Overweight, hungry, diabetic, and fat-free

15. December 2009 William Davis (52)
Let me tell you about my low-fat experience from 20 years ago.

At the time, I was living in Cleveland, Ohio, and served on the faculty at a large metropolitan university-affiliated hospital, supervising fellows-in-training and developing high-tech cath lab procedures like directional athererectomy and excimer laser coronary angioplasty. (Yes, another life.)

I was concerned about personal heart disease risk, though I knew next to nothing about lipids and coronary risk prediction outside of the little I learned in training and what the drug industry promoted.

I heard Dr. Dean Ornish talk while attending the American College of Cardiology meetings in Atlanta. Dr. Ornish spoke persuasively about the dangers of fat in the diet and how he "reversed" coronary disease using a low-fat, no added oils, no meat, vegetarian diet that included plenty of whole grains. So I thought I'd give it a try.

I eliminated all oils; I removed all meat, eggs, and fish from my diet. I shunned all nuts. I ate only low-fat products like low-fat yogurt and cottage cheese; and focused on vegetables, fruit, and whole grains. Beans and brown or wild rice were a frequent staple. I loved oatmeal cookies--low-fat, of course!

After one year of this low-fat program, I had gained a total of 31 lbs, going from 155 lbs to 186 lbs. I reassessed some basic labs:

HDL 28 mg/dl
Triglycerides 336 mg/dl
Blood sugar 151 mg/dl (fasting)


I became a diabetic. All through this time, I was also jogging. I ran on the beautiful paths along the Chagrin River in suburban Cleveland for miles north and south. I ran 5 miles per day most days of the week.

It was diabetes that hit me alongside the head: I was eating low-fat meticulously, exercising more than 90% of the population, yet I got fat and diabetic!

I have since changed course in diet. Last time I checked, my lipid values on NO statin agent:

HDL 67 mg/dl
Triglycerides 57 mg/dl
Blood sugar 91 mg/dl

That was my lesson that fat restriction is a destructive, misguided notion. The data since then have confirmed that restricting total fat is unnecessary, even undesirable, when fat calories are replaced by carbohydrate calories.

This is your brain on wheat

10. December 2009 William Davis (32)
Here's just a smattering of the studies performed over the past 30 years on the psychological effects of wheat consumption.

Oddly, this never makes the popular press. But wheat underlies schizophrenia, bipolar illness, behavioral outbursts in autism, Huntington's disease, and attention deficit hyperactivity disorder (ADHD).

The relationship is especially compelling with schizophrenia:

Opioid peptides derived from food proteins: The exorphins.
Zioudrou C et al 1979
"Wheat gluten has been implicated by Dohan and his colleagues in the etiology of schizophrenia and supporting evidence has been provided by others. Our experiments provide a plausible biochemical mechanism for such a role, in the demonstration of the conversion of gluten into peptides with potential central nerovus system actions."


Wheat gluten as a pathogenic factor in schizophrenia
Singh MM et al 1976
"Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten."


Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates
Huebner FR et al 1984


Is schizophrenia rare if grain is rare?
Dohan FC et al 1984
"Epidemiologic studies demonstrated a strong, dose-dependent relationship between grain intake and the occurrence of schizophrenia."

Small LDL: Perfect index of carbohydrate intake

8. December 2009 William Davis (15)
Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.


Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.

Fat "conditioning"

4. December 2009 William Davis (0)
Here's a great study from the prolific laboratory of Dr. Jeff Volek from the University of Connecticut. (Full text here.)


http://jn.nutrition.org/cgi/content/full/134/4/880

Video Teleconference with Dr. William Davis

2. December 2009 William Davis (0)

Dr. Davis is available for personal
one-on-one video teleconferencing

to discuss your heart health issues.


You can obtain Dr. Davis' expertise on issues important to your health, including:

Lipoprotein assessment

Heart scans and coronary calcium scores

Diet and nutrition

Weight loss

Vitamin D supplementation for optimal health

Proper use of omega-3 fatty acids/fish oil


Each personalized session is 30 minutes long and by appointment only. To arrange for a Video Teleconference, go to our Contact Page and specify Video Teleconference in your e-mail. We will contact you as soon as possible on how to arrange the teleconference.


The cost for each 30-minute session is $375, payable in advance. 30-minute follow-up sessions are $275.

(Track Your Plaque Members: Our Member cost is $300 for a 30-minute session; 30-minute follow-up sessions are $200.)

After the completion of your Video Teleconference session, a summary of the important issues discussed will be sent to you.

The Video Teleconference is not meant to replace the opinion of your doctor, nor diagnose or treat any condition. It is simply meant to provide additional discussion about your health issues that should be discussed further with your healthcare provider. Prescriptions cannot be provided.

Note: For an optimal experience, you will need a computer equipped with a microphone and video camera. (Video camera is optional; you will be able to see Dr. Davis, but he will not be able to see you if you lack a camera.)

We use Skype for video teleconferencing. If you do not have Skype or are unfamiliar with this service, our staff will walk you through the few steps required.

Track Your Plaque challenges

1. December 2009 William Davis (31)
Of all the various factors we correct in the Track Your Plaque program in the name of achieving reversal of coronary plaque, there are two factors that are proving to be our greatest challenges:

1) Genetic small LDL

2) Lipoprotein(a)

More and more people are enjoying at least marked slowing, if not zero change or reduction, in heart scan scores following the Track Your Plaque program. We achieve this by correcting a number of factors. Some factors, like vitamin D deficiency, are easily corrected to perfection--supplement sufficient vitamin D to achieve a blood level of 25-hydroxy vitamin D of 60-70 ng/ml. Correcting standard lipid values--LDL cholesterol, HDL cholesterol, and triglycerides--child's play, even to our strict targets of 60-60-60.

However, what I call "genetic small LDL" and a subset of lipoprotein(a) are proving to be the most resistant of all.

Let's first consider genetic small LDL. Small LDL is generally the pattern of the carbohydrate-ingesting, overweight person. It has exploded in severity over the past decade due to overconsumption of carbohydrates due to the ridiculous low-fat notion. Reduce or eliminate carbohydrates, especially wheat, which permits weight loss, and small LDL drops like a stone. But there is a unique subset of people who express the small LDL pattern who start at or near ideal weight. Take Chad, for instance. At 6' 2" and 152 lbs and BMI of 19.6, there's no way excess weight could be triggering his small LDL. Yet he starts with 100% small LDL particles. All efforts to reduce small LDL, such as wheat, cornstarch, and sugar elimination; niacin; vitamin D normalization; thyroid normalization; and several supplements that yield variable effects, such as phosphatidylcholine, all leave Chad with more than 90% small LDL.

Lipoprotein(a) is a bit different. Over the past 5 years, our choices in ways to reduce Lp(a) expression have improved dramatically. Beyond niacin, we now have high-dose EPA + DHA, thyroid normalization that includes use of T3, and hormonal manipulation. In the Track Your Plaque experience, approximately 70% of people with Lp(a) respond with a reduction in Lp(a). (In fact, the 4 out of the 5 record holders for reduction of heart scan scores have Lp(a) that was successfully treated.) But about 30% of people with Lp(a) prove resistant to all these treatments--they begin with a Lp(a) of, say, 260 nmol/L and, despite niacin, high-dose EPA + DHA, and various hormones, stay at 260 nmol/L. It can be frustrating and frightening.

So these are the two true problem areas for the Track Your Plaque program, genetic small LDL and a subset of Lp(a).

We are actively searching for better options for these two problem areas. Given the collective exploration and wisdom that develops from such collaborative efforts as the Track Your Plaque Forum, I am optimistic that we will have better answers for these two stumbling blocks to plaque reversal in the future.

I'll supply the tar if you supply the feathers

30. November 2009 William Davis (13)
The results of the latest Heart Scan Blog poll are in.


DIRECT-TO-CONSUMER PHARMACEUTICAL ADVERTISING HAS:

Increased public awareness of medical conditions and their treatment
19 (11%)

Has had little overall effect on health and healthcare
29 (18%)

Needlessly increased healthcare costs
81 (50%)

Further empowered the revenue-obsessed pharmaceutical industry
130 (81%)


Clearly, there's a lot of negative sentiment against direct-to-consumer (DTC) drug advertising.

It looks as if a small minority believe that good has come from DTC advertising, judging by the meager 11% who voted for increased awareness. In fact, the poll results are heavily weighed towards the negative: 50% voted for "needlessly increased healthcare costs," while an astounding 81% voted for "empowered the revenue-obsessed pharmaceutical industry."

It is, indeed, an odd situation: Pharmaceutical agents available only by prescription being hyped directly to the consumer.

Personally, I would vote for choices 1,3, and 4. While awareness has increased, it has come with a hefty price, not all of it well spent. I believe the pharmaceutical industry still adheres to the rule that, for every $1 spent on advertising, $4 is made in revenue. They are, in effect, printing money.

What goes up can't come down

28. November 2009 William Davis (13)
According to conventional wisdom, heart scan scores cannot be reduced.

In other words, say you begin with a heart scan score of 300. Conventional wisdom says you should take aspirin and a statin drug, eat a low-fat "heart healthy" diet, and take high blood pressure medications, if necessary.

If your heart scan score goes up in a year or two, especially at an annual rate of 20% or more, then you are at very high risk for heart attack. If the heart scan score stays the same, then your risk is much reduced. These observations are well-established.

But more than 99% of physicians will tell you that reducing your heart scan score is impossible. Don't even try: Heart scan scores can go up, but they can't go down.

Baloney. Heart scan scores can indeed go down. And they can go down dramatically.

It is true that, following conventional advice like taking a statin drug, following a low-fat diet, and taking aspirin will fail to reduce your heart scan score. A more rational approach that 1) identifies all causes of coronary plaque, 2) corrects all causes while including crucial strategies like omega-3 fatty acid supplementation, vitamin D supplementation, and thyroid function normalization, is far more likely to yield a halt or reduction in score.

While not everybody who undertakes the Track Your Plaque program will succeed in reducing their heart scan score, a growing number are enjoying success.

A small portion of our experience was documented this past summer. (I collected and analyzed the data with the help of Rush University nutrition scientist, Dr. Susie Rockway, and statistician, Dr. Mary Kwasny.)


Effect of a combined therapeutic approach of intensive lipid management, omega-3 fatty acid supplementation, and increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic adults.

Davis W, Rockway S, Kwasny M.

The impact of intensive lipid management, omega-3 fatty acid, and vitamin D3 supplementation on atherosclerotic plaque was assessed through serial computed tomography coronary calcium scoring (CCS). Low-density lipoprotein cholesterol reduction with statin therapy has not been shown to reduce or slow progression of serial CCS in several recent studies, casting doubt on the usefulness of this approach for tracking atherosclerotic progression. In an open-label study, 45 male and female subjects with CCS of > or = 50 without symptoms of heart disease were treated with statin therapy, niacin, and omega-3 fatty acid supplementation to achieve low-density lipoprotein cholesterol and triglycerides < or = 60 mg/dL; high-density lipoprotein > or = 60 mg/dL; and vitamin D3 supplementation to achieve serum levels of > or = 50 ng/mL 25(OH) vitamin D, in addition to diet advice. Lipid profiles of subjects were significantly changed as follows: total cholesterol -24%, low-density lipoprotein -41%; triglycerides -42%, high-density lipoprotein +19%, and mean serum 25(OH) vitamin D levels +83%. After a mean of 18 months, 20 subjects experienced decrease in CCS with mean change of -14.5% (range 0% to -64%); 22 subjects experienced no change or slow annual rate of CCS increase of +12% (range 1%-29%). Only 3 subjects experienced annual CCS progression exceeding 29% (44%-71%). Despite wide variation in response, substantial reduction of CCS was achieved in 44% of subjects and slowed plaque growth in 49% of the subjects applying a broad treatment program.

Gretchen's postprandial diet experiment

27. November 2009 William Davis (11)
Gretchen sent me the results of a little experiment she ran on herself. She measured blood glucose and triglycerides after 1) a low-fat diet and 2) a low-carb diet.









Gretchen describes her experience:

Several years ago I received a windfall of triglyceride strips that would expire in a week or so. I hated to waste them, so I decided to use them to test my triglyceride and BG responses to two different diets: low carb and low fat.

The first day I followed a low-fat diet. For breakfast I ate a lot of carbohydrate, including 1 oz of spaghetti cooked al dente and ¾ cup of white rice. For the rest of the day I ate less carbohydrate but continued to eat low fat.

The second day I followed a low-carb diet. For breakfast I ate a lot of fat, including a sausage, mushrooms fried in butter, 2 slices of bacon, and ¼ cup of the creamy topping of whole-milk yogurt. For the rest of the day I ate less fat, especially less saturated fat, but continued to eat low carb.

Both days I measured both BG and triglyceride levels every hour until I went to bed. On the low-carb day I had 3 meals. On the low-fat day, I was constantly hungry, had 4 meals, and kept snacking.

You can see the results in Figure 1. On the low-fat diet, after a “healthy” low-fat breakfast of low-glycemic pasta with low-fat sauce, my BG levels shot up to over 200 mg/dL and took more than 6 hours to come down. My triglycerides, however, remained low, and at first I thought perhaps the low-fat diet might be better overall. However, after about 6 hours, the triglyceride levels started to increase steadily, and by the next morning, they were higher than they had been the day before.
On the low-carb diet, my BG levels stayed low all day. However, after meals, the triglyceride levels skyrocketed. After meals they came down, and by the next morning they were lower than they had been the day before.

As I interpret these results, the high triglyceride levels after eating the high-fat meals represent chylomicrons, the lipoproteins that transport fat from your meals to the cells of your body. The high triglyceride levels the morning after eating the low-fat meals represent very low density lipoprotein, which takes the cholesterol your liver synthesizes when your intake of dietary cholesterol is low and distributes it to cells that need it, or again, to the fat for storage.

There are several interesting factors to consider here. First, when you have a lipid test done at the lab, it’s usually done fasting, which means first thing in the morning after not eating for 8 to 12 hours. It tells you nothing about what your triglyceride levels were all day.

Second, the low-carb diet resulted in lower fasting triglyceride levels, but much higher postprandial triglyceride levels. Which are more dangerous? I’m afraid I don’t know. You should also note that the high-fat, low-carb breakfast was extremely high in fat, including saturated fat. I don’t normally eat that much fat but wanted to test extremes.

Third, although the low-fat diet didn’t produce the very high postprandial triglyceride levels that the high-fat diet did, it produced extremely high BG levels that persisted for 6 hours. Some people think that it’s oxidized and glycated lipids that are the dangerous ones, so high BG levels and normal triglyceride levels might be more dangerous than very high triglyceride levels and normal BG levels. Note that high BG levels also contribute to oxidation rates.

Fourth, this shows the results of an experiment with a sample size of one. My physiology might not be typical. If you want to know how your own body’s lipids respond to different types of diets, you should get a lipid meter and test yourself. Unfortunately, your insurance is unlikely to want to pay for this, so it will be an expensive experiment.

The main point of this is that the results of different diets are complex. We have to eat. And what we eat can affect many different systems in our bodies. Finding the ideal diet that matches our own physiology and results in the best lipid levels as well as BG levels is a real challenge.



This was a lot of effort for one person. Thanks to Gretchen for sharing her interesting experience.

Gretchen makes a crucial point: Some of the effects of diet changes evolve over time, much as triglyceride levels changed substantially for her on the day following her experiment. Wouldn't it be interesting to see how postprandial patterns develop over time if levels were observed sequentially, day after day?

The stark contrast in blood sugars is impressive--Low-carb clearly has the advantage here. Are there manipulations in diet composition in low-carb meals that we can make to blunt the early (3-6 hour) postprandial lipoprotein (triglyceride) peak? That's a topic we will consider in future.

More of Gretchen's thoughts can be found at:

http://wildlyfluctuating.blogspot.com
http://www.healthcentral.com/diabetes/c/5068

After-eating effects: Carbohydrates vs. fats

25. November 2009 William Davis (17)
In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

High-carbohydrate was defined as 15% protein; 10% fat; 75% carbohydrate (by calories), with starch:sugar 70:30.

High-fat was defined as 15% protein; 40% fat; 45% carbohydrate, with starch:sugar 70:30. (Yes, I know. By our standards, the "high-fat" diet was moderate-fat, moderate-carbohydrate--too high in carbohydrates.)

Blood was drawn over 6 hours following the test meal.




Roberts R et al. Am J Clin Nutr 2008

The upper left graph is the one of interest. Note that, after the high-carbohydrate diet (solid circles), triglyceride levels are twice that occurring after the high-fat diet (open circles). Triglycerides are a surrogate for chylomicron and VLDL postprandial lipoproteins; thus, after the high-carbohydrate diet, postprandial particles are present at much higher levels than after the high-fat diet. (It would have been interesting to have seen a true low-carbohydrate diet for comparison.) Also note that, not only are triglyceride levels higher after high-carbohydrate intake, but they remain sustained at the 6-hour mark, unlike the sharper decline after high-fat.

It's counterintuitive: Postprandial lipoproteins, you'd think, would be plentiful after ingesting a large quantity of fat, since fat must be absorbed via chylomicrons into the bloodstream. But it's carbohydrates (and obesity, a huge effect; more on that in future) that figure most prominently in determining the pattern and magnitude of postprandial triglycerides and lipoproteins. Much of this effect develops by way of de novo lipogenesis, the generation of new lipoproteins like VLDL after carbohydrate ingestion.

We also see this in our Track Your Plaque experience. Rather than formal postprandial meal-testing, we use intermediate-density lipoprotein (IDL) as our surrogate for postprandial measures. A low-carbohydrate diet reduces IDL dramatically, as do omega-3 fatty acids from fish oil.
Salvation from halogenation

Salvation from halogenation

24. September 2010 William Davis (26)
Iodine is a halogen.

On the periodic table of elements (remember the big chart of the elements in science class?), the ingenious table that lays out all known atomic elements, elements with similar characteristics are listed in the same column. The elegant genius of the periodic table has even allowed prediction of new, undiscovered elements that conform to the "laws" of atomic behavior.

Column 17 (also called "group VIIa") contains all the halogens, of which iodine is one member. Other halogens include fluorine, chlorine, and bromine.

Odd phenomenon in biologic systems: One halogen can often not be distinguished from another. Thus, a chlorinated compound can cleverly disguise itself as an iodinated compound, a brominated compound can mimic an iodinated compound, etc.

What this means in thyroid health is that, should sufficient iodine be lacking in the body, i.e., iodine deficiency, other halogens can gain entry into the thyroid gland.

While a polychlorinated biphenyl (PCB) molecule may be recognized as an iodinated compound, it certainly doesn't act like an iodinated compound once it's in the thyroid's cells and can disrupt thyroid function (Porterfield 1998). Another group of chlorine-containing compounds, perchlorates, that contaminate groundwater and are found as pesticide residues in produce, are extremely potent thyroid-blockers (Greer 2002). Likewise, bromine-containing compounds, such as polybrominated diphenyl ethers (PBDEs), widely used as flame retardants, also disrupt thyroid function (Zhou 2001). Perfluorooctanoic acid (PFOA), found in Teflon non-stick cookware and stain-resistant products,  has been associated with thyroid dysfunction (Melzer 2010). PFOA, incidentally, can disrupt thyroid dysfunction that will not show up in the TSH test used by primary care physicians and endocrinologists to screen for thyroid dysfunction. (In fact, the presumed champions of thyroid health, the endocrinology community, have proven a miserable failure in translating and implementing the findings from  toxicological science findings to that of preserving or restoring thyroid health. They have largely chosen to ignore it.)

We therefore navigate through a world teeming with halogenated thyroid blocking compounds. We should all therefore avoid such exposures as perchlorates in produce by rinsing thoroughly or purchasing organic, avoid non-stick cookware, avoid use or exposure to pesticides and herbicides.

Another crucial means to block the entry of various halogenated compounds into your vulnerable thyroid: Be sure you are getting sufficient iodine. While it doesn't make your thyroid impervious to injury, iodine circulating in the blood in sufficient quantities and residing in sufficient stores in the thyroid gland provides at least partial protection from the halogenated impostors in your life.

I make this point in the context of heart disease prevention, since even the most subtle degrees of thyroid dysfunction can easily double, triple, or quadruple heart disease risk. See related posts, Is normal TSH too high? and Thyroid perspective update.
Tags :

Comments (26) -

  • Anonymous

    9/24/2010 2:52:02 PM |

    What is the mechanism by which the thyroid problems lead to heart disease? I have typically had a tsh of 4-5, my doc always said that was OK, but more recently it is down to 2, not sure what caused the chang, but we have started using iodized salt again instead of the "Kosher salt" Coudld this alone be the difference?

  • Anna

    9/24/2010 3:54:17 PM |

    It's my understanding that everyday PFOA exposure isn't so much a result of daily *use* of products with Teflon/non-stick coatings,  but rather is due to the contamination of the environment during a mid-stage manufacturing process.  PFOA contamination is now essentially global and shows up even where the end-products are not in widespread use.

    So even if one doesn't have any or use any Teflon/stain-resistant items in daily life  one can still be exposed to PFOA in the environment (even unborn children show evidence of exposure though fetal cord testing) because it is extremely persistent and doesn't break down (one if the characteristics that has made non-stick/stain-resistance so popular and "desirable").  

    There is a completely different issue with non-stick cookware surfaces; toxic gas that is emitted if the item is overheated (esp without enough food contents to moderate the temperature).  Birds are esp susceptible to those toxic fumes and many pet birds have been harmed by non-stick pans overheated on ranges.  But that's not the same as the PFOA contamination during manufacturing.

    So it is not enough to not personally own and not use Teflon/non-stick and stain-resistant fabrics/textiles (though that's a great step in the right direction).  The environmental exposure still continues.  Even persons in remote areas can't completely avoid contact with PFOA contamination at this point.

    If the items are still in production for the market, more PFOA is still being released into the environment during manufacturing.  

    There are new non-stick coatings now on the market, but how long will be it be before we discover an unintended consequence to their production?  

    I try to reduce my own demand for such products.  Whenever I can, I choose products without non-stick and stain-resistant finishes.  The short-term benefits aren't worth it in the long run if we are exposing our children while still in the womb and subjecting them at critical developmental stages to such powerful endocrine-disruptors.  Kids shouldn't be the "canaries in the coal mine".  

    http://www.ewg.org/node/21715
    www.ewg.org/pfc-manufacturers

  • Ed Terry

    9/24/2010 4:33:06 PM |

    Many drugs also contain fluorine molecules in order to slow down metabolism and excretion.

    All semi- and synthetic statins have fluorine atoms in the molecule.  While the main metabolic pathways are known, there could also be lesser alternate metabolic products formed.  

    I've been unable to find free research papers describing all possible metabolic pathways of drugs.  Once the main products are known, no one pays additional attention.

  • Kevin

    9/24/2010 4:57:24 PM |

    Could this be the result of our national salt phobia?  I have low blood pressure so I add iodized salt to everything.  I also run 50+ miles a week and eat salt during long runs.  

    kevin

  • Anonymous

    9/24/2010 6:11:38 PM |

    I have a question completely off subject.  My cardiologist just prescribed Livalo and when I tried to research it online there is not much reported.  Have you heard much about it and what is your opinion of it?  I have had a bad reaction to all the statins I have tried to date and am a little afraid to try it.  Any information on this drug would be appreciated.

  • Dr. William Davis

    9/24/2010 6:18:42 PM |

    Anonymous about TSH 4-5--

    Please enter "iodine" in the site-specific search for past posts about iodine use.

    Iodine restoration could indeed explain your improved TSH, though there is great variation in both thyroid status and in thyroid testing to consider, as well. However, if your TSH is again in the 4-5 range, I would get another opinion from someone more up-to-date or at least open minded.

  • Laura

    9/24/2010 7:42:37 PM |

    Thank you for sharing, very informative.

  • kellgy

    9/25/2010 2:50:33 PM |

    Interesting perspective on halogens Dr. Davis. I suppose drinking water from plastic bottles even from the ubiquitous "water coolers" puts us at risk with halogens and/or petrochemicals. I think we have forgotten about the beauty and safety of glass as a useful product.

  • Dr. William Davis

    9/25/2010 4:31:14 PM |

    Hi, Kell--

    Yes, indeed.

    We got rid of the polycarbonate water cooler in our office a while back and replaced it with a glass one. Polycarbonate is the standout problem, leaching out bisphenol A.

  • Anonymous

    9/25/2010 9:50:39 PM |

    Geez "Ed TerrY" ...
    I guess I am wondering where the fluorine atom is located in
    (1S,3R,7S,8S,8aR)-8-{2-[(2R,4R)-4-hydroxy-6-oxooxan-2-yl]ethyl}-3,7-dimethyl-1,2,3,7,8,8a-hexahydronaphthalen-1-yl 2,2-dimethylbutanoate; otherwise known as simvastatin (Zocor). All statins (not just simvastatin) act by competitively inhibiting 3-hydroxy-3-methylglutaryl coenzyme A HMG-CoA reductase, the rate-limiting enzyme of the HMG-CoA reductase pathway, the metabolic pathway responsible for the endogenous production of cholesterol. The presence of a fluorine atom in a statin molecule would most likely destroy this inhibitory activity. Lets at least try to have a basic understanding of what we say in our comments, or keep them to ourselves.

  • Peter

    9/26/2010 2:26:44 PM |

    The levels of BPA on two fifths of all supermarket receipts is apparently as much as a thousand times higher than that in can linings, for example.

  • Saddam

    9/27/2010 12:33:55 PM |

    Heart  disease is one of the most  dangerous disease which takes thousands of life every years all over the world. If we know its symptoms and Treatment for heart disease>. We can prevent is to large extent.

  • Anonymous

    9/27/2010 1:48:23 PM |

    Anonymous said, “I guess I am wondering where the fluorine atom is located in”

    Your Zocor example belongs to a hydrophilic statin of the type 1 class. You must research lipophilic statins of the type 2 class, for instance Lipitor: by far the most extensively prescribed blockbuster drug in the history of medical science.

    (3R,5R)-7-[2-(4-FLUOROPHENYL)-
    3-phenyl-4-(phenylcarbamoyl)-5-(propan-2-yl)- 1H-pyrrol-1-yl]-3,5-dihydroxyheptanoic acid

    Examine the chemical structure of all synthesized statins: Crestor, Baycol, Vytorin, Zetia/Ezetimibehave, they contain para-fluorophenyl groups. Generally, organofluorines in pharmaceuticals are meant to protect breakdown by metabolic enzymes and strengthen bonds to target proteins.

    In regards to type 2 statins, the fluorophenyl group replaces the butyryl group in order to strengthen binding to the HMGR enzyme. Lithopholic statins are especially insidious due to their ability to cross the blood brain barrier and easily penetrate cell membranes.

  • julianne

    9/28/2010 2:16:51 AM |

    Just discovered there is a the polycarbonate water container in our coffee espresso machine at home.

    When I took iodine with my Hashimotos, it flared up badly? In my case (and other Hashis sufferers) what is the answer, besides avoiding other halogens?

  • steve

    9/28/2010 5:16:41 PM |

    any thoughts on Bill Clinton's new near vegan Ornish/Esselstyne diet?

  • Anonymous

    9/28/2010 7:23:15 PM |

    "Your Zocor example..."

    Well said, and thank you for the update.

  • Anand Srivastava

    9/28/2010 7:31:39 PM |

    @julianne

    My brother has the same problem. Hashi, which he detected when he tried to supplement iodine.

    Do you have an idea regarding possible remedies or good websites?

    thanks

  • Anonymous

    9/28/2010 7:35:33 PM |

    Polycarbonate bottles are a minor problem compared with the thermal credit card receipts that are everywhere.  Many of these have BPA levels that are off the charts, and a lot of people touch their mouths after handling them.

  • Dr. William Davis

    9/28/2010 8:42:22 PM |

    Julianne and Anand--

    Hashimoto's can indeed be flared by iodine.

    What I've been doing is to start with minimal doses, e.g., 100 mcg per day--not much more than a few shakes of the salt shaker--and build up over time. This has worked well, so far.

    It may also be important to supplement selentium, 200 mcg per day, since this tends quiet Hashimoto's inflammation.

  • Dr. William Davis

    9/28/2010 8:51:31 PM |

    Hi, Anna--

    Thanks for the great clarification.

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    9/29/2010 5:37:59 AM |

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  • Anonymous

    10/3/2010 9:56:22 PM |

    I expect this comment to get struck off the blog because it suggests the BPA scare is overblown........

    The European Food Safety Authority (EFSA; Brussels) has concluded  it
    could not identify any new evidence that would lead it to revise the
    current Tolerable Daily Intake (TDI) for bisphenol A (BPA) of 0.05
    mg/kg body weight, which EFSA set in 2006. The EFSA advisory panel
    also says data currently available “do not provide convincing evidence
    of neurobehavioural toxicity of BPA.”

    source:
    http://www.chemweek.com/home/top_of_the_news/29910.html

  • Anonymous

    10/5/2010 8:50:33 PM |

    This is all so unproductive.  

    You cannot micromanage your chemical exposure in America in 2010.  If our environment is  thoroughly suffused with "toxins" (in insidious micro-amounts or in great big chunks as per comments on thermal credit card receipts and grocery store shelves) there is nothing you can do about it.  

    This is all a big distraction from what is important for your health (eat approximately right, exercise enough) and for your life (love, work, use your brain, and play. And vote, thoughtfully).

    Just my two cents.

  • Ross4Teflon

    10/19/2010 3:10:34 PM |

    Hi -- Because there's so much misinformation out there about Teflon, I'm not surprised that you are concerned. I'm a representative of DuPont though, and hope you'll let me share some information with you and your readers, so that everyone can make truly informed decisions.

    The recent Exeter study tried to determine whether there is a potential relationship between PFOA and thyroid changes.  The study’s authors state that the observed association is a correlation, which may or may not be causal.  This is inconsistent with other studies, including studies of workers who have had much higher levels of PFOA exposure than the general public.  These workers have not shown any changes that would indicate impact on the thyroid.  The weight of evidence gathered from a number of significant health studies continues to indicate to us that there is no health risk to the general public from exposure to PFOA.  Please take a look at http://www2.dupont.com/PFOA2/en_US/pfoa_thyroid.html for more info.

  • qualia

    10/28/2010 3:26:58 PM |

    with regard to hashimoto: ALWAYS go 100% off gluten when having hashimoto, as it is 90% of the time an autoimmune disease which is almost always triggered and maintained by gluten and leaky gut. secondly, as with all autoimmune diseases - be sure to be in a high-optimal range of your vitamin d (like 60-80ng/L).

  • lala

    11/17/2010 6:29:57 AM |

    Thanks for your post and welcome to check: here.

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