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.
How to Give Yourself Hashimoto's Thyroiditis: 101

How to Give Yourself Hashimoto's Thyroiditis: 101

25. January 2009 William Davis (18)
I borrowed this from the enormously clever Dr. BG at The Animal Pharm Blog.


How to Give Yourself Hashimoto's Thyroiditis: 101

--lack of sunlight/vitamin D/indoor habitation
--mental stress
--more mental stress
--sleep deprivation... (excessive mochas/lattes at Berkeley cafes)
--excessive 'social' calendar
--inherent family history of autoimmune disorders (who doesn't??)
--wheat, wheat, and more wheat ingestion ('comfort foods' craved in times of high cortisol/stress, right? how did I know the carbs were killing me?)
--lack of nutritious food containing EPA DHA, vitamin A, sat fats, minerals, iodine, etc
--lack of play, exercise, movement (or ?overtraining perhaps for Oprah's case)
--weight gain -- which begins an endless self-perpetuating vicous cycle of all the above (Is it stressful to balloon out for no apparent reason? YES)


If you haven't done so already, take a look at Animal Pharm you will get a real kick out of Dr. BG's quick-witted take on things.


We are systematically looking for low thyroid (hypothyroidism) in everyone and findings oodles of it, far more than I ever expected.

Much of the low thyroid phenomena is due to active or previous Hashimoto's thyroiditis, the inflammatory process that exerts destructive effects on the delicate thyroid gland. It is presently unclear how much is due to iodine deficiency in this area, though iodine supplementation by itself (i.e., without thyroid hormone replacement) has not been yielding improved thyroid measures.

I find this bothersome: Is low thyroid function the consequence of direct thyroid toxins (flame retardants like polybrominated diphenyl ethers, pesticide residues in vegetables and fruits, bisphenol A from polycarbonate plastics) or indirect toxins such as wheat via an autoimmune process (similar to that seen in celiac disease)?

I don't know, but we've got to deal with the thyroid-destructive aftermath: Look for thyroid dysfunction, even in those without symptoms, and correct it. This has become a basic tenet of the Track Your Plaque approach for intensive reduction of coronary risk.
Tags :

Comments (18) -

  • Bad_CRC

    1/25/2009 7:07:00 PM |

    Hmm, really?  So if I eat wheat (or was it 'carbs' generally?) and not enough animal fat, drink coffee, don't sleep enough, etc., Hashimoto's autoantibodies will start showing up in my blood?  And when I reverse the above, the antibodies will disappear and TSH, etc., will revert to normal?

    Any support for this in the literature?

  • dubyaemgee

    1/25/2009 8:12:00 PM |

    I suspect there needs to be some reeducation as to what is considered "normal" within the medical community as a whole. My TSH was last measured at 4.32, and is considered well within the range of normal, even though I've been complaining of hypothyroidism for a while now. Seems like we have to go into the doctor's office with steely determination to have these problems addressed.

  • mike V

    1/26/2009 2:03:00 AM |

    Drs Davis and BG:
    I think you are both on target with the attention you pay to hypothyroidism in relation to heart disease, and other related diseases such as obesity, diabetes, kidney and other hormone related problems.

    Question please:
    In your opinions:
    1 Is the high incidence of hypothyroidism in the population throwing 'off' the lab  norms for TSH, FT3, FT4 or can we assume the numbers used by most labs are based on world wide or historical values?

    2 Is 'Subclinical Hypothyroidism' real, or could it simply be a function of #1, or inadequate vitamin D3/iodine etc. I understand that 60% of the US population may be in that category.

    Thank you
    Mike V

  • Anne

    1/26/2009 2:26:00 PM |

    You mention the connection between wheat and thyroid. If you want to read more about that, go to The Gluten File. www.theglutenfile.com There you will find a section on thyroid disease.

    It is known that about 4-6% of those with Hashimoto's have celiac disease. I am sure that percentage would go even higher if one included those with non-celiac gluten sensitivity. There has been at least one study showing that thyroid antibodies disappear with the use of a gluten free diet.

  • Nameless

    1/26/2009 8:46:00 PM |

    Are there any studies showing wheat, vitamin D, etc. causing Hashimoto's? I suspect there isn't, but if population studies are looked into, perhaps you could find a correlation? Look at populations that generally don't consume much wheat, and see what their rates of Hashimoto's are. Or populations at upper latitudes vs those near the equator, and their rates of Hashimoto's.

    However, if wheat, lack of sleep, poor diet, etc. does cause Hashimoto's, wouldn't it alter the male/female ratio of who gets the disease? Why would women still be more likely to contract Hashimoto's, if the cause is diet?

    And in my case, several years ago I went to a low carb diet, restricted wheat, desserts consist of fruits/berries only, corrected my vitamin D levels, took fish oil, etc. I also tested negative for Celiac. Before these changes my thyroid tested normal (TSH in the low 1s). I was never overweight and exercised regularly too.

    And this past month I was  diagnosed with Hashimoto's (high antibodies, TSH in the 3s, thyroid scan all lumpy). So... if there is a correlation, shouldn't my thyroid have improved, not gotten worse?

  • G

    1/26/2009 10:00:00 PM |

    Bad_CRC,

    I think you need to have the genetic susceptibility. On the animal pharm blog, I've listed a few that scientists have already correlated to Hashimoto's
    --VDR polymorphs
    --HLA polymorphs

    I'm certain there will only be dozens others b/c these things (autoimmunity) don't happen alone.

    Add'l, perhaps these things are also just signals for 'hibernation'...??  Perhaps we are only inducing ancient signals that are meant to protect and increase survival (low melatonin, high carbs, wheat/stress, fructose (from the Italian sodas I forgot to mention!), gaining weight, slowing down to Eat-Eat-Eat/stress, etc).

    Any thoughts?

    There are a few links in the literature regarding higher TSH, lower T3/T4 during winter months and lower vitamin D in the serum. Of course!

    -G

  • mike V

    1/27/2009 2:32:00 AM |

    G
    I have no personal doubt that how well you choose your parents is of primary importance.
    My late mother, and two brothers and sisters have all been  hypothyroid.
    As in most diseases, I think other immune factors can be involved, some in the womb, some exposures in early childhood, while the immune system is still being 'programmed', others from bacterial or viral exposures.
    It is said that vitamin D is quite important in a balanced immune system, but it starts very low in typical breast milk, and in very young children, and can remain low throughout life in much of the population.
    Iodine deficiency was a critical factor in people not living near the coasts, until iodized salt was introduced in the early 20th century.
    Lack of timely exposure to bright light is well known to "mess" with our biological clock, moods, and immunity.
    I did not become aware that I was hypothyroid until my forties, and since have not found nutrition a major factor, until perhaps vitamin D.
    With the exception of vitamin D, I have not personally been aware that other nutrition has affected my treatment.
    Is there any co-relation between Hasimoto's, and other auto-immune conditions?

    MikeV

  • Dr. William Davis

    1/27/2009 11:53:00 AM |

    Mike V--

    The newest data, e.g., the HUNT Study, are analyses of events based on TSH. It therefore factors out the effect of population distributions.

    You are correct, however, in pointing out that previous analyses were flawed precisely for this reason.

  • mike V

    1/27/2009 5:13:00 PM |

    As usual thanks to all for the education, and for all you do to penetrate the blood brain barrier between the specialties, Big Medica, and us (the great 'unwashed'. Smile)

    MikeV

  • Pat Elliott ND

    1/27/2009 5:44:00 PM |

    Hi Doc,
    We are seeing a very high % of our patients with zinc deficiency - similar to the whole vitamin D thing. Just wanted to share this with you since zinc is also correlated to blood sugar and cholesterol problems. Would love to see what you find in your patients with regard to this nutrient as well.
    Regards,
    Pat Elliott ND
    www.elliotthealthcare.com

  • Anonymous

    1/28/2009 3:51:00 AM |

    Pat Elliott  --

    How do you define a zinc deficiency? I've read that serum zinc is pretty inaccurate (as is copper or magnesium serum testing).

    Looking at other biomarkers, or a zinc taste test?

  • Lou

    4/1/2009 11:54:00 PM |

    I'm guessing that when "Nameless" took up the low-carb eating plan, they may have also increased eating soy.  Soy can really mess up the hormones.  I think we can blame soy for all this thyroid trouble and fibromyalgia and fatigue related troubles.  Add to that inadequate fish oils, butter, after years of telling us to avoid fats and sunlight (vitamin D) and you get a nice picture of what has happened to far too many of us.

  • scall0way

    11/10/2009 8:35:12 PM |

    I know this is an old post but I'm just going through all the thyroid-related posts. My TSH got flagged at a 9 when I went for a physical a couple weeks ago, and further tests came back with a Hashimoto's diagnosis.

    I just don't know. I follow a gluten-free diet, in fact I avoid all grains. I avoid all sugars, I don't consume any high-PUFA vegetables oils. I have not eaten any sort of soy (except for rare splashes of fermented soy sauce here or there) in a dozen years. I always cook any veggies I might eat  that call into the goitrogenic category. I supplement with 5000 IU of D3 in gelcap format daily. I consume most of my fats as sat fats/animal fats. I take fish oil, cod liver oil. I love to eat sardines.

    Yet my thyroid apparently has slowly been getting worse over the last couple years. My TSH is definitely higher than it was in 2007, and that was higher than it was in 2006 - slowly been climbing over the last few years until finally the doctor red-flagged it.

  • Anonymous

    7/29/2010 10:42:48 AM |

    I have Hashimotos. Was diagnosed at 15. Had it long before then. I am convinced it is genetic when I look at other family members (although no-one else has been diagnosed). I am on 'correct' dosage of thyroid hormones but many of the symptoms still exist and I would LOVE to blame my GP but the fact is that they are overworked and are doing the best with what they have - like the rest of the population. Recently diagnosed with anxiety by a psychologist. Does this cover the hashimotos symptoms completely or partially? Who knows? All I know is that I am drunk now as I am bone tired from trying and failing from everything from relationships to work - alcohol seems to be the only way out...although my psychologist has told me it isn't - just being tired and weak I guess. I'm sure you will delete this post as soon as you see it blog owner, but before you do, I hope a few Hashimotos/anxiety sufferers see one person struggling to be better despite the messy interference of life. Having a temporary failure right now but will be back on the horse again tomorrow like every other day.

    Love you all.

    XXX.

  • buy jeans

    11/3/2010 6:58:15 PM |

    JMC at the blog animal pharm has linked some fantastic resources from Loren Cordain and how the Paleo diet reverses autoimmune diseases (incl JMC's own rheumatoid arthritis). Wheat is not the ONLY culprit. Legumes, Dairy/casein, nutr'l deficiencies, excessive fruit/HFCS, lack of exercise, lectins, etc are part of the equation for autoimmunity disorders as well.

  • PureAlan

    1/24/2011 10:46:15 AM |

    What a brilliant idea! Thanks for sharing this information. I have hypothyroidism for almost 4 years and it was terrible. I am currently taking porcine thyroid .  Now I'm gaining back my normal life.

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