Take the time to watch/listen to the following lecture by Dr. Bruce German from UC Davis. It will help to explain why we have this conundrum.

http://www.researchchannel.org/prog/displayevent.aspx?rID=29854&fID=567

Then read the writings of a Venetian gentleman who lived to be almost 100 yars of age (Born 1467 - Died 1566).

http://www.soilandhealth.org/02/0201hyglibcat/020105cornaro.html


Both of these together put nutrition and health in perspective for me.

Tom

Dr. Davis, please comment on the study released today by the Harvard medical School.  How does one avoid saturated fats and still get proteins if he is a low carber??   http://news.bbc.co.uk/2/hi/health/8580899.stm  Thanks!

Hi, David--

Studies are meant to make observations. That is the reason for the unnatural intake of fats.

People on the Track Your Plaque Diet approach rarely show such high levels because they've reduced or eliminated the foods that form the basis for high postprandial responses (wheat, cornstarch, and sugars) and do not indulge in high fat intakes that cause near-term surges of postprandial particles.

Hi, Gretchen--

I agree, but I believe that the observations are still relevant. It shows us that postprandial responses are sensitive to carbohydrate intake over time. It also shows us that average people have substantial surges postprandially with fat challenges on an average American diet.

While I advocate carbodrate restriction and weighing diet more heavily in fats and oils, you can see that the emerging conversation is that unlimited quantities of oils, low-carb or no, have the potential to generate extravagant postprandial responses.

I tested my postprandial triglycerides after having been on a LC diet for about 11 years and wheat-free even longer (because I discovered that it was wheat that was giving me acid reflux). With about 50 g of fat, the TGs went very high, over 400.

Someone else said his rarely went over 100 after only a year on a LC diet.

The author of "Life Without Bread" presented a graph showing that younger people reduced cholesterol on a LC diet but older people didn't.

We may all react slightly differently to different diets (as well as interpreting them differently, as someone else has pointed out; you can be on a LC diet that includes mostly LC junk food or a LC diet that includes a lot of greens and lean meat).

I have type 2 diabetes, and some people think that metabolic syndrome/type 2 diabetes is basically a disease of disturbed lipid metabolism.

So what worries me is that people with insulin resistance, who may not respond the same way as people without IR, are taking LC advice to eat a lot of fat that is based on the experiences of people without IR.

Here's an article that addresses this issue:

http://www.lipidworld.com/content/4/1/21

This is why some time ago I felt the "GO Diet" by Jack Goldberg and Karen O'Mara, which is LC but emphasizes monounsaturated fat, yogurt, and fiber, was the best solution and helped them rewrite it as "The Four Corners Diet."

Apparently very few people agreed with me, and the book bombed.

I still think LC with restrained fat intake, meaning restrained calorie intake, and real foods along with reasonable exercise is the best solution on the basis of today's evidence.

@Tom (anonymous)

Although there are many voices and styles of presentation, I can state, through frequent communication with them, that my approach at PaNu is a tent that fully covers the diets of Eades, Dr. Stephan, Peter at Hyperlipid, Sisson, Nikoley, and although I do not correspond with them, Bernstein and Groves. There is also significant overlap with the Weston A Price Foundation and even Matt Stone.

If you look for a common element in all of our approaches, and indeed the crux move in choosing a healthy alternative to the SAD, it is actually nothing to do with paleo so much as the simple and total rejection of Ancel Keys and the multiple versions of the lipid hypothesis he spawned 50 years ago.

This then allows the realization that humans are evolved to eat substantial calories from animal products, including animal fats, and further including (on purpose, and without limitation or fear) SATURATED FAT.

All versions of the lpid hypothesis have in common the belief that somehow, somewhere, there is a molecule that is fat, tastes like fat, is  kind of like fat, is associated with fat, or reminds us of fat, and that molecule is perversely designed to give us atherosclerosis and coronary heart disease.

Start to view all these dietary approaches through the filter of whether they reject the lipid hypothesis instead of "low carb" or "paleo" and the dividing line will start to look much much brighter.

So for someone that works out a lot and is suppost to gte something in the 3000-4000 calories per day... what would be the addecuate kind of food to use as high calories source?
I was taking unlimited almonds, but this post makes that look like way too much fats.

@ Dr. Harris,

You obviously did not read/listen to the two links that I provided in my comment.  I happen to believe every word you wrote in your response.   My contention is that personal optimal health and longevity is beyond the simplicity of following 12 simple steps (though I do think they are a huge step in the right direction).  Health is determined at the molecular level based upon an individuals genetics as affected by many factors, particularly, stress. Please Google nutrigenomics, epigenetics and metabolomics.

My apologies to Dr. Davis.

(I may have inadvertantly sent a another version of this comment previously.)

Tom

Isn't this just normal for a well adjusted human? I mean TGs are how fuel (free fatty acids) is transported through the blood from its sources (liver and fat cells) to the places where it is needed i.e. everywhere else.

@ Pythonic Avocado

Yup, eating fat raises TG levels temporarily.  I consume a high-fat diet with lots of nuts, and, based on results from a TG meter, do not see extraordinarily high TG levels (starting from a fasting level near 70).  I also spread meals out during the day, thereby reducing both BG and TG spikes.

The only time I saw a high TG spike was after consuming 2 raw egg yolks!  This influenced how I approach eggs (always cooked, one at a time, mixed with other foods).

btw, if you consume too much fat in one meal, a lot of the fat will end up in your stools, since there is a limit to the lipase that your pancreas can generate on short notice.  Another complication when trying to compare diets.

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

Here is the list of over 20 publications about iodine consumption, trials, findings etc. the normal intake may be between 6 to 12.5 mg. it depends on the individual. when i started taking iodine, i took 50 mg a day for a week before i felt any uneasiness. now one drop of lugol's iodine every second day and i can feel it. according to these studies some vitamins along with iodine play major role in coping with iodine.  
http://www.optimox.com/pics/Iodine/opt_Research_I.shtml

What's your opinion of potassium salt?  I've been using an iodized mixture of sodium and potassium chloride lately, and it seems to be working well.

I use sea salt that contains iodine naturally.  I also eat a little seaweed a couple of times a week.  Is this sufficient?  Who knows, I guess.  I definitely do not have any trace of a goiter.  I eat fish, too, and live on the East Coast, so I assume I'm okay.

The full text of the article "Iodine: deficiency and therapeutic considerations" (Altern Med Rev 13 (2): 116–27. PMID 18590348) published last year can be found here.

From that article: "The safety of therapeutic doses of iodine above the established safe upper limit of 1 mg is evident in the lack of toxicity in the Japanese population that consumes 25 times the median intake of iodine consumption in the United States. Japan’s population suffers no demonstrable increased incidence of autoimmune thyroiditis or hypothyroidism."

StephenB

This is the second time in a week the volatility of iodine has come to my attention.  I'm wondering now about the iodine content in the dried kelp and sea vegetable I have in my cupboards.  Anyone have any idea how stable that iodine is?

What do you reckon about "Celtic" salt (unprocessed sea salt)? I know there's a lot of websites out there granting it near-magical health properties, about which I am extremely skeptical, however it does have a notable amount of minerals in it (about 8% I believe) whereas regular salt is refined to 99.99% purity. So it seems if you switched to using that kind of salt in your diet (including avoiding processed food which uses pure salt) it may have some benefit. It does contain iodine naturally, too.

I'm taking Lugol's solution too, about 10 drops a day. My iodine was measured at "<1" by the lab four months ago.

Australian readers should note that Australian soil has an extremely low iodine content (it's official), so our food is unlikely to be a source of pretty much any iodine at all. A case where being a "localvore" won't help your health.

I take Iosol iodine, which I get from iherb.com for $12 a bottle (http://bit.ly/6qLtp). Each drop has 1,830 mcg of iodine, and there are over 600 drops per bottle. Great price, and seems to be working well for me. My feet aren't nearly as cold as they used to be, and my usually low morning temperature has started increasing a bit, too.

My sense is that goiter is the least of the problems with iodine deficiency.  Kris has pointed to the optimox link.  Optimox manufactures Iodoral which is iodine in convenient tablet form.  The liquid form, Lugol's Solution is available here: http://www.jcrows.com/iodine.html

My sister began taking iodine supplements last year at my suggestion.  She had experienced 5 years of bad mammograms so she was delighted to have a flawless mammogram three months after starting iodine.  It seems that iodine is so important to the baby that breasts concentrate iodine as well as thyroid glands.  Fibrocystic breast disease seems to be the equivalent of goiter in breast tissue.

She also reports better sleep, fresh moist skin, quicker reactions, more energy and most recently, iodine applied to poison ivy stopped the itch.  

Dr Flechas reports here, http://iodine4health.com/disease/diabetes/flechas_diabetes.htm, that half of his diabetic patients are no longer diabetic when they get enough iodine.  The other half improve, needing less medication.  It seems to me that iodine should be the first step in treating diabetes of either form.

Iodine deficiency is reported to be the number one preventable cause of mental retardation in the world.  Looking around, goiter is not the most visible evidence of iodine deficiency.

Having read the papers at Optimox and others, iodine looks to be under appreciated and quite valuable.

I cut out all salt from my 'nutritarian'-style diet a few weeks ago.  But as a result of reading this blog, I started taking 4 kelp tablets a day at about the same time. I'm thinking of taking even more tablets to try to help increase my low (according to the endocrinologists and this blog, not my doctor) thyroid numbers.

I rarely use salt except when I make popcorn.  I do occasionally take an Iodoral and sometimes add a drop of aquarium Lugols iodine in my 7 gallon water jugs of thermal spring water.

When I run in 90°+ weather I do take salt.  So far, at age 70, no goiter.

You might want to let Michael Bloomberg know that cutting back on salt will increase iodine deficiency.  His health commissioner, Thomas Frieden, was picked to head the CDC.

Remember to reduce bromine exposure which competes with iodine.

Thanks for conducting the poll - very interesting.
We use kosher and sea salt at home - about a year ago, this late realization (regarding iodine) led me to a bit of a panic, as my pregnant wife was nearing full term...  I was especially worried because I had been all along encouraging heavy broccoli consumption as well, and brassica vegetables are known to have goitrogenic properties (as do many other types of plants).  I then learned she was taking a multi-supplement that contained a fair amount of iodine. Whew.  Our 10 month old is doing great now, fortunately.   
We consume a fair amount of garlic and seafood as well, though I don't really know what the variance is when it comes to garlic's iodine content - presumably it depends quite a bit on the soil and water supply (Apparently, California garlic and broccoli assimilate a fair amount of selenium from the water used for irrigation, for instance).

k1wuk,

I'd love ot know if you have any more info on iodine and breast health.

I checked the Lo-Salt I've been using since I decided I might not be getting enough potassium (a good guess as electrolytes came back spot on) and realise it is NOT iodised.

Not a problem personally I suspect as I eat plenty of fish and shellfish but I'm now trialling various seaweeds, sea vegetables etc. Even without a deficiency these are tasty!

Goiter is not common in the UK AFAIK, nowhere near as common as hypothyroid. However when young my father was hyperthyroid, which damaged his heart before being treated. Didn't stop the tough old goat from living into his eighties, but in retrospect I believe he may well have become hypothyroid in later life as a result of the operation (not diagnosed), and probably also became Type 2 (not diagnosed)in his last years.

Probably wouldn't have lengthened his life but diagnosis and treatment would certainly have improved the quality a lot. All power to you for continuing your posts on these issues. They will suffice until Endocrine System SP1 is released.

Anna

Here are few links to dr. david derry's answer to patients(in case you haven't found it your self). My wife had painted lugol's iodine externally for breast lumps, with unbelievable results only after applying it twice. she was having hard time sleeping on one side. her mother passed away few years ago with Breast cancer. just being extra careful now.
http://thyroid.about.com/library/derry/bl1a.htm

http://thyroid.about.com/library/derry/bl2a.htm

My endo told me to avoid iodine because it exacerbates goiter in hypothyroid.  Also, those of you who know nursing mothers, PLEASE be aware of this risk:

from pubmed:
1: Hypothyroidism in a breast-fed preterm infant resulting from maternal topical iodine exposure.
Smith VC, Svoren BM, Wolfsdorf JI.
Pediatr. 2006 Oct;149(4):566-7.
PMID: 17011335 [PubMed - indexed for MEDLINE]

2: Transient hypothyroidism in a breastfed infant after maternal use of iodoform gauze.
L'Italien A, Starceski PJ, Dixit NM.
J Pediatr Endocrinol Metab. 2004 Apr;17(4):665-7.
PMID: 15198299 [PubMed - indexed for MEDLINE]

3: Early childhood caries: an overview with reference to our experience in California.
DenBesten P, Berkowitz R.
J Calif Dent Assoc. 2003 Feb;31(2):139-43. Review.
PMID: 12636318 [PubMed - indexed for MEDLINE]

4: Transient neonatal hypothyroidism during breastfeeding after post-natal maternal topical iodine treatment.
Casteels K, Pünt S, Brämswig J.
Eur J Pediatr. 2000 Sep;159(9):716-7. No abstract available.
PMID: 11014479 [PubMed - indexed for MEDLINE]

5: [Iodine antiseptics are not harmless]
Arena Ansotegui J, Emparanza Knörr JI.
An Esp Pediatr. 2000 Jul;53(1):25-9. Review. Spanish.
PMID: 10998400 [PubMed - indexed for MEDLINE]

6: The newborn should be protected from dangerous transient induced hypothyroidism.
López-Sastre JB, Rivas-Crespo MF.
Acta Paediatr. 1995 Oct;84(10):1211. No abstract available.
PMID: 8563243 [PubMed - indexed for MEDLINE]

7: [Thyroid function disturbances in an infant following maternal topical use of polydine]
Rakover Y, Adar H.
Harefuah. 1989 May 10; 116(10):527-9. Hebrew.
PMID: 2792927 [PubMed - indexed for MEDLINE]

8: Topical iodine, breastfeeding, and neonatal hypothyroidism.
Delange F, Chanoine JP, Abrassart C, Bourdoux P.
Arch Dis Child. 1988 Jan;63(1):106-7. No abstract available.
PMID: 3348642 [PubMed - indexed for MEDLINE]

Leslie.
here is another study from the same site search. i just copied the whole paragraph.

1: Public Health Nutr. 2007 Dec;10(12A):1600-1.Click here to read Links
    Iodine nutrition of pregnant and lactating women in Hong Kong, where intake is of borderline sufficiency.
    Kung AW.

    Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong SAR, China.

    OBJECTIVE: To describe the iodine nutrition of pregnant and lactating women in Hong Kong, where intake is of borderline sufficiency.DESIGN: Review of cross-sectional and prospective studies.SETTING: China, Hong Kong Special Administrative Region (SAR).SUBJECTS: Pregnant and lactating women.RESULTS: Studies of pregnant women in Hong Kong SAR have revealed an increase in the urinary iodine (UI) concentration as pregnancy advances. A significant percentage of women had a sub-normal serum thyroid hormone concentration at full term. Although iodine is concentrated by the mammary gland, 19% of all mothers had low iodine concentrations in their breast milk. The moderate correlation between the concentrations of iodine in breast milk and urine suggests that an adequate maternal urinary iodine concentration cannot reliably indicate that an infant is getting enough iodine in breast milk. Therefore, some breast-fed infants may still be at risk of low iodine intake, and additional iodine supplements, other than salt iodisation, would be warranted in this population.CONCLUSIONS: The currently recommended intake of iodine through universal salt iodisation may not be adequate for pregnant and lactating women, and supplementation during pregnancy and lactation should be further considered in light of the latest recommendations.

here is another one.

1: J Am Coll Nutr. 2004 Apr;23(2):97-101.Click here to read Links
    Maternal thiocyanate and thyroid status during breast-feeding.
    Dorea JG.

    Faculdade de Ciências da Saúde, Universidade de Brasília, Brasília, Brazil.

    Cyanogenic glucosides are naturally present in plant foods especially in staple foods (cassava) consumed by millions of people in tropical countries. Most traditional processing methods are effective in detoxifying such goitrogens to safe levels of consumption. Nevertheless, residual cyanide (CN) is rapidly metabolized to thiocyanate (SCN) by existing metabolic pathways. There are concerns that goitrogens may reach the nursing infants through breast feeding or cow's milk based formulas. SCN adverse effects are commonly observed in relation to cigarette smoking. Breast-feeding is effective in protecting infants from anti-thyroid effects of eventual or habitual maternal exposure to CN exposure in food (cassava) or recreation habits (cigarette smoking). SCN goitrogenic effects occur secondary to iodine deficiency in special circumstances of high consumption of incomplete detoxified cassava and insufficient protein intake. Only during inadequate protein nutrition can SCN aggravate endemic iodine-deficient disorders (IDD).

More and more one reads about these, more and more it becomes a muddy and confusing subject.
despite the fact that we have all sorts of studies and experts to educate people, all it takes is few drug profit driven experts studies to confuse the less money spending route.
Please read this
"The Wolff-Chaikoff Effect"
"crying wolf".
http://www.optimox.com/pics/Iodine/IOD-04/IOD_04.html
Please don't take me wrong. i am not trying to contradict the studies that you have posted here. i am merely trying to show as to what else is available out there.

The Safe and Effective Implementation of Orthoiodosupplementation In Medical Practice

This section had me laughing out loud. Much the same applies to the use of effective amounts of D3.
Medicoiodophobes suffer from: A) a split personality which results in iodophobia within the orthoiodosupplementation range previously used safely and successfully in medical practice and iodophylia for megadoses of iodide (up to 12 gm/day); B) double standards, which render those physicians intolerant to the minor side effects of the inorganic forms and extremely tolerant to the severe side effects of the radioactive and organic forms; C) amnesia pertaining to the inorganic, non-radioactive forms when making therapeutic decisions; D) confusion, attributing the severe side effects of organic iodine-containing drugs to inorganic iodine/iodide; and E) an altered state of consciousness, allowing doublethink, doublespeak, and contradictory logic to become acceptable. Although the factors involved in medical iodophobia are still unknown, decreased cognition seems involved. Since low iodine intake is associated with intellectual impairment, deficiency of this essential element cannot be ruled out, and if present, would create a self-perpetuating phenomenon. Needless to say, medical iodophobia is contagious and can be transmitted to patients and other physicians (iatrogenic iodophobia). Medical iodophobia will remain a syndrome until the causes are discovered and effective therapy implemented. It is very likely however, that medical iodophobia will eventually be classified as an iodine-deficiency disease.

My endo told me not to take iodine because he said living in the UK, it being an island, people here get enough iodine from their diets.

He also said that because I eat a lot of fish (once or twice per day) that gives me additional iodine.

He said some of his German patients take iodine against his wishes (must be a popular supplement among Germans), and if they are pregnant it's really bad for the fetus.

Anne

Fish.
according to Dr. david derry,"Fish of the great lakes still shows Goiter formation".
http://books.google.ca/books?id=PVWOyP68OMsC&pg=PP1&dq=dr+david+derry&client=firefox-a#PPA6,M1
So even fish's origin is important. apart from fluoride in the tooth paste and fluoride added municipal water which depletes us from iodine. never mind chlorine in the water and bromine in the food and many other goods around us, helps to deplete iodine.

I wonder about the huge amount of food that is imported into the UK from distant locations One can't assume enough iodine universally throughout the UK based on UK soil content.

Kris - you should eat sea fish and shell fish.

Anne,
Thank you for your advise.
now i am eating sea fish twice a week. but iodine is must for me. my mother's right side elbow and knee was in bad shape for 35 years. The knee joint was so bad that the joint would come off of it's position. we had to learn our to self to place it back. as usual, she went to many doctors but no help. she is vegetarian all her life. about six months ago she started applying lugol's iodine externally on the knee. she was applying religiously 3 times a day for 2 weeks on and one week off. at the end of the two weeks application, the knee would look like war zone. after about month and half, the knee starting to look like normal knee. now she is able to walk about mile and a half every day on the tread mill. she also been taking 3 drops a day internally too. i personally believe in more iodine than we can find in our the food.

Anna:
"Breast Cancer and Iodine" by Dr David M. Derry, Canada

What am I missing here? Has it not been proven that Statin + Niacin combo is like 90% affective in stopping plaque progression in its tracks? Why does that not say that LDL reduction AND particle size reduction,(Niacin for LP(a),works best? Its not just LDL, I developed heart disease with a 90-100 LDL before my Dr discovered  high LP (a). Treated with 10mg statin,1500 Niacin, diet,I am at a30/30 count. OVER&OUT

Let's just summarise. First there was Keys with his total cholesterol. This turned out to be garbage. Then there was LDL vs HDL. But LDL is calculated and, as we know from this site, tells us nothing about anything. Then we have LDL particle size. Small dense is bad, big fluffy is good, noting that big fluffy contains lots of cholesterol per particle and can increase your calculated, or even absolute, LDL. Two factors, most studies use calculated LDL. The bin is there, file promptly.

The second is that something controls your LDL particle size. How, on a practical basis, does Dr Davis control LDL size and density? No wheat and no sugar. Does wheat and sugar elimination alter anything in the body? Wheat contains both an insulin mimetic and two insulin potentiators, plus starches and sugars both increase blood insulin levels per se. Perhaps there is a message here. It's been known for decades that insulin drives the proliferation of the arterial media we call arteriosclerosis.

If insulin also controls LDL particle size (I have no information on this, but I'm willing to bet it does) then Yudkin and Stout are correct, Keys is wrong and the cholesterol hypothesis, what remains of it, describes the effects of insulin on blood lipids. While insulin and glucose do the damage to the arteries.

Just a cholesterol skeptic view.

Peter

Statins are anti-inflammatory, antioxidant, anti-proliferative and probably anti other things too. Unfortunately they drop cholesterol levels (in humans anyway). Zetia, like torcetrapib and clofibrate, does the cholesterol dropping thing without the anti everything else that statins bring along. No wonder they killed so many people in the clinical trials. Clofibrate. Torcetrapib.

If a drug company develops a drug which converts small dense LDL to light fluffy LDL without affecting insulin sensitivity or glucose, I predict it will go the way of clofibrate and torcetrapib. There's the bin.

I especially find it interesting that, among the so-called pleiotropic, or non-lipid, effects of statin drugs is a modest rise in 25-OH-vitamin D3 levels.

I think this just once again shows that statins DO reduce heart disease but NOT because of the reduction in LDL. I'm always amazed at the Dr. who say you don't need to be on a statin your LDL is fine. Statins have been proven to reduce death rates in cardiovascular disease by 30 to 40% and yes with niacin by 90%!!!!!!!! Anybody worried about heart disease should be taking them. And save me the "side effects" alarm of statins that is so over blown. The fact is we invented a drug to reduce LDL, it does that but thats not why it reduces heart attacks and we're still not sure why they do. We accidently created a great class of drugs.

I remember in Taubes reading that small LDL are the result of particles being formed in a high-triglyceride environment--if so there is a more direct link to diet than through insulin.

About the merits of statins, can't we at least say that through reducing the number of all LDL particles and hence the number of small particles arteries are protected?

Keith

The drug company slanted this study so that they'd get a wonderful result, that they didn't and the lengths that they went to hide or misrepresent the data that came out of the study has to make you suspicious of what ELSE they have learned.

Did you catch that they also suppressed other study results showing liver damage from Zetia?

Also, did you catch the BMJ story today about the calcium supplementation trial that lowered LDL raised HDL and increased cardiac and stroke events in older women?

While that too isn't a death blow to the LDL hypothesis, it certainly doesn't bolster it.

Peter,

Good post; you have an impressive grasp of the literature on this!  I have a question for you, though:  Besides the epidemiology (which I know you don't buy), aren't there still tons of animal studies linking atherosclerosis to dietary saturated fat?  In fact, to promote atherogenesis in lab animals so they can study it, don't they feed them a diet rich in palmitic, stearic, myristic and lauric acids from animal and tropical plant fats, which works predictably?

Drug companies are actually scrutinized fairly closely, though plenty of shenanigans still go on.

What scares me even more is what may have been going on BEFORE the intensified scrutiny began a few years ago.

Nowadays, the return on investment for treatment of chronic diseases like cholesterol, osteoporosis, and hypertension are so substantial that it is causing them to see a blur between right and wrong.

Yes. I believe that the evidence for that effect of statin drugs is quite confident.

When I question the Lipid Hypothesis, what I really mean is that I question the wisdom of the simple "high cholesterol means more atherosclerosis" philosophy, a belief that is clearly oversimplified, though it contains a germ of truth.

For anonymous,

Of course statins reduce cardiac mortality and obviously it's nothing to do with LDL cholesterol lowering. But before you pop one on the off chance (they are available OTC in the UK) go very carefully through this paper.

You need the full text, the abstract tells you nothing, so here's a summary:

There were 2913 patients in the placebo group. A total of 306 died during their 3 years of not taking a statin. That is 10.5% died. In the treatment group there were 2891 patients and 298 died, that's 10.3%. Bear in mind that these were high risk cardiovascular patients, the sort for whom statin therapy is supposed to be effective in saving lives.

There was undoubtedly a significant improvement in cardiac mortality WITHOUT improvement in overall mortality. To sum up the PROSPER trial, you can have the cause of death changed from heart attack to cancer, but not the date on the death certificate. You choose. Perhaps you're too young to be in the PROSPER trial, but live long enough and you won't be!

PS if you EVER see a statin trial without the overall mortality figures, just assume there was no benefit or worse. If there is even a miniscule benefit it will be broadcast far and wide.

Keith,

Thanks for the pointer. Obviously high triglycerides are a classic marker of hyperinsulinaemia and insulin resistance. I'll follow that one when I get that far in to Taubes' book. Seems it's looking good for Yudkin.

bad_crc,

Yes, there are thousands of papers like that. They usually use D12451 or something like it. High fat alright, 45% calories from lard. As the rest is? A bit of corn starch, a mass of maltodextrin and an even bigger mass of sucrose!!!!! But of course it's the lard that kills....

Whereas using a real high fat diet you get this paper. I would suggest the 60% of calories from fat us a little low for a rodent. Choosing for themselves they can go to around 80%, get plump but don't develop insulin resistance.

Peter

My understanding is that studies show that statins are effective in reducing heart attacks ONLY in people who have already HAD heart attacks. Not in the general population.

This would confirm the growing suspicion that statins work by limiting the inflammation associated with heart disease. Not through their effect on lipids.

To get back to Zetia/Vytorin, what Dr. Nissen pointed to, which IS in my mind worth noting, was that while the variation in individual endpoints did not rise to statistical significance every single endpoint measured went in the wrong direction. That argues against random effects in my mind.

Beyond that, we know that in most people heart disease develops over a longer period than that spanned by this study, which only lasted 2 years. If all these parameters measured were trending negatively at 2 years, what happens at 5? Or 10? This is one of those drugs that once they put on on it, you take them forever. So the 5 or 10 year result could be devastating if this turns out to be a significant finding.

My suggestion would be continue testing this drug in small studies involving people who are very well informed of the risks, but end the writing of the current 1 million prescriptions a month. That's a LOT of guinea pigs, and if there turned out to be an accelerating pace of problems with it, a lot of people could die unnecessarily.

Statins reduce the number of LDL particles, which is very poorly represented by the conventional (Friedwald)calculated LDL cholesterol.

More importantly, when someone with heterozygous hypercholesterolemia (as in this Vytorin study) has a high number of SMALL LDL particles, then statin drugs, in my view, do provide benefit. But a superior effect would be to specifically reduce the number of small LDL particles, best accomplished with such strategies as elimination of wheat, weight loss via low carbohydrate diet, fish oil, vitamin D, and niacin.

This raises the question of how well the two groups in this study were matched for the number of small LDL particles. To my knowledge, this was not measured.

Let me also remind everybody that the measure obtained and used for comparison was carotid IMT, not carotid plaque.

I'm certain I'm not alone in feeling bewildered that such a dominant theory of the disease could turn out to have been so wrong for so long at such great cost in lives and treasure.

Just as a question of historical interest, how far back in the history of science do we have to look to find this kind of reversal of understanding of what the facts are with such broad and great consequence?

Hi, WC--

I'm not sure, but it's not the first time.  

Is the earth still flat?

Hi Dr. D.

I was thinking of Galileo also and his remarkable discovery that the earth orbits the sun.

But then I thought "surely we don't have to go that far back do we to get to such a broad and consequential paradigm shift?"

Maybe we do.

Could zetia be interfering with the absorption  of simvastatin?

Hi wccaguy,

You may enjoy this discussion article from PLoS. The authors intend it to be provocative, put it does pose the question "on which day did medicine stop making mistakes?"

Peter

In response to Jenny, not all studies on reducing heart attack death havwe been done on people who already had a heart attack. The reduction of 30 to 40% is whether you've had one or not.

Our saturated fat question keeps coming up, but the current common wisdom is that saturated fats are "neutral" in the sense that they raise both LDL and HDL. But do we know what they do to the number of small particles? Of course, if LDL is raised by making particles fluffy then saturated fats are clearly protective.

Keith

Hi, Richard-
No, there was indeed a substantial further drop in LDL with Vytorin over simvastatin.

There is a very modest shift from small to large LDL.

Zetia dropped my very high, inherited LDL to normal, BUT I afer a couple months on Zetia my post-menopausal body stopped making estrogen--my gynecologist remarked on it.  

I also started having a problem with persistent visual afterimages which the ophthalmologist said might also be from having too little cholesterol.

Both problems went away when I stopped the Zetia. I have very high LDL but I also have the "longevity" cholesterol gene which makes for big fluffy LDL as well as very low Apo(b). My doctors--including the cardiologist I saw--are ignorant about the implications of both findings and just obsess about the high LDL.

Since naturally produced estrogen seems to be protective for heart disease, I wonder if some people with inherited high LDL are like me have the large fluffy LDL molecules which give a deceptively high LDL value on tests. For them lowering it with Zetia drops LDL TOO low, so that the body doesn't have the cholesterol it needs for important functions, like making the naturally produced female hormones that may be protective against heart disease.

Hi, Jenny-
Keep in mind that conventional LDL is a flagrantly inaccurate number. In my experience, LDL of 150 when accurately measured (we use the NMR LDL particle number as the "gold standard"), the true number is between 80 and 270 mg/dl.

In my view, conventional LDL is a silly number. It is also the basis of a $23 billion (annual revenue) industry.

In Dec 05 I had a heart scan score of 145.  I went from 10 mg of Lipitor to 80mg of Vytorin and 1000 Niacin, 1 fish oil.  At that time my particle number was 1325 and small particle # 977.  A year later it went to 1503/1277.

In Nov 07 my heart scan went to 291. I then went to 2000 mg of Niacin and 150 COQ10,4 fish oil, 500 mg C, Vitamin D.

My new liposcience profile taken Dec 27 07 shows small particle down to 249 and particle number down to 279.

I dont know why my plaque increased so much but the new lipo profile is impressive in reduction.

Is there anything here that seems weird or is it just the plaque grew fast and is likely now under control with the much improved scores?  All other factors on the profile were great and my Vitamin D is very good and CRP excellent too.  My homosistine was 15.7 is the only thing a bit high.

Thanks!!

Sorry, but I do not assess entire programs on this blog.

I would invite you to participate in the conversations in the Track Your Plaque Forum for detailed discussions like this. There is also a free report on "10 steps to take if your heart scan score increases" on the www.trackyourplaque.com website.

I would not automatically conclude that Zetia causes carotid plaque. This is absurd. And I am definitely not one to come to the rescue of a drug or drug manufacturer. I am simply after understanding and truth.

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