Vitamin D: Treatment for metabolic syndrome?

Metabolic syndrome is that increasingly common collection of low HDL cholesterol, high triglycerides, high blood sugar, and high pressure that now afflicts nearly 1 in 4 adults, rapidly gaining ground to 1 in 3. Beyond these surface factors, metabolic syndrome also creates small LDL particles, VLDL, intermediate-density lipoproteins (IDL), increased imperceptible inflammation measured as higher c-reactive protein, and greater blood clotting tendencies. Metabolic syndrome is usually, though not always, associated with a big tummy ("beer belly," though I call it "wheat belly").

In short, metabolic syndrome creates a metabolic mess that leads to dramatic increases in heart disease, vascular disease and stroke, and cancer. The medical community has been paying increasingly greater attention to this condition because of its booming prevalence and because of the big bucks invested in "education" by the manufacturers of the diabetes and pre-diabetes drugs, particularly makers of Actos and Avandia.

But here's a curious observation:

Replacement of vitamin D to healthy levels (we aim for 50-60 ng/ml, or 125-150 nmol/l) yields:

--Higher HDL
--Lower triglycerides
--Lower blood sugar
--Reduced c-reactive protein
--Reduced blood pressure
--Reduced small LDL
--Enhanced sensitivity to insulin

(Whether blood clotting and effects on IDL should be added to this list is uncertain.)

It's obvious: Vitamin D is proving to be a very important and powerful corrective influence on many of the facets of the metabolic syndrome. In fact, I would go as far as saying that, side by side, vitamin D yields nearly the same effect as prescription drugs Actos and Avandia--without the extravagant cost (nearly $200 per month), leg swelling, congestive heart failure and heightened heart attack risk (with Avandia), and average 8 lb weight gain. Of course, vitamin D also provides benefits beyond metabolic syndrome like facilitation of coronary plaque regression, increased bone density, reduced arthritis, and reduced risk of several cancers.

You'd think that agencies like the American Diabetes Association (ADA) would be all over vitamin D like white on rice. Yet they remain curiously quiet about the entire issue. (That should come as no surprise to anyone familiar with the behavior and politics of this organization, the same outfit that has widely propagated the ADA diet, a program that accelerates diabetes and its complications. In my view, the ADA is an embarassment.)



For a really great story and video on vitamin D that includes a terrific interview with vitamin D guru and Track Your Plaque friend, California psychiatrist Dr. John Cannell, go to What's the Real Story on Vitamin D?. While the video will yield little new to readers of The Heart Scan Blog or Track Your Plaque members, it just feels really good to see a well-made, high-class video production echoing many of the things we've been talking about these past two years.

Comments (44) -

  • Anonymous

    12/21/2007 5:52:00 PM |

    > Whether blood clotting and effects on IDL
    >should be added to this list is uncertain.

    Meaningless anecdote: I've noticed an increased tendency to bruise easily since I've been taking higher doses of vitamin D, and had been wondering whether it was the cause. I definitely have metabolic syndrome.

  • mo79uk

    12/21/2007 7:36:00 PM |

    I wish Dr. Cannell would come talk the British media. We need a tank load of D talk to infiltrate here.

  • Mike

    12/22/2007 3:49:00 PM |

    An irrational fear of skin cancer prevents most people from getting their vitamin D from sunshine. The doses that the medical establishment recommends are so small as to be almost worthless.

  • MarilynMann

    12/22/2007 10:36:00 PM |

    It would be helpful if you could tell us where the research on vitamin D you are referring to is published.  Some of us like to go to the original source.

  • Dr. Davis

    12/23/2007 12:38:00 AM |

    See our special reports on the Track Your Plaque website with detailed references. Or, go to Dr. John Cannell's www.vitamindcouncil.com website.

  • Sue

    12/23/2007 2:38:00 AM |

    Is cod liver oil the best way to get vitamin D or just vitamin D3 capsules?
    Is there are connection with hypothyroidism and low vitamin D levels?

  • Dr. Davis

    12/23/2007 1:57:00 PM |

    Either source for vitamin D works.

    I do believe that correction of vitamin D has, in occasional instances, modestly increased thyroid function.

  • MarilynMann

    12/23/2007 3:45:00 PM |

    Cod liver oil has a lot of vitamin A, which in excess can lead to low bone density.  It is better just to take the vitamin D by itself.

  • g

    12/23/2007 9:20:00 PM |

    I agree -- over 20yrs ago it was suggested that increased thyroid doses are required in the winter time for hypothyroid pts on replacement (see below). IT sure seems to suggest that Vitamin D deficiency exacerbates hypothyroidism (and I'd go as far to say it even CAUSES it)?  I've observed this as well. (it's corrected with D3)

    In the second study, a corollary phenomenon occurred -- thyroid replacement in hypothyroid pts caused 25(OH)D to INCREASE (in the autumn when you'd normally expect it to decrease).  

    Isn't it fascinating how thyroid hormone and D3 hormone are interrelated.
    ---When D3 hormone (sunlight) is lacking, thyroid function suffers
    ---When thyroid hormone is lacking, a high D3 dose fails to increase 25(OH)D much....
    ---When thyroid hormone is NOT lacking, high dose D3 causes a large increase in 25(OH)D (in normal euthryoid controls)

    it all sounds very familiar to me...  Smile

    THANK YOU FOR ALL YOUR WORK AND INSIGHTS!! Keep up the strong work, g


    Metabolism. 1984 Mar;33(3):215-8. Links
    Is it necessary to adjust the replacement dose of thyroid hormone to the season in patients with hypothyroidism?Hamada N, Ohno M, Morii H, Jaeduk N, Yamakawa J, Inaba M, Ikeda S, Wada M.
    Hypothalamo-pituitary-thyroid activity varies with the temperature of the environment; we therefore measured variables involved with thyroid function in summer and winter in normal controls and in patients with primary hypothyroidism. All seven patients had impalpable thyroid glands and had received a set replacement dose of thyroxine for over a year. In the patients, serum T3 and FT4 levels were slightly but significantly lower in winter, and TSH levels and delta TSH at 30 minutes in the TRH tests were significantly higher. In the controls, there were no significant differences between summer and winter in these values. These findings suggest that the dose required for replacement of thyroid hormone in patients with hypothyroidism may be higher in winter than in summer.

    PMID: 6420646 [PubMed - indexed for MEDLINE]



    Acta Endocrinol (Copenh). 1986 Nov;113(3):329-34.Links
    Effect of vitamin D3 loading and thyroid hormone replacement therapy on the decreased serum 25-hydroxyvitamin D level in patients with hypothyroidism.Bársony J, Lakatos P, Földes J, Fehér T.
    Twelve hypothyroid subjects, 13 healthy and 12 healthy women with a slight deficiency of vitamin D were studied to distinguish seasonal changes from the thyroxine-dependent ones. Serum 25-hydroxyvitamin D levels of hypothyroid patients were lower than those of healthy individuals when the sera were obtained in the autumn. In hypothyroid patients a single oral dose of 100,000 IU vitamin D3 resulted in a smaller increase in 25-hydroxyvitamin D concentration than in controls having subclinical exogenous vitamin D deficiency. Substitution therapy with thyroid hormone, started in our study always in autumn, increased the 25-hydroxyvitamin D concentration in hypothyroid patients, which was opposite to the autumn-to-spring variation of this hormone observed in healthy controls. The increase of 25-hydroxyvitamin D, dehydroepiandrosterone and its sulphate values following substitution therapy in the hypothyroid patients may indicate that thyroid hormone(s) is (are) involved in the regulation of steroid hormone synthesis.

    PMID: 3024434 [PubMed - indexed for MEDLINE]

  • g

    12/23/2007 9:32:00 PM |

    This is very hopeful...Vitamin D3 stalls thyroid cancer, one case report:

    Endocr J. 2005 Oct;52(5):613-6. Links
    Vitamin D3 treatment for locally advanced thyroid cancer: a case report.Morishita M, Ohtsuru A, Kumagai A, Namba H, Sato N, Hayashi T, Yamashita S.
    Department of Molecular Medicine, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Japan.

    There are many intricacies in the surgical treatment of locally advanced thyroid cancer, including the medical management of the remaining functional organ and any cosmetic impairments, which are sometimes very difficult to manage and eventually carry a relatively high morbidity and mortality. Here, we report on a case of a 65-year-old female with an extremely locally-advanced thyroid cancer involving both lobes of the thyroid, blood vessels, trachea and esophagus. Despite the severity of her condition, oral administration of vitamin D3 (alphacalcido) has stalled both the tumor growth and further increases of serum thyroglobulin (Tg) level, and has led to a good preservation of quality of life for the last two years. Several reports have previously demonstrated the efficacy of vitamin D3 to inhibit the proliferation of thyroid cancer cell lines in vitro, but clinical evidence has been limited so far. Therefore, this case report provides important evidence for the effectiveness of vitamin D3 therapy against advanced thyroid cancers.

    PMID: 16284441 [PubMed - indexed for MEDLINE]

  • g

    12/23/2007 9:42:00 PM |

    Another good story... 3mon old child with depressed thyroid function, CHF and profound Vitamin D deficiency in Oslo, Norway -- corrected with a Vit D analogue:

    Acta Paediatr. 1995 Jan;84(1):106-8
    Congestive heart failure caused by vitamin D deficiency?Brunvand L, Hågå P, Tangsrud SE, Haug E.
    Department of Paediatrics, Ullevål Hospital, Oslo, Norway.

    We describe a child, 3.5 months old, with severe vitamin D deficiency, profound hypocalcaemia, hyperphosphataemia, dilated left ventricle, severely reduced myocardial contractility and congestive heart failure. She also had depressed thyroid function with subnormal thyroxine and non-detectable serum thyrotropin (TSH) levels. The child promptly responded to calcium infusions, conventional anticongestive therapy and calcitriol. She is now 3 years old and received no medication. Myocardial function is normal but she has motor delay. We believe that her transitory congestive heart failure was caused by severe vitamin D deficiency with profound hypocalcaemia.

    PMID: 7734890 [PubMed - indexed for MEDLINE]

  • Dr. Davis

    12/23/2007 11:31:00 PM |

    Thanks, Marilyn. You're absolutely right.

    In all honesty, I virtually never use cod liver oil, but for some reason some people gravitate towards it, perhaps since they took it as children.

  • Jerome

    12/24/2007 1:55:00 PM |

    I went to a local vitamin supplier yesterday to get some Vitamin D after reading your blog, which is most interesting I might add.  At this store they had Vitamin D2 and D3 but no D1.  Is there such a thing (D1) and which is the one I should be taking to benefit as suggested in the blog?

  • Dr. Davis

    12/24/2007 4:59:00 PM |

    Hi, Jerome--

    Vitamin D3 is the only form I recommend. In my view, vitamin D2 is a worthless scam, whether it's in milk, a multivitamin, or a prescription product. I've never heard of vit D1.

  • jpatti

    12/24/2007 4:59:00 PM |

    I liked the *idea* of cod liver oil, as it would replace both fish oil and vitamin D tablets - a total of 8 pills in my 26-pill regimen.

    I bought what was supposed to be one of the best tasting ones and... it made me retch.  It also sort of tingles in your mouth.  And because it's oily, you can't rinse it out of your mouth.  It's just icky.

    I gave some to the cats, figuring it would be a healthy snack for them... and all four of them refused it.

    If someone can get it down, I think it's great stuff.  For me, I'll stick to the extra 8 pills...

  • Sue

    12/25/2007 2:20:00 AM |

    Thanks for all the helpful comments.  I've got cod liver oil in the fridge so I think I will use it up and then get D3 capsules.
    I take the cod liver oil with lemon juice.  I put the cod-liver oil in a little shot glass and squeeze some fresh lemon into the shot glass aswell and drink it in one swoop.  I then wash it down with some water with fresh lemon squeezed into it.  Gets rid of some of the icky fishy taste. The lemon also helps with digesting the fat.

  • cheron

    12/27/2007 7:19:00 AM |

    I wouldn't necessarily be afraid of the A, as we can be deficient in the A as well.  Perhaps alternating between A-containing and A-less forms of D supplements would work.  That way you get a vacation from the A periodically.

    As for surviving the fish taste...try following it up with a bite of something else that's strong tasting and contains fat, like cured olives or a tuna salad sandwich.

  • Anonymous

    1/1/2008 11:37:00 AM |

    Hi Dr. Davis,

    Have you seen literature making a connection to the plaque linked to Alzheimer's disease with the plaque responsible for heart disease?  I was asked this question by a distant cousin yesterday that wondered if the supplements recommended for TYP ,like vitamin D and K2, could help prevent those at risk for Alzheimer's (his grandmother, and mother both came down with Alzheimer's)

  • Dr. Davis

    1/1/2008 2:37:00 PM |

    No, sorry, they are two completely unrelated phenomena, despite the use of the word "plaque" to describe both.

  • MarilynMann

    1/1/2008 11:31:00 PM |

    Fish oil benefits
    Medical Research News
    Published: Sunday, 30-Dec-2007  

    It's good news that we are living longer, but bad news that the longer we live, the better our odds of developing late-onset Alzheimer's disease.
    Many Alzheimer's researchers have long touted fish oil, by pill or diet, as an accessible and inexpensive "weapon" that may delay or prevent this debilitating disease. Now, UCLA scientists have confirmed that fish oil is indeed a deterrent against Alzheimer's, and they have identified the reasons why.

    Reporting in the current issue of the Journal of Neuroscience, now online, Greg Cole, professor of medicine and neurology at the David Geffen School of Medicine at UCLA and associate director of UCLA's Alzheimer Disease Research Center, and his colleagues report that the omega-3 fatty acid docosahexaenoic acid (DHA) found in fish oil increases the production of LR11, a protein that is found at reduced levels in Alzheimer's patients and which is known to destroy the protein that forms the "plaques" associated with the disease.

    The plaques are deposits of a protein called beta amyloid that is thought to be toxic to neurons in the brain, leading to Alzheimer's. Since having high levels of LR11 prevents the toxic plaques from being made, low levels in patients are believed to be a factor in causing the disease.

    Alzheimer's is a debilitating neurodegenerative disease that causes memory loss, dementia, personality change and ultimately death. The national Alzheimer's Association estimates that 5.1 million Americans are currently afflicted with the disease and predicts that the number may increase to between 11 million and 16 million people by the year 2050.

    The researchers examined the effects of fish oil, or its component DHA, in multiple biological systems and administered the oil or fatty acid by diet and by adding it directly to neurons grown in the laboratory.

    "We found that even low doses of DHA increased the levels of LR11 in rat neurons, while dietary DHA increased LR11 in brains of rats or older mice that had been genetically altered to develop Alzheimer's disease," said Cole, who is also associate director of the Geriatric Research Center at the Veterans Affairs Medical Center.

    To show that the benefits of DHA were not limited to nonhuman animal cells, the researchers also confirmed a direct impact of DHA on human neuronal cells in culture as well. Thus, high levels of DHA leading to abundant LR11 seem to protect against Alzheimer's, Cole said, while low LR11 levels lead to formation of the amyloid plaques.

    Fish oil and its key ingredient, omega-3 fatty acids (found in fatty fish like salmon), have been a mainstay of alternative health practitioners for years and have been endorsed by the American Heart Association to reduce the risk of cardiovascular disease.

    Fatty acids like DHA are considered "essential" fatty acids because the body cannot make them from other sources and must obtain them through diet. Years of research have shown that DHA is the most abundant essential fatty acid in the brain, Cole said, and that it is critical to fetal and infant brain development. Studies have also linked low levels of DHA in the brain to cognitive impairment and have shown that lower levels may increase oxidative stress in the brains of Alzheimer's patients.

    Based on the positive results, the National Institutes of Health is currently conducting a large-scale clinical trial with DHA in patients with established Alzheimer's disease. For those patients, Cole said, it may be too late in the disease's progression for DHA to have much effect. But he is hopeful that the NIH will conduct a large-scale prevention clinical trial using fish oil at the earliest stages of the disease - particularly because it is unlikely that a pharmaceutical company will do so, since fish oil in pill form is readily available and inexpensive.

    Still to be determined, he said, "is what the optimal dose should be. It could be that a smaller amount might be helpful, especially in a place like the south of France, where people are already on a Mediterranean diet."

    Here in the United States, though, where fish consumption is not very high, the dose may need to be higher.

    "There's a deficiency of DHA to begin with," Cole said, "and this may contribute to the low LR11 seen in many Alzheimer's patients."

    http://www.ucla.edu/

    This is for the person asking about Alzheimer's.

    Marilyn
      




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  • Anonymous

    1/2/2008 6:43:00 PM |

    Hi Marilyn,

    Thanks for sharing the great information on fish oil/DHA!  I'm going to pass this on to my relative.

  • J. Michael

    1/3/2008 2:07:00 PM |

    It is rather difficult to find good D3-sources in Europe. Swanson's seems to be available; gelatine capsules although with a white powder inside. Are they any good?

  • Dr. Davis

    1/3/2008 9:08:00 PM |

    I do not advocate use of powder preparations of vit D. The absorption is simply too erratic. oil-based gelcaps are best.

  • moblogs

    1/4/2008 1:25:00 PM |

    I wonder what you think of this report? http://www.eurekalert.org/pub_releases/2008-01/bu-vdi010208.php I'm guessing that this is probably Hollick's idea of infiltration - get them to at least accept profitable D2 more before winning them over with D2.

    Also, last year I was prescribed 400IU of D2 which raised my 10nmol/L to 21nmol/L; in realising this is inadequate what would you recommend is a good plan for me?

  • Dr. Davis

    1/4/2008 1:35:00 PM |

    I don't know what to make of Holick's study. He is a source of reliable observations. However, his experience is dramatically different from my experience and that of many others. I have seen D2 have no effect whatsoever repeatedly. I had one woman who had been taking 50,000 units D2 per day have a blood level of D3 of 4 ng/ml.

    Most of my patients take somwhere in the 4000-6000 units per day of vit D3 to generate a blood level of 50-60 ng/ml.

  • Anonymous

    1/4/2008 4:35:00 PM |

    I saw the study about the vitamin D2 being just as good as D3 also.  Here is the link I read: http://www.nutraingredients.com/news/ng.asp?n=82331-vitamin-d-cholecalciferol-ergocalciferolI thought the article was interesting, until I read the part of the company that made the softgels.  I'd question  what where the Q/C of the content? Did an independent lab test the softgels?

  • Dr. Davis

    1/5/2008 1:52:00 AM |

    Excellent point.

    To me, there is absolutely no reason to take vit D2, given the uncertainty. It is not cheaper, more effective, nor more available. It may, however, be more profitable for a drug company. D3 is the human form; D2 is the plant form.

    Is there any reason at all to take D2? I don't think there is.

  • g

    1/7/2008 12:29:00 AM |

    Thanks for the information on Alzheimer's (AD) known now as 'Type 3 Diabetes.' It's conjectured that profound Insulin Resistance in the brain occurs prior to amyloid development in AD patients.  The brain can only use two types of fuel -- ketones (ie like during starvation) and glucose.  There appears to be a problem with excessive glucose.  Some neurobiologist experts believe a mildly ketotic diet may be beneficial for preventing this type of insulin resistance.

    Many benefits in recent studies have shown that fish oil significantly decreases IR associated with Type 2 Diabetes, NAFLD (a precursor to diabetes and believed to be a new indicator for Metabolic Syndrome, non-alcoholic fatty liver dz) and even cancers -- including prostate (shown by Vieth) and glioblastoma -- a rare malignant brain cancer -- thought to be incurable but now being 'cured' with fish oil (and tamoxifen, etc cocktail).

    Thanks ! !  g

  • g

    1/7/2008 4:36:00 PM |

    sorry -- Vieth is in vitro data -- don't know if in vivo data exists yet

  • Anonymous

    1/8/2008 12:23:00 PM |

    Seems word is leaking into the mainstream press about vitamin D.  Last night NBC Nightly News ran an article about the connection between low vitamin D levels and increased risk for heart disease.

  • Paul Kelly - 95.1 WAYV

    1/8/2008 7:28:00 PM |

    Hi Dr. Davis,

    I know that you recommend oil-based / gel caps for Vitamin D as opposed to tablets. Does the same hold true for daily multi-vitamins? Is a capsule and a gelcap the same thing?

  • Renee

    1/8/2008 8:57:00 PM |

    Wow another sickness that not enough Vitamin D is contributed to.  I just read an article at Here Comes The Sun talking about ways you can intake more Vitamin D.  Check it out.

  • Dr. Davis

    1/9/2008 3:33:00 AM |

    Paul--
    Vit D gelcaps contain oil. Gelcaps are capsules. However, not all capsules are gelcaps; some contain powder.

    Oil-based vitamins like A, D, and E are best taken as an oil. The D, for instance, in your multivitamin probably doesn't work at all, or absorption is erratic.

    Gelcaps are no more expensive, so why bother with tablet or powder forms?

  • moblogs

    1/21/2008 11:54:00 AM |

    Just wondered what your opinion on this anti-D report is? http://www.prweb.com/releases/2008/1/prweb639651.htm

    For what it's worth, I think this guy is going too far. His Marshall Protocol might be entertainable for those with certain autoimmune diseases, but saying D is bad for everyone based on his *personal* model seems nuts. Furthermore, his basic assumption is that everyone with low D 'is' ill, rather than has the potential to. And yet we know treating D in associated illness restores health.

    Would this guy withhold blood because a bullet causes bleeding? No wonder he's not an MD.

  • Dr. Davis

    1/21/2008 1:05:00 PM |

    Is this guy from the same planet?

    I've witnessed such extraordinary effects of vitamin D replacement that, for me, there is no turning back. Thus far, the effects of vitamin D replacement have paralleled the effects of sun exposure (except for the tan, of course).

    For every new idea, there will always be those who protest. Some have validity, some are plain kooks.

  • Anonymous

    1/24/2008 3:40:00 AM |

    Dear Dr. Davis,

    Thank you for your support of Vitamin D. I recently was tested and found to have a level of 37. I do have a question or two, though. I was on the mega-dose (50000IU twice a week for four weeks).

    I am now on 2000IU per day (just started this past Sunday). I have all of the Metabolic Syndrome symptoms except the high glucose (my last fasting was 81).

    How long do you think I should continue on this does before I have my level checked again? And how long before I would start to see results?

    My doctor seems very concerned about my CRP (3.1), and I'm really hoping that this vit d. regime helps.
    Thank you.

  • Dr. Davis

    1/24/2008 12:50:00 PM |

    Unfortunately, the "mega-dose" you refer to probably yielding nothing--it was probably vitamin D2 (ergocalciferol). In my experience, this synthetic form fails to be converted to the active form in humans, D3.

    We wait at least 4 weeks before checking a blood level, ideally 8 weeks.

  • Linda

    7/20/2009 7:30:21 PM |

    Just found out that I have
    vitamin D deficiency.  I have
    neuropathy, muscle weakness
    and arthritis.
    I hope taking the 50,000 units
    three times a week helps.
    We must certainly need our D,
    I'm proof.

  • Anonymous

    1/16/2010 2:53:37 AM |

    I have been detected with high TSH levels - 6 (the thyroid hormones are within range)and low Vit D - 25.
    Additionally, my cholesterol is 223 (good one is 81).
    I also seem to be getting ovarian cysts.
    Is all this related?

  • Anonymous

    2/15/2010 1:20:25 PM |

    quite interesting post. I would love to follow you on twitter.

  • shaheel

    9/27/2010 1:00:12 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.

  • buy jeans

    11/3/2010 6:51:49 PM |

    In short, metabolic syndrome creates a metabolic mess that leads to dramatic increases in heart disease, vascular disease and stroke, and cancer. The medical community has been paying increasingly greater attention to this condition because of its booming prevalence and because of the big bucks invested in "education" by the manufacturers of the diabetes and pre-diabetes drugs, particularly makers of Actos and Avandia.

  • liposculpture guide

    1/31/2011 4:15:52 AM |

    Vitamin D is proving to be a very important and powerful influence on many of the facets of the metabolic syndrome. Because the metabolic syndrome increases the risk of diabetes and cardiovascular disease, an adequate vitamin D level in the body might be important in the prevention of these diseases.

  • robrob

    2/5/2011 6:42:42 PM |

    I was wondering can you have a genetic compenont against making enough vit d by the sun? I bask in the sun for hours (since I love it so much and I am drawn to it like postive charge does to negative charge) yet I am d deficient, I suffer terrible metabolic syndrome, the whole nine yards just short of type 2. my doctor calls me prediabetic.

    I have even improved my diet big time over the last 3 years. lower gi, lower sat fat, more veggies etc. omega 3 fish oil

    I never use sunscreen and I never burn. just a nice light brown tan.I keep this tan by the way almost the whole winter. I started to take a cal vita d mag supplement chewables and I drink whole milk with it to make sure I absorb them being fat soluable and all. I can't expose my belly for more than a few minutes that will burn. ouch!

    being obese I am sure whatever cal vita d I take is going to end up in storage hoarding it an all. what can I do? I now drink more whole milk, eat organic bacon per suggestion from article the obesity epidemic is metabolic syndrome a nutritional deficiency. by stephanic seneff. real nice lady by the way.

    anyway slowly after implementing her suggestions my fasting hypoglycemic especially at night has improved, i don't run to the bathroom like i used to, I am more relaxed too. I have more energy, all this is a slow process not overnight. over many months.

    I don't have to eat at 3 in the morning anymore because of getting super hungry, nervous sweaty etc.

    but I still suffer some of the symptoms just not as severe. is there anything else I can do to speed up the improvments in mets?

    reduced cal diets do not work I get to hungry can't sleep and lose all energy. even a slight reduction which I have done makes me to hungry to sleep at night. or forces me up to eat after a couple of hours of sleep.

    forcing my body to get by on less caloires is not an option. (losing weight is always touted by my doctor to cure mets but mets was caused by my dieting history) I have lost hundreds of pounds over my 35 dieting history.

    I would like to hear any suggestions you may have. my doctor keeps pushing weight loss but that is what got me like this in the first place.

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All posts by william-davis

Cholesterol follies

Rudy is a 59-year old man. He's had three heart catheterizations, two of which resulted in stent implantations. Obviously, Rudy should be the beneciary of a prevention program.

His basic cholesterol values:

Total cholesterol 164 mg/dl--pretty good, it seems.

LDL cholesterol 111 mg/dl--Wow! Not too bad.

HDL cholesterol 23 mg/dl--Uh oh, that's not too good.

Triglycerides 148 mg/dl--By national (NCEP ATP-III) guidelines, triglycerides of 150 mg/dl and below fall within the desirable range.


So we're left with an apparently isolated low HDL cholesterol, nothing more. On the surface, it doesn't seem all that bad.

Of course, we need to keep in mind that this pattern landed Rudy in the hospital on several occasions and prompted several procedures.

Should we rely on these results? How about Rudy's lipoproteins?

Here they are (NMR; Liposcience):

LDL particle number 2139 nmol/l--Representing an effective LDL of 213--over 100 mg higher than the standard value (above) suggests.

Small LDL particles 2139 nmol/l--In other words, 100% of all Rudy's LDL particles are small. (Thus, weight-based measures of LDL cholesterol fail to tell us that he has too many small particles.)

Large HDL 0 (zero) mg/dl--Rudy has virtually no functional HDL particles.


If we had relied only on Rudy's standard cholesterol values, we would have focused on raising HDL. However, lipoprotein analysis uncovered a smorgasbord of additional severe patterns. The high LDL particle number comprised 100% of small particles is especially concerning.

Truly, conventional cholesterol testing is a fool's game, one that time and again fails to fully uncover or predict risk for heart disease. One look at Rudy's lipoproteins and it becomes immediately obvious: This man is at high risk for heart disease and the causes are clear.

Of course, many physicians and insurance companies argue that the added information provided by this portion of the lipoprotein test added around $70 more to the expense.

When you see results like this, is there even a choice?

Equal calories, different effects

A great study was just published in the Journal of the American College of Cardiology:

Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects.

88 obese adults with metabolic syndrome were placed on either of two diets:

1) A very low-carbohydrate, high-fat diet (VLCHF): 4% calories from carbohydrates (truly low-carb); 35% protein; 61% fat, of which 20% were saturated. In the first 8 weeks, carbohydrate intake was severely limited to <20 grams per day, then <40 grams per day thereafter.

2) A high-carbohydrate, low-fat diet (HCLF): 46% calories from carbohydrates; 24% protein; 30% total fat, of which <8% were saturated.

Both diets were equal in calories (around 1400 calories per day--rather restrictive) and participants were maintained on the program for six months.

At the end of the six month period, participants on the VLCHF diet lost 26.4 lb, those on the HCLF diet 22.2 lbs (though the difference did not reach statistical significance). Thus, both approaches were spectacularly successful at weight loss.

Surprisingly, blood pressure, blood sugar, insulin and insulin sensitivity (a measure called HOMA) were all improved with both diets equally. Thus, these measures seemed to respond more to weight loss and less to the food composition.

Lipids differed between the two diets, however:


VLCHF:
Total cholesterol: initial 208.4 mg/dl final 207.7 mg/dl

LDL: initial 125 mg/dl final 123 mg/dl

HDL: initial 55 mg/dl final 64.5 mg/dl

Triglycerides: initial 144 mg/dl final 74 mg/dl

Apoprotein B: initial 98 mg/dl final 96 mg/dl


HCLF
Total cholesterol: initial 208.4 mg/dl final 187.5 mg/dl

LDL: initial 126 mg/dl final 108 mg/dl

HDL: initial 51 mg/dl final 54.5 mg/dl

Triglycerides: initial 157.6 mg/dl final 111 mg/dl

Apoprotein B: initial 100 mg/dl final 95 mg/dl


Some interesting differences became apparent:
--The VLCHF diet more effectively reduced triglycerides and raised HDL.
--The HCLF diet more effectively reduced total and LDL.
--There was no difference in Apo B (no statistical difference).

The investigators also made the observation that individual responsiveness to the diets differed substantially. They concluded that both diets appeared to exert no adverse effect on any of the parameters measured, both were approximately equally effective in weight loss with slight advantage with the carbohydrate restricted diet, and that lipid effects were indeed somewhat different.


What lessons can we learn from this study? I would propose/extrapolate several:

When calories are severely restricted, the composition of diet may be less important. However, when calories are not so severely restricted, then composition may assume a larger role. When calories are unrestricted, I would propose that the carbohydrate restriction approach may yield larger effects on weight loss and on lipids when compared to a low-fat diet.

The changes in total cholesterol are virtually meaningless. Part of the reason that it didn't drop with the VLCHF diet is that HDL cholesterol increased. In other words, total cholesterol = LDL + HDL + trig/5. A rise in HDL raises total cholesterol.

Despite no change in Apo B, if NMR lipoprotein analysis had been performed (or other assessment of LDL particle size made), then there would almost certainly have seen a dramatic shift from undesirable small LDL to less harmful large LDL particles on the VLCHF diet, less change on the HCLF diet.

The lack of restriction of saturated fat in the VLCHF that failed to yield adverse effects is interesting. It would be conssistent with the re-analysis of saturated fat as not-the-villain-we thought-it-was put forward by people like Gary Taubes (Good Calories, Bad Calories).

In the Track Your Plaque experience, small LDL is among the most important measures of all for coronary plaque reversal and control. Unfortunately, although this study was well designed and does add to the developing scientific exploration of diet, it doesn't add to our insight into small LDL effects. But if I had to make a choice, I'd choose the low-carbohydrate, high-fat approach for overall benefit.

Is skinny necessary for reversal?

Nothing we do in the Track Your Plaque program guarantees that coronary atherosclerotic plaque or your heart scan score is reduced or reversed.



But everything we do weighs the odds in your favor of successfully achieving reversal: correction of lipoprotein patterns, uncovering hidden patterns like Lp(a), vitamin D, being optimistic--it all tips the scales in your favor.

But how necessary is it to be skinny, meaning somewhere near your ideal weight?

It is important, but not as important as it used to be. Let me explain.

I used to tell people that plaque would not regress unless ideal weight was achieved and all the parameters of abdominal obesity and metabolic syndrome were corrected. This includes blood pressure, blood sugar, low HDL, small LDL, high triglycerides, and high c-reactive protein. Curiously, though, as we've gotten better and better at reducing coronary calcium scores, I've been finding that complete correction of all parameters, including achieving ideal weight, don't seem to be as necessary to achieve plaque reversal.

I almost hate to say this, but I've even witnessed significant drops in heart scan scores in people with body mass indexes (BMI) of 30--obese.

The necessary change doesn't seem to be weight, per se, but the consequences of weight. In other words, if you remain overweight, but blood sugar, HDL, small LDL, etc. have shown substantial improvement, then reversal is still achievable.

Then is it okay to be fat or overweight?

Reducing weight to ideal weight does indeed tip the scales in your favor, since it represents an observable, perceptible measure of all associated patterns. Dropping weight can also minimize the need for efforts to correct the consequences of overweight--you might need less niacin, fish oil, exercise, blood pressure medication, etc. to succeed at plaque reversal. Achieving ideal weight may also provide benefits like reduced risk of cancers and degenerative diseases of the hips and knees. But, to my recent surprise over the last two years, achieving ideal weight is not an absolute requirement to achieve reversal.

This is contrary to what some others say. For instance, in an upcoming interview with Dr. Joel Fuhrman on the Track Your Plaque website, Dr. Fuhrman argues that 10% body fat for males, 22% body fat for females, accelerates plaque and symptom reversal. Dr. Fuhrman is author of Fasting and Eating for Health, Eat to Live, and a new upcoming 2-part book, Eat for Health, and proponent of high-nutrient vegetarian diets and fasting. Dr. Fuhrman has been helpful in teaching us some important lessons on how to apply periodic fasting to accelerate plaque reversal.

So, which is it, fat or skinny?

If given a choice (which everyone has), I'd choose skinny. But, provided all the parameters associated with overweight are corrected, then remaining overweight doesn't necessarily mean that you can't still succeed at plaque reversal.

If you are interested in knowing what your ideal weight is, there are a number of software calculators and tables available, including the HealthCentral.com calculator and the National Heart, Lung, and Blood Institute BMI Calculator.


Image courtesy Wikipedia.

Copyright William Davis, MD 2008

MESA Study: Track Your Plaque-Lite?

The long-awaited data analyses from the Multi-Ethnic Study of Atherosclerosis (MESA) are finally making it to press.

The MESA Study is an enormously ambitious and important study of 6800 people, 45 to 84 years old, that includes white, black, Hispanic, and Chinese participants from six communities around the U.S. (Forsyth County, NC; Northern Manhattan and the Bronx, NY; Baltimore and Baltimore County, Md; St Paul, Minn; Chicago, Ill; and Los Angeles County, California.) Participants had no history of heart disease at enrollment. All underwent a heart scan (either EBT or multi-detector heart scans) at the start. It is therefore the largest prospective study involving heart scans ever performed. It is, not unexpectedly, yielding some fascinating observations relevant to the Track Your Plaque program. The MESA study is, incidentally, funded by the non-commercial, publicly-funded National Heart, Lung, and Blood Institute and is therefore presumably free of commercial bias.

Among the most recent publications is Risk factors for the progression of coronary artery calcification in asymptomatic subjects: Results from the Multi-Ethnic Study of Atherosclerosis (MESA) In this analysis of 5700 of the MESA participants, a repeat heart scan was obtained an average of 2.4 years after the first. Conventional risk factors for heart disease were obtained at the start (see below for details under Measurement of Covariates.)

After analyzing the data and risk factors assessed, such as age, sex, race, blood pressure, body mass index (BMI), presence of diabetes, blood sugar, and family history of heart disease, two questions were asked:

1) What risk factors predict heart scan scores?

2) What risk factors predict progression (i.e., increase) in heart scan scores?

(The second question is particularly relevant to us and the Track Your Plaque experience.)

The MESA analysis showed that essentially all the risk factors assessed correlated with both the initial heart scan score, as well as the rate of progression. No surprises here.

But the most eye-opening finding was that the conventional risk factors assessed explained only 12% of the variation and progression in heart scan scores (coefficient of determination, or R squared, = 0.12.) In other words:

--Conventional risk factors like LDL cholesterol, diabetes, and excess weight explain only a tiny fraction of why someone develops coronary atherosclerotic plaque as represented by a heart scan score.

--The great majority of risk for a high heart scan score remains unexplained by conventional risk factors.

--The great majority of risk for progressive increase in heart scan scores also remains unexplained by conventional risk factors.


In light of the MESA analysis, it's no surprise that strategies like reducing LDL cholesterol with statin drugs fails to prevent most heart attacks. It's no surprise that conventional prevention programs that talk about "knowing your numbers," eating a "balanced" or low-fat diet, etc., fail miserably to prevent the vast majority of heart attacks and heart procedures.

MESA confirms what we've been saying these past few years: If you want control over coronary heart disease, you won't find it in Lipitor, a low-fat diet, and other limited conventional notions of risk. Correction of conventional risk factors like cholesterol and blood pressure are, in a word, a failure. I wouldn't even call the conventional approach Track Your Plaque-Lite. They don't even come close.

If conventional risk factors can explain only 12% of the reason behind heart disease, we've got to look elsewhere to understand why you and I develop this process.



Measurement of Covariates
Information on demographics, smoking, medical conditions, and family history was collected by questionnaire at the initial examination. Height and weight were also measured at the baseline examination, and blood was drawn for measurements, including lipids, inflammation, fasting glucose, fibrinogen, and creatinine. Resting blood pressure was measured 3 times in the seated position, and the average of the last 2 measurements was used in the analysis. Medication use was determined by questionnaire. Additionally, the participant was asked to bring to the clinic containers for all medications used during the 2 weeks before the visit. The interviewer then recorded the name of each medication, the prescribed dose, and frequency of administration from the containers.


Copyright 2008 William Davis,MD

Risks for coronary disease 2008

According to conventional thinking, there are identifiable risks for coronary disease and heart attack. These risk factors are:

* smoking
* high blood pressure
* high blood cholesterol and excessive saturated fat intake
* diabetes
* being overweight or obese
* physical inactivity

I'd agree with all the factors listed (though I would argue about the importance of high blood cholesterol and saturated fat; they are not as important as commonly made to be.)

Is the list complete?

From the unique perspectives gained in the Track Your Plaque program, I'd offer a significantly different list. Trying to stop or reduce coronary atherosclerotic plaque and heart scan scores makes you a whole lot smarter about what works and what doesn't work.

So, in addition to the risk factors listed above, I would add:

* Small LDL particles--Lots of small LDL particles is MORE important than high LDL.
* High blood pressure with exercise
* Excessive wheat intake and other processed carbohydrates--An issue of explosive importance today. Wheat creates large numbers of small LDL particles, among other adverse effects.
* Vitamin D deficiency--Among the most powerful risks I know of. It belongs at the top of the list.
* Vitamin K2 deficiency
* Low HDL cholesterol
* Blood sugar >100 mg/dl
* High triglycerides--While some argue about whether triglycerides are a risk that behaves independently of patterns like low HDL, they are neglecting the potent force of this risk. Sure, it occurs in tandem with low HDL (usually, though not always), but it is a factor that can leave you with risk even when HDL is raised to healthy levels.
* Lipoprotein(a)--It is eminently, positively crystal clear that lipoprotein(a) is a powerful risk for heart disease. The lack of a profitable treatment keeps it hidden in the shadows.
* Pessimism--Be happy, do better. Be a constantly angry, frustrated, complaining sourpuss and you are more likely to succumb to heart disease, cancer, or other undesirable fate.


These are the risk factors that we address through the Track Your Plaque program, a list that yields a far more powerful and comprehensive approach to control over coronary plaque/atherosclerosis, sufficient to achieve reversal in many (though not in all) instances.

I view the list of conventional risk factors as a "no brainer" list. Sure, smoking is a risk factor. But there are virtually no smokers in the Track Your Plaque program. If you smoke, you clearly don't care enough to engage in a high-intensity prevention program like this.

Saturated fat? Perhaps, but the battlefield of heart disease is riddled with the bodies of those who employed this as their sole strategy and failed catastrophically.

Diabetes, hypertension, and overweight all represent a continuum of risk; the solutions offered in the conventional scheme (i.e., low-fat diet, etc.) make these patterns worse, not better.

The conventional response to heart disease risk is trapped somewhere in 1973 and has not changed in over 30 years. Heart disease continues to be a growth industry for hospitals and the pharmaceutical and medical device industries. The "official" organizations continue to deliver an antiquated, outdated message.

If you want heart disease, follow the American Heart Association diet. If you want established heart disease to get worse, follow the American Heart Association diet. If you want diabetes or, if you already have diabetes or pre-diabetes, if you want it to worsen and develop organ damage (eyes, kidneys, nervous system, etc.), then follow the American Diabetes Association diet. USDA food pyramid? Loosen your belt!

The list of conventional risk factors for heart disease is woefully inadequate. If that is as far as your prevention program takes you, heart disease will not be controlled or prevented. At best, it might be slowed; at worst--and more likely--it might be accelerated.

Food sources of vitamin K2



Vitamin K2 is emerging as an exciting player in the control and possible regression of coronary atherosclerotic plaque. Only about 10% of dietary vitamin K intake is in the K2 form, the other 90% being the more common K1.

The ideal source of K2 is natto, the unpalatable, gooey, slimy mass of fermented soybeans that Japanese eat and has been held responsible for substantial decreases in osteoporosis and bone fractures of aging. Natto has an ammonia-like bouquet, in addition to its phlegmy consistency that makes it virtually inedible to anyone but native Japanese.

I say that the conversation on vitamin K2 is emerging because of a number of uncertainties: What form of vitamin K2 is best (so-called MK-4 vs. MK7 vs. MK-9, all of which vary in structure and duration of action in human blood)? What dose is required for bone benefits vs. other benefits outside of bone health? Why would humans have developed a need for a nutrient that is created through fermentation with only small quantities in meats and other non-fermented foods?

Much of the developing research on vit K2 is coming from the laboratories of Drs. Vermeer, Geleijnse, and Schurgers at the University of Maastricht in the Netherlands, along with several laboratories in Japan, the champions of K2.

MK-7 and MK-8,9,10 come from bacterial fermentation, whether in natto, cheese, or in your intestinal tract; MK-4 is naturally synthesized by animals from vitamin K1. While natto is the richest source of the MK-7 form, egg yolks and fermented cheeses are the richest sources of the MK-4 form.

Chicken contains about 8 mcg MK-4 per 3 1/2 oz serving; beef contains about 1 mcg. Egg yolks contain 31 mcg MK-4 per 3 1/2 oz serving (app. 6 raw yolks). Hard cheeses contain about 5 mcg MK-4 per 3 1/2 oz serving, about 70 mcg of MK-8,9; soft cheeses contain about 30% less. Natto contains about 1000 mcg of MK-7, 84 mcg MK-8, and no MK-4 per 3 1/2 oz serving.











Feta cheese

Thanks to the research efforts of the Dutch and Japanese groups, several phenomena surrounding vitamin K2 are clear, even well-established fact:

--Vitamin K2 supplementation (via frequent natto consumption or pharmaceutical doses of K2) substantially improves bone health. While K2 by itself exerts significant bone density/strength increasing properties in dozens of studies, when combined with other bone health-promoting agents (e.g., vitamin D3, prescription drugs like Fosamax and calcitonin), an exaggerated synergy of bone health-promoting effects develop.



--The MK-4 form of vitamin K2 is short-lived, lasting only 3-4 hours in the body. The MK-7 form, in contrast, the form in natto, lasts several days. MK-7 and MK-8-10 are extremely well absorbed, virtually complete.

--Bone health benefits have been shown for both the MK-7 and MK-4 forms.

--Coumadin (warfarin) blocks all forms of vitamin K.





Interestingly, farm-raised meats and eggs do not differ from factory farm-raised foods in K2 content. (But please do not regard this as an endorsement of factory farm foods.)

Another interesting fact: Since mammals synthesize a small quantity of Vit K2 forms from vitamin K1, then eating lots of green vegetables should provide substrate for some quantity of K2 conversion. However, work by Schurgers et al have shown that K1 absorption is poor, no more than 10%, but increases significantly when vegetables are eaten in the presence of oils. (Thus arguing that oils are meant to be part of the human diet. Does your olive oil or oil-based salad dressing represent fulfillment of some subconscious biologic imperative?)

If we believe the data of the Rotterdam Heart Study, then a threshold of 32.7 micrograms of K2 from cheese yields the reduction in cardiovascular events and aortic calcification.

It's all very, very interesting. My prediction is that abnormal (pathologic) calcium deposition will prove to be a basic process that parallels atherosclerotic plaque growth, and that manipulation of phenomena that impact on calcium depostion also impact on atherosclerotic plaque growth. Vitamins D3 and K2 provide potential potent means of at least partially normalizing these processes.

As the data matures, I am going to enjoy my gouda, Emmenthaler, Gruyere, and feta cheeses, along with a few egg yolks. I'm going to be certain to include healthy oils like olive and canola with my vegetables.


All images courtesy Wikipedia.

Copyright 2007 William Davis, MD

Track Your Plaque: Naughty or nice?



Among the many wonderful surprises we've had at Track Your Plaque this holiday season was a letter from Santa Claus himself!

It seems that Santa, like the rest of us, has been busy surfing the web for useful health information the last few months. He was struck with this curious discussion we've been having about "wheat belly" and all the unhealthy consequences of wheat products in our diet.

He writes:

"I wouldn't have believed it myself, except that my waist size has grown four inches in as many years. Sure, I'm known for my healthy girth, but now even Mrs. Claus calls me fat!

"I was open to new ideas when I came across this crazy discussion about eliminating wheat from your diet. So I said, "What have I got to lose?" Well, four weeks later and 12 lbs lighter, I'm convinced. Now comes the tough part: I've got to deliver all the toys and resist all those cookies the children put out for me. I wonder if wheat makes reindeer fat, too?

"Anyway, thanks to your program I'm back to my old weight again. Doc says my blood sugar and blood pressure are also back down to normal. Thanks, Track Your Plaque! (You'll find something extra special under the tree this year.)"

And so it goes. I'm tempted to put Santa's testimonial on our homepage, but I think that may be tooting our own horn a bit too much.

Have a wonderful holiday!

Vitamin D: Treatment for metabolic syndrome?

Metabolic syndrome is that increasingly common collection of low HDL cholesterol, high triglycerides, high blood sugar, and high pressure that now afflicts nearly 1 in 4 adults, rapidly gaining ground to 1 in 3. Beyond these surface factors, metabolic syndrome also creates small LDL particles, VLDL, intermediate-density lipoproteins (IDL), increased imperceptible inflammation measured as higher c-reactive protein, and greater blood clotting tendencies. Metabolic syndrome is usually, though not always, associated with a big tummy ("beer belly," though I call it "wheat belly").

In short, metabolic syndrome creates a metabolic mess that leads to dramatic increases in heart disease, vascular disease and stroke, and cancer. The medical community has been paying increasingly greater attention to this condition because of its booming prevalence and because of the big bucks invested in "education" by the manufacturers of the diabetes and pre-diabetes drugs, particularly makers of Actos and Avandia.

But here's a curious observation:

Replacement of vitamin D to healthy levels (we aim for 50-60 ng/ml, or 125-150 nmol/l) yields:

--Higher HDL
--Lower triglycerides
--Lower blood sugar
--Reduced c-reactive protein
--Reduced blood pressure
--Reduced small LDL
--Enhanced sensitivity to insulin

(Whether blood clotting and effects on IDL should be added to this list is uncertain.)

It's obvious: Vitamin D is proving to be a very important and powerful corrective influence on many of the facets of the metabolic syndrome. In fact, I would go as far as saying that, side by side, vitamin D yields nearly the same effect as prescription drugs Actos and Avandia--without the extravagant cost (nearly $200 per month), leg swelling, congestive heart failure and heightened heart attack risk (with Avandia), and average 8 lb weight gain. Of course, vitamin D also provides benefits beyond metabolic syndrome like facilitation of coronary plaque regression, increased bone density, reduced arthritis, and reduced risk of several cancers.

You'd think that agencies like the American Diabetes Association (ADA) would be all over vitamin D like white on rice. Yet they remain curiously quiet about the entire issue. (That should come as no surprise to anyone familiar with the behavior and politics of this organization, the same outfit that has widely propagated the ADA diet, a program that accelerates diabetes and its complications. In my view, the ADA is an embarassment.)



For a really great story and video on vitamin D that includes a terrific interview with vitamin D guru and Track Your Plaque friend, California psychiatrist Dr. John Cannell, go to What's the Real Story on Vitamin D?. While the video will yield little new to readers of The Heart Scan Blog or Track Your Plaque members, it just feels really good to see a well-made, high-class video production echoing many of the things we've been talking about these past two years.

Appetite stimulants

Ever have days when you just can't seem to get enough to eat, your stomach gnawing just a hour after a meal? We all get them, some more than others. Other days, you can be content with a few simple foods and hunger is subdued, temptation easy to control.

Why such contrasts on different days?

A major part of the reason can be the presence of appetite stimulants, factors that trigger appetite beyond rational control. The list of common appetite stimulants includes:

--Sleep deprivation--A very important factor. Lack of sleep drives tremendous appetite, and often for the wrong foods (processed carbohydrates). I personally have experienced my most shamefully indulgent days when sleep-deprived. The solution is obvious: Sleep. Another factor that is based purely on personal observation is that of waking mid-phase. In other words, waking up while you're still enjoying the deeper phases of sleep (e.g., phase 3,4, or REM). This can oddly disrupt your day and your impulse control. I usually try and time sleep to increments of 90 minutes to coincide with the average duration of the full cycle of sleep. For example, 7 1/2 hours is better than 8 hours, since the extra half hour puts your square into a deeper sleep cycle.

--Excessive caffeine--Caffeine stimulates stomach acid. This triggers the impulse to eat . . . and eat and eat.













Image courtesy Wikipedia

--Aspirin and other anti-inflammatory agents--If you take aspirin (as many of our Track Your Plaquers do), then beware of the gastritis that can develop. Like excessive caffeine, it also triggers the impulse to eat, likely a protective mechanism, since food sops up excess acid. I ask patients to take periodic breaks from aspirin, e.g., a week off every two or three months, to allow the stomach to heal. Alternatively, an occasional dose of acid-suppressing medication is a safe practice, e.g., Pepcid AC 10-20 mg; Prilosec 10-20 mg.

--Wheat-containing foods--Followers of The Heart Scan Blog know my feelings on this. Wheat is a potent appetite stimulant: Eat something containing wheat like a pretzel or whole wheat bagel, and you want more. You may want more immediately, or a little later when your blood sugar plunges after the wheat-driven insulin surge. Solution: Dump the wheat, one of the most unhealthy food groups around.

--Alcohol--Though perhaps not a direct appetite-stimulating effect, the loss of impulse-control with alcoholic drinks can lead to overindulgence, often in the worst foods. Just beware.

--Hanging around with heavy people. Remember peer pressure? It can be subliminal. People with poor eating habits provide the silent message that it's okay to yield to impulse, overeat, overindulge, and choose the wrong foods.

--Stress--Whether through cortisol stimulation or other means, stress triggers appetite in some people. If you experience this and must give in, reach for raw nuts or nuts, rather than wheat snacks or chips. The effect will be minimal, perhaps even beneficial, rather than the bloating, appetite-stimulating, fattening effect of crackers, chips, or pretzels. This may be the same phenomenon as taking prescription steroids like prednisone.

--Short dark days, long nights--In other words, winter. Though just an anecdotal observation, I am convinced that vitamin D supplementation is an effective antidote to this effect. The short, dark days just don't bother you as much, perhaps not at all, and there's no impulse for comfort foods.


How about appetite suppressants? In this list I would include 1) raw nuts--especially almonds, walnuts, pecans, and pistachios, the sort with a fibrous covering and rich in monounsaturates, 2) other sources of plentiful healthy oils, e.g, use more olive oil in your salad or add it to hummus for your veggie dip, 3) space-occupying fibers such as glucomannan, inulin (such as in Fiber Choice), and psyllium seed products. Counteracting the above appetite stimulants like sleep deprivation is, of course, important.

The coming wheat frenzy, otherwise known as the holidays, is an especially important time to be aware of these effects. Eat, drink, and be merry--but with rational impulse control not driven by subconscious appetite stimulants.

"Heart scans are experimental"

Let me warn you: This is a rant.

It is prompted by a 44-year old woman. She has a very serious lipoprotein disorder. Her family experiences heart attacks in their 40s and 50s. I asked for a heart scan. Her insurance companied denied it.

This is nothing new: heart scans, like mammograms, have not enjoyed reimbursement from most insurers despite the wealth of data and growing acceptance of this "mammogram" of the heart.

However, 10 minutes on the phone, and the "physician" (what well-meaning physician can do this kind of work for an insurance company is beyond me) advised me that, while CT heart scans for coronary calcium scoring are not covered, CT coronary angiograms are.

Now, I've been witnessing this trend ever since the big players in CT got involved in the game, namely Philips, Siemens, Toshiba, and GE. These are enormous companies with hundreds of billions of dollars in combined annual revenues. They, along with the lobbying power of cardiology organizations like the American College of Cardiology, have gotten behind CT coronary angiograms. This is most likely the explanation of why CT coronary angiograms have rather handily obtaining insurance reimbursement. Interestingly, the insurance company I was speaking to is known (notorious?) for very poor reimbursement practices.

A CT heart scan, when properly used, generates little revenue, a few hundred dollars to a scan center, barely enough to pay for a device that costs up to $2 million. However, CT coronary angiograms, in contrast, yield around $2000 per test. More importantly, they yield downstream revenues, since CT angiograms are performed as preludes to conventional heart catheterizations, angioplasty, stents, bypass surgery, etc. Now we're talking tens or hundreds of thousands of dollars revenue per test.

What puzzles me is that much of that increased cost comes out of the insurance company. Why would they support such tests if it exposes them to more costs? I'm not certain. It could be the greater pressures exerted by the big CT companies and powerful physician organizations. I seriously doubt that the insurance companies truly believe that heart scans for coronary calcium scoring are "experimental" while CT coronary angiograms are "proven." If all we did was compare the number of clinical studies that validate both tests, we'd find that the number of studies validating heart scans eclipses that of coronary angiograms several fold. Experimental? Hardly.

The smell of money by physicians eager to jump on the bandwagon of a new revenue-producing procedure is probably enough to have them lobby insurers successfully. In contrast, plain old heart scans just never garnered the kind of vigorous and vocal support, since nobody gets rich off of them.

If CT coronary angiograms are sufficiently revenue producing that my colleagues and the CT scanner manufacturers have managed to successfully lobby the health insurers, even one as financially "tight" as the one I spoke to today, well then I take that as testimony that money drives testing, as it does the behavior of hospitals, many of my colleagues, and can even force the hand of insurers.