Vitamin D Newsletter-Autism and Vitamin D

Although Dr. John Cannell's most recent Vitamin D Newsletter concerns the connection between autism and vitamin D, and has nothing to do with coronary plaque reversal, this fascinating discussion between a mother of an autistic boy and Dr. Cannell is so enlightening that I thought that it was still worth passing on.

I also feel very deeply for parents with autistic children, who I see struggle with the developmental difficulties their children encounter. (I even have several patients who are parents of 2 or 3 autistic children.)

As always, Dr. Cannell is at the cutting-edge of converting hard scientific information into practical use. You will note several points or questions raised:

1) Dr. Cannell advocates a powdered capsule form of vitamin D. In my experience, most powdered or tablet forms do not work. But some do. He apparently has success with the brand he specifies.

2) Are there vitamin D-receptor (VDR) genotypes that respond differently? Should there be different 25 (OH) vitamin D blood level targets for different VDR genotypes? Nobody knows yet, but it will be an important question to explore in the future.

3) Is heavy metal toxicity, at least in its milder forms, a surrogate for vitamin D deficiency? (Are chelationists unwittingly treating vitamin D deficiency?)

4) If this is a genuine association, and vitamin D replenishment exerts profound neurologic effects in autistic children, does a similar, though less marked effect, hold in non-autistic children? Will children perform better, learn more effectively, etc. with vitamin D supplementation to normal levels?

5) Vitamin A--Is vitamin A with vitamin D good or bad? This one I do not have an answer to. Reading the literature Dr. Cannell cites didn't help much. (Dr. BG--Any comments? Dr. BG is a vitamin A advocate.)


Perhaps, should the association between autism and vitamin D hold, it raises more questions than it settles. But, true to my experience with vitamin D, every day I stumble on some unique, fascinating effect, all beneficial. We continue to learn new lessons about vitamin D and Dr. Cannell's insights as a practicing psychiatrist deeply concerned with vitamin D issues have helped enormously.

(Sorry, but I did not copy the links to the literature Dr. Cannell cites. To obtain the links, go to the original Vitamin D Newsletter.)

The Vitamin D Newsletter
June 2008




This month we feature a remarkable series of letters from a mother of an autistic son who treated her child with vitamin D. It is the first case report in the medical literature suggesting vitamin D has a treatment effect in autism.

First, a brief case report and then a more detailed exchange of emails between the mother and me.

Case Report:

John is a seven-year old boy living in the northeastern U.S. with a long-standing diagnosis of autism. Symptoms include temper tantrums, repetitive self-stimulatory behavior, impaired language, mood swings, fear of being alone, toileting problems, dysbacteriosis, and impaired muscle strength. John spends a lot of time outdoors starting in the spring and his mother noticed a distinct seasonal variation in his symptoms in that he improved in the summer and regressed in the winter. A 25-hydroxy-vitamin D in April of 2008 was 25 ng/ml and obtained after John had begun to play outside. Due to the seasonality of John's symptoms the mother consulted me. I advised the mother to stop all products containing vitamin A including cod liver oil and begin John on 5,000 IU of vitamin D3 per day for two weeks followed by 2,000 IU per day in the form of powdered vitamin D dissolved in juice. Within a week of starting the vitamin D, John's language began to return and he was no longer as fearful of being alone. At the end of two weeks his language showed further improvement, he began to toilet himself, counted to 10 and knew the spelling of his name. After three weeks language continued to improve and some improvements were noted in his dysbacteriosis. After four weeks of vitamin D treatment, the mother noted improvements in muscle strength as well as continued improvements in language. A repeat 25-hydroxy-vitamin D is pending while John continues taking 2,000 IU of vitamin D per day.

Before you read the series of emails between the mother and me, I'd like to caution that this is only a case report of sorts and does not prove a treatment effect. Spontaneous remissions, while rare in autism, have been reported, thus the supplemental vitamin D may have had nothing to do with his improvement. If the response is due to vitamin D, there is no assurance it will prove lasting. I think it unlikely that older autistic children or individuals with severe autism will show these sorts of apparent improvements. Furthermore, autism is a multifactorial disease with strong genetic roots and it is highly unlikely that treatment of vitamin D deficiency in all autistic children will result in similar improvements. Finally, I did not examine this child, and I am relying on the child's mother to report both his condition and his apparent response to vitamin D treatment. However, the mother agreed to speak with the press about her son and allow for independent confirmation of the apparent treatment response.

Below are the emails, edited for brevity, clarity, and confidentiality.



Dear Dr. Cannell:

I am writing because I believe my son John is strongly affected by vitamin D and I need some advice. John is seven and autistic and weighs 50 pounds. We live in the northeastern part of the United States . He starts spending lots of time outside in May and continues until September. Every year, like clockwork, he has the same patterns of behavior and ability. After about six weeks of sun exposure, every July, he begins feeling much better, seems to be comfortable in his skin, does not have as much self-stimulatory behavior, can eat a variety of foods and has language. This past summer, he was using 14-word sentences. By the end of November, he can't even ask you for a cup of juice. He becomes more exclusive, has emotional highs and lows, has tantrums and is easily frustrated.

His 25(OH)D level on April 15th was 25 ng/ml but he had already been going out in the sun so his level must have been lower in the winter. I have had his genetics tested (Nutrigenomic) and he has mutations in his vitamin D receptors:

VDR Bsm/Taq ++
VDR Fok --
VDR Taq ++

My first question, does it sound like the changes in his behaviors and abilities could be caused by lack of vitamin D? Could you elaborate on the time it would take to get adequate amounts of vitamin D to start seeing positive results? For example, even if he starts going out in the sun in May, it's usually not until July that I see positive changes. Then would it take a month or two to go back to being deficient, thus explaining his 'regression' by the time November comes around. Secondly, I am looking at different forms of vitamin D therapy: a vitamin D lamp, vitamin D3 cream, or oral vitamin D. Can you tell me what might be the best form during the winter months?

Thank you very much for your time and attention.

Jane, Boston MA



Dear Jane:

Yes, it is possible your son's autism is related to vitamin D. Such seasonality has been reported before in autism, both in an individual and in autistic children at a summer camp. Although suggestive, such seasonality does not prove a vitamin D connection. Sun exposure, unless it is full body, takes several months to get vitamin D levels up. If sunblock or clothes are worn sun exposure will not get 25(OH)D levels much above 30 ng/ml. As far as the "mutations" you list, they are actually vitamin D receptor (VDR) polymorphisms and not referred to as mutations although all such changes occurred through mutations at some time in the past. VDR polymorphisms are simply the different structures of the vitamin D receptor that different people have and they are widely distributed. A pilot study of actual VDR receptor mutations did not detect VDR mutations in 24 autistic individuals but they did not assess for VDR polymorphisms. However, a highly significant association exists between one VDR polymorphism and larger head size. Mean head circumference is larger in autism.

Yan J, et al. Vitamin D receptor variants in 192 patients with schizophrenia and other psychiatric diseases. Neurosci Lett 2005;380(1-2):37-41.

Handoko HY, et al. Polymorphisms in the vitamin D receptor and their associations with risk of schizophrenia and selected anthropometric measures. Am J Hum Biol 2006;18(3):415-7.

Lainhart JE, et al. Head circumference and height in autism: a study by the Collaborative Program of Excellence in Autism. Am J Med Genet A 2006;140(21):2257-74.

Lainhart JE, et al. Macrocephaly in children and adults with autism. J Am Acad Child Adolesc Psychiatry 1997;36(2):282-90.

I emailed the world's foremost expert on VDR polymorphisms asking him about your son's polymorphisms and his reply, quite technical, is below.



Dear John:

I apologize for the delay in getting back to you regarding VDR polymorphisms. Initial studies by Eisman and coworkers many years ago suggested that several of the polymorphs identified above in the VDR gene (Bsm/Tag) correlated strongly with osteoporosis. Despite the hoopla, subsequent analyses by many different investigators did not really confirm these results, i.e. only a very modest (3%) correlation. This spawned multiple studies searching for correlations between VDR polymorph's and cancer, autoimmune disease and so forth. It is fair to say from all of these studies that the correlation is at best weak, and in most cases non-existent. Part of this may be due to the fact that the Bsm and Taq polymorphs are located in VDR gene introns and as a first approximation cannot affect the VDR protein's function. This is not an absolute statement, however, as our work is now showing that regulatory regions that control the VDR's expression are located within introns as well as upstream. Therefore the possibility exists that these polymorphs could affect expression, although we have not found these regions to contain enhancers yet. This is clearly where gene and disease studies are going. The only polymorph that could affect function is the Fok1 site, which we identified many years ago following our initial cloning and structural analysis of the human VDR gene. The presence of this site leads to the expression of a shorter VDR protein (424 aa) that is purported to have a slight increase in transcriptional activity (10%?) vs the large protein (427 aa). The above analysis suggests that this polymorph is absent, leading to production of the larger perhaps less active protein. On a single patient basis, it is really difficult to conclude anything regarding this finding. Indeed, despite large numbers of patients, the VDR polymorph have not really revealed any significant insight. Given the summer correlations, it is probably more likely that the individual is low in vitamin D3 in winter.

Sincerely,

Professor John Doe




Thus, one of your son's polymorphisms may have less functionality but that should be easily overcome by higher vitamin D levels. The first thing to do is stop all vitamin A, multivitamins containing vitamin A, or cod liver oil and start vitamin D. As you will see below, vitamin A antagonizes the action of vitamin D and he should have plenty of vitamin A if he eats colorful vegetables, colorful fruit, eggs and fortified oatmeal. As far as vitamin D, I think the easiest way to give vitamin D is powdered capsules, not a cream. You can open the capsule and put the powder in about anything, such as juice. To buy the capsules, go toBio Tech Pharmacal and buy both a bottle of the 5,000 and the 1,000 IU capsules. He should take one 5,000 IU capsule a day for two weeks then take 2,000 IU per day. After a month, go to the doctor and have another 25-hydroxy-vitamin D blood test. Do not let your doctor order a 1,25-dihydroxy-vitamin D as it will give you and your doctor false information about your son's vitamin D status. The other option is buying a Sperti vitamin D light. Daily use of the light on both sides of his trunk will raise levels fairly quickly but he should still have a 25(OH)D blood test every month to assure his levels rise to the mid level of normal ranges, about 70 ng/ml. Vitamin D is very safe. Your son would have to take more than 10,000 IU a day for more than a year to have any risk of toxicity. If he improves and his level is 50 ng/ml, the next question is would he improve even more if his level was 70 ng/ml? Some lifeguards have levels of 80-100 ng/ml; normal ranges in the labs in the USA are 30 -100 ng/ml (ideal ranges are 50 -100 ng/ml.) If you have any more questions, let me know. I certainly want to know how he is doing.

Sincerely,

John Cannell



Dear Dr. Cannell:

It has been one week on 5,000 IUs of vitamin D3 daily and already we're getting some language back! We haven't had original language since probably around the end of November. The only language we have had in the past five months has been verbal scripting. Today John has already told me "turn off the TV" and "clean up the water". This is all very exciting. Will it last? I will continue to keep you updated on progress and change in behavior. One more thing, all winter long he was afraid to be by himself anywhere. Now he is starting to be able to be in another room or outside by himself.

Thanks so much,

Jane



Dear Jane:

I can't tell you how happy I am for you. I suspect John will continue to improve. Do you have any parent rating scales or does his treating pediatrician have any objective rating scales? If you have before and after rating scales or his treating doctor does then it becomes important to track his progress on an objective measure. Jane, if you are a member of any autism discussion groups, you should post about this, including doses used. If your son's case is typical, then hundreds of thousands of autistic children may be helped with vitamin D.

John Cannell



Dear Dr. Cannell:

It has been two weeks on 5,000 IU per day and I want to inform you that we are having continued success with language. Continued in the sense that it is consistent, it wasn't just a one day fluke. In addition, he is taking himself to the bathroom; this is another thing that goes away in winter months. I usually have to catch him holding it in and then suggest he go, but now he is going completely by himself. In therapy last week, he started drawing again. He drew a bee and then ran around the room buzzing. His toileting is consistent with his therapists, not just mommy. Last night, I asked him to count to 10 for me and he did - quite enthusiastically. Then I said what does J-O-H-N spell? It took him a bit but then he said "John."

Unfortunately, the last scale taken was when he was 3 when he had his first developmental evaluation. But we do track behavior and language on a weekly basis. The forms we fill out give a good indication as to how he is doing.

I belong to a parent forum. It was created by a doctor named Amy Yasko. She's a PhD, a researcher, not a medical doctor. It was through her that I got John's genetics tested. She advocates vitamin D as being very crucial. I will post something on her forum for the parents there. However, if the parents on the forum are following her recommendations, they should be taking it already - 2000 IUs in winter and 1000 IUs in summer is her recommendation. I will post something on the forum to really emphasize how important vitamin D is.

Jane



Dear Jane:

I'm glad the improvements are continuing. I see Dr. Yasko recommends 10,000 IU of vitamin A/day as well as cod liver oil. I strongly disagree. Make sure your son is taking neither vitamin A nor cod liver oil. Rather, make sure he eats colored fruits and vegetables as well as fortified oatmeal. Vitamin A interferes with vitamin D's function, especially at the doses Dr. Yasko recommends.

Vitamin A antagonizes the action of vitamin D. In humans, even the vitamin A in a single serving of liver impairs vitamin D’s rapid intestinal calcium response. Furthermore, the consumption of preformed retinols, even in amounts consumed by many Americans in both multivitamins and cod liver oil appears to be causing low-grade, but widespread, bone toxicity, perhaps through its antagonism of vitamin D. In a recent dietary intake study, Kyungwon et al found high retinol intake completely thwarted vitamin D’s otherwise protective effect on distal colorectal adenoma and they found a clear relationship between vitamin D and vitamin A intakes as the women in the highest quintile of vitamin D intake also ingested almost 10,000 IU of retinols/day. As early as 1933, Hess et al warned about vitamin A consumption, concluding, “as to a requirement of thousands of units of vitamin A daily, the unquestionable answer is that this constitutes therapeutic absurdity, which, happily, will prove to be only a passing fad.”

Rohde CM, Deluca HF. All-trans retinoic acid antagonizes the action of calciferol and its active metabolite, 1,25-dihydroxycholecalciferol, in rats. J Nutr. 2005;135(7):1647-1652.

Johansson S, Melhus H. Vitamin A antagonizes calcium response to vitamin D in man. J Bone Miner Res. 2001;16(10):1899-1905.

Penniston KL, Tanumihardjo SA. The acute and chronic toxic effects of vitamin A. Am J Clin Nutr. 2006;83(2):191-201.

Oh K, Willett WC, Wu K, Fuchs CS, Giovannucci EL. Calcium and vitamin D intakes in relation to risk of distal colorectal adenoma in women. Am J Epidemiol. 2007;165(10):1178-1186.

Hess AF, Lewis JM, Barenberg LH. Does our dietary require vitamin A supplement? JAMA. 1933;101:657-663.

Unfortunately, Hess’s prophecy of a passing fad proved premature and many Americans continue to consume “absurd” and dangerous quantities of vitamin A. For example, multivitamins, until recently, had small amounts of vitamin D (200 to 400 IU) but high amounts of preformed retinols (5,000 to 10,000 IU). This pales in comparison to a tablespoon of modern cod liver oil, which contains sub-physiological amounts of vitamin D (400 to 1200 IU) but supra-physiological amounts of completely preformed retinols (5,000 to 15,000 IU or in some cases 30,000 IU).

John Cannell



Dear Dr. Cannell:

It has been three weeks and he went from 5,000 IU of vitamin D per day to 2,000 IU per day a week ago. His language is increasing. He's now back to saying the things he wants with some prompting. He also has gut dysbiosis and I'm sure the D is helping with microbes in his gut. He has a lot of problems with his immune system and bacteria and viruses. Also, doesn't vitamin D aid in the production of glutathione? I feel that could be a big part of his increased language.

Jane



Dear Jane:

Yes, abnormal immune responses are associated with both autism and vitamin D deficiency. For example, autistic individuals have immune abnormalities that show a striking similarity to the immune functions affected by vitamin D. Animal evidence indicates some vitamin D deficiency induced brain damage may be malleable, that is, vitamin D may partially reverse the brain damage, if given early enough. These studies offer hope that sunlight or oral vitamin D, especially in young autistic children, may have a treatment effect.

Ashwood P, et al. The immune response in autism: a new frontier for autism research. J Leukoc Biol 2006;80(1):1-15.

Cantorna MT, et al. Vitamin D status, 1,25-dihydroxyvitamin D3, and the immune system. Am J Clin Nutr 2004;80(6 Suppl):1717S-20S.

Burne TH, et al. Combined prenatal and chronic postnatal vitamin D deficiency in rats impairs prepulse inhibition of acoustic startle. Physiol Behav 2004;81(4):651-5.

Both the brain and the blood of autistic individuals show evidence of ongoing chronic inflammation and oxidative stress. That is, the disease process is probably increasingly destructive. Further hope for a treatment effect rests in activated vitamin D's powerful anti-inflammatory properties. Its administration reduces production of inflammatory cytokines in the brain, which have consistently been associated with cognitive impairment. Furthermore, activated vitamin D is remarkably neuroprotective by stimulating neurotropin release, reducing toxic cellular calcium levels in the brain, inhibiting the production of nitrous oxide, and by its immunomodulating properties, especially in reducing inflammatory cytokines and by increasing brain glutathione.

Moore ME, Piazza A, McCartney Y, Lynch MA. Evidence that vitamin D3 reverses age-related inflammatory changes in the rat hippocampus. Biochem Soc Trans 2005;33(Pt 4):573-7.

Cohen-Lahav M, Shany S, Tobvin D, Chaimovitz C, Douvdevani A. Vitamin D decreases NFkappaB activity by increasing IkappaBalpha levels. Nephrol Dial Transplant 2006;21(4):889-97

Kalueff AV, Eremin KO, Tuohimaa P. Mechanisms of neuroprotective action of vitamin d(3). Biochemistry (Mosc) 2004;69(7):738-41.

This last function of vitamin D, increasing cellular levels of glutathione, may explain the purported link between heavy metals, oxidative stress, and autism. For example, activated vitamin D reduces iron-induced and zinc-induced oxidative injuries in rat brain. The primary route for the neurotoxicity of most heavy metals is through depletion of glutathione and subsequent generation of reactive oxygen and nitrogen species. Besides its function as a master antioxidant, glutathione acts as a chelating (binding) agent to remove heavy metals. Several studies indicate autistic individuals have difficulty excreting heavy metals, especially mercury. If vitamin D deficient brains are unable to utilize glutathione properly, and thus unable to remove heavy metals, they may be oxidatively damaged by heavy metal loads normal children easily excrete. The amount of activated vitamin D in the brain directly depends on how much vitamin D is made in the skin or put in the mouth.

Garcion E, Wion-Barbot N, Montero-Menei CN, Berger F, Wion D. New clues about vitamin D functions in the nervous system. Trends Endocrinol Metab 2002;13(3):100-5.

Chen KB, Lin AM, Chiu TH. Systemic vitamin D3 attenuated oxidative injuries in the locus coeruleus of rat brain. Ann N Y Acad Sci 2003;993:313-24.

Lin AM, Chen KB, Chao PL. Antioxidative effect of vitamin D3 on zinc-induced oxidative stress in CNS. Ann N Y Acad Sci 2005;1053:319-29.

Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem 2005;12(10):1161-208

Kern JK, Jones AM. Evidence of toxicity, oxidative stress, and neuronal insult in autism. J Toxicol Environ Health B Crit Rev 2006;9(6):485-99.

Sincerely,

John Cannell



Dear Dr. Cannell:

It has been a month now and John's Improvements are continuing. In the last week, he has been using his muscles more, he goes on the swing outside and lifts his legs and bends in ways that take core muscle strength. This is yet another skill or interest that left and is returning. I will report more next week.
Jane




Conclusion:

It is too early to say vitamin D has a treatment effect in autism. However, a simple risk/benefit analysis suggests that autistic children should be diagnosed and aggressively treated for vitamin D deficiency. If readers want to learn more about vitamin D and autism, they can obtain the entire paper on the link below. Unfortunately, Elsevier charges $31.50 to download it. You can read a similar document for free on the website, where we first published the theory a year ago.

Cannell JJ. Autism and vitamin D. Med Hypotheses. 2008;70(4):750-9.

http://vitamindcouncil.org/newsletter/2007-may.shtml

In summation, autistic children should be given enough vitamin D to get their 25(OH)D levels up to the mid to high range of normals, that is, 70 ng/ml (175 nmol/L in countries that use the metric system). In the absence of sun exposure, this usually requires long-term administration of about 1,000 IU/day per 20 pounds of body weight with a loading dose of 2,000 IU of vitamin D/day for every 20 pounds of body weight for the first two weeks. As individual variation in response is very high, they should have 25(OH)D blood tests every month until their level has stabilized around 70 ng/ml. They should stop all products containing preformed retinols (vitamin A), especially cod liver oil.

John Cannell, MD
The Vitamin D Council

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. As we are a 501(3)(c) non-profit corporation, dedicated to ending vitamin D deficiency and not making money, the Vitamin D Council does not copyright this newsletter. Please reproduce it and post it on Internet sites. If this newsletter proves useful to a child you know with autism, the Vitamin D Council asks for a donation as we have not been able to secure a grant and our bank account balance is again below $5,000. Send your tax-deductible contributions to:

The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422

"Make big money fast with CT scans"

Rather than the headline New Study Could Change Heart Disease Diagnosis And Treatment being run in Utah TV and newspapers, instead it should read:


Make big money fast with CT scans!

Is your bottom line shrinking? Have you fallen on hard economic times? Is competition from other hospitals and providers threatening your financial health?

Then we have a solution: Do a CT coronary angiogram on everybody! Look for disease in people with no symptoms, scare the heck out of them, and voila! Instant need for bypass surgery!

Ka-ching!! That'll be $100,000, please.

Do it again, and again, and again, and your hospital will be quickly in the black in no time!

And, for the savvy marketer, tell the newspapers that you're going to conduct a study to see if this approach works--even before the study gets started! Even if the study pans, you'll come out a winner because you did it in the name of "research"!




Apparently a group of cardiologists at the Intermountain Medical Center and LDS Hospital in Salt Lake City, with the financial assistance of Siemens, a manufacturer of CT scanners, is funding a 1000-patient study of diabetics, all without symptoms of heart disease, half of whom will undergo "screening" CT coronary angiograms (not heart scans) followed by bypass surgery, if "needed". The other half will receive conventional, "aggressive" medical therapy. "Aggressive" means cholesterol treatment, blood pressure control, and blood sugar control (no kidding).

The outcomes of the two groups will be compared after two years.

To understand the absurdity of this study, note that they are proposing what amounts to "prophylactic" bypass surgery, since the participants are without symptoms. Since there are no stress tests, a measurement of flow or functional capacity (exercise tolerance) cannot be factored in. Decisions will be made on the basis of severity of "blockages" in asymptomatic people, a hazardous notion that has never been shown to provide benefit. No doubt: Some diabetics with extensive disease may obtain benefit from screening, but many more will undergo what amounts to unnecessary bypass that provides no benefit. We already know from studies dating back over 20 years to the days of the original CASS (Coronary Artery Surgery Study) that putting asymptomatic people through bypass surgery willy-nilly does not reduce mortality.

Of course, the "aggressive" preventive treatment they propose is more like the least common denominator level of treatment. In fact, I would characterize the "aggressive" preventive treatment as ridiculous. Doing less would be malpractice. Much more could be done, but doing a lot more would pose a real challenge to the bypass arm of the trial.

But the smell of money drives such efforts: More CT angiograms, more hospitalization for bypass surgery. The payoff to the hospitals from this effort is likely to exceed $5 to $10 million, all money that they might not have otherwise seen. The ill-informed people in the local media gush with enthusiasm, the hospital acts like they are at the cutting edge of medical technology, the doctors pose as saviors.

All this time, real preventive efforts go unmentioned. No fish oil (28% reduction in heart attack, 45% reduction in sudden death from heart attack), no genuine diet efforts (i.e., not the diabetes-promoting American Diabetes Association diet), no effort to identify sources of coronary risk beyond LDL cholesterol (low HDL,small LDL,and postprandial or after-eating abnormalities, for instance, are prominent sources of risk in diabetics), no vitamin D. In my view, the preventive arm of the study amounts to doing virtually nothing beyond prescribing statin drugs.

Don't fall for it.

Is DHEA dangerous?

















The Fountain of Youth, Louis Cranach the Younger (1546)




In the Track Your Plaque program, we sometimes use the adrenal hormone, DHEA. It is a fascinating and--surprisingly--an over-the-counter hormone that can be useful and safe when used properly.

DHEA can be useful for:

--Reduction of Lp(a)--Though more effective in females, it can also be useful in males. In the women, DHEA often reduces Lp(a) 15-18%, somewhat less in males. The lower the starting DHEA, the greater the Lp(a) reduction.

--Improved libido--in both men and women. The effect is modest. It's magnified when used with other strategies. Although this is not specifically a goal in the program, it sure helps to get side-benefits like this, rather than unwanted side-effects.

--Increased energy and mood--The boost in mood is, for many, the most perceptible effect: More ambition, more stamina, greater staying power in work and exercise.

--Reduction in abdominal (visceral) fat--A modest effect, but one that, over a long period of use (>6 months) can yield improved insulin responses.


Most commonly, I will suggest DHEA supplementation when blood levels allow. Some people, however, Google "DHEA" and come back horrified that I would suggest such a dangerous supplement.

"I read that it makes women grow mustaches and makes their voices deeper!"

And it does--if you take a lot.

10-15 years ago, when the benefits of DHEA became apparent, some people wanted to believe that DHEA was the fountain of youth. People interested in the anti-aging potential for DHEA figured that, if 50 mg per day made you feel energized and vigorous, what would be the effect of 1000 mg, 2000 mg, or 3000 mg per day? A number of clinical trials were conducted using these doses and, interestingly, depression can lift, men and women increase muscle mass, there is a slight increase in bone density, even pain symptoms from rheumatoid arthritis and lupus may improve. But . . . women grow mustaches, become sexually aggressive, and develop deep voices. Men can become hyperaggressive or overly emotional.

No wonder: Any hormone taken in extraordinary, supraphysiologic doses will exert wacky effects. Imagine taking testosterone or estrogen at 50 times the usual dose.

The doses we use for the above benefits, including Lp(a) reduction, range from 25-100 mg per day; most people do fine with 50 mg. We also adjust doses to starting blood levels. In this dose range, I have never seen any of the above side-effects.

The only side-effects I see at these doses are 1) excessive assertiveness or crabbiness, and 2) insomnia if taken at bedtime.

In my experience, DHEA is a benign hormone, provided it is taken in limited doses and not abused. An occasional female younger than 55 years old will be able to tolerate only 10-20 mg per day before developing the edgy side-effects, but I've never witnessed masculinizing side-effects at these low doses, nor have I ever seen excessive increases in testosterone in men or women. (Women can raise testosterone levels slightly, but almost never enough to exert much effect beyond modestly increased libido.)



Copyright 2008 William Davis, MD

Wheat addiction: 140 lbs lost

Here is detailed comment from a reader who figured out the wheat (and dairy) issue on her own with impressive results.

Though it seems an unpardonable over-simplification of diet, this concept of eliminating wheat-based products (along with obvious unhealthy foods like candy and soda) yields unexpectedly large results, as our reader relates.


Hi Dr. Davis,

Several years ago, chronic untreated asthma infections hospitalized me. I thought it was recurring bronchitis as I'd never had asthma in my life. Killed much of the alveoli... took awhile to de-crap the lungs and regrow the alveoli. Got assigned a cardiologist sort-of by accident while in the hospital for that (couple days of constant heated steroid, stress, a pain + situation combined, elevated my heart rate to 298 for a brief time). When I went to see him, he wrote me a prescription for the Eades' PPLP [Protein Power LifePlan] book.

It's taken awhile, since it's required radical gradual changes in most aspects of my overly Type-A life, but I'm now about 140 lbs lighter, and hopefully much more in the future.

Miraculously, after 10 days on a hard meat-eggs-cheese-veggie-berry approach (which I sadly confess was mostly pepperoni & mozz nuked... I was busy! ;-)), all my medical symptoms disappeared too. Acid reflux, acne, brain-fog, rashes, 'severe asthma', allergies, etc. etc. By trial and error I realized I wrongly attributed that to lowcarbing when it was getting off gluten that actually did it for me. Which since I'm lowcarb also means all the crap my celiac boyfriend can eat, I can't. Lowcarb does many great things for me (just dropping all the bloating and increasing the energy level are awesome), but getting off wheat was critical.

I've since found that a single tablespoon of "milk" in the morning, or something with wheat (say a tortilla), will make me ravenous *specifically for milk and wheat* all day. Conversely, I can be eating lowcarb and then eat total junk--but something without gluten--and not have it bother me much at all. But one pumpernickel slice at Outback and I am DOOMED. It doesn't always happen that instant; will-power has some sway; but the odds of my making a 'poor decision that leads to cascade failure and totally abandoning my eating plan' in the next 48 hours is astronomically higher if milk or wheat were involved. Oddly, cheese does not seem to affect me this way.

When I was younger (I'm 42 now) I had to stop drinking milk. If I drank some I wanted more. If I drank more I needed more. If I drank more, that was it: I'd be stumbling to the kitchen in the dark at 3am, drinking out of the carton, falling gasping against the refrigerator after several long gulps, like a heroin addict who just got a fix. I finally realized that since I'd lived on a ton of milk my whole life, maybe this was a milk problem; so I usually stayed away from it. So then it turned out wheat/gluten were an issue too. Which made me realize how much of my life was filled with not-eating most of the time (very busy, workaholic, but very sedentary), but when I did eat, ingesting amazing amounts of wheat products. I'm astounded that my whole life I mostly ate things I am apparently intolerant to "or something." Sometimes I wonder how much different even my brain would be if it'd been different.

This might contribute to my ending up weighing 500# at one point. The only amazing thing is that I didn't get a disease. (Well I did--obesity--but I mean any others.) I'm from a family of people who are mostly fat, mostly alcoholic, and mostly dead of cancer. I'm just fat, worse than the others but otherwise seemingly ok. Now I'm starting to think that maybe my whole family may have some 'issue' with the primary foods of our culture.

I tell friends that my horrible chronic acid reflux was solved merely by getting off gluten. They nearly all say, "I could never give up bread!" (Isn't it funny, you never hear people say, "Oh man, I could never give up broccoli!") I tried to convince one young friend to try it; her doctor told her eating more protein and fat was unhealthy, and gave her a prescription (this is lifetime--it doesn't cure it, merely treats the symptom) to a drug to help with acid reflux. I said you're kidding me, you think taking a drug the rest of your life is healthier than trading your pasta for a steak?? Go figure.

I still haven't figured out the milk connection (or why I seem ok with cheese for some reason; maybe there is a dosage-difference, or the sugar combined with it has some effect), but I think it's pretty clear that dropping milk and wheat has very radically changed my life for the better. I may actually live, which being a single mom to an awesome 11 year old girl, is a good thing.

Best,
P.

Diet: Don't be angry, be GRATEFUL


Given the confusion over what constitutes the "ideal" diet, a discussion that has been hotly debated for decades, some people become very angry that we still don't agree on what is truly healthy.

"Why should I even try if the experts don't agree? They say something is bad one day, then say it's okay the next!"

But that's a short-sighted half-truth born of frustration. We have certainly zigzagged in our understanding of diet over the years. The grand national experiment in low-fat eating, for instance, clearly failed to improve our health. In fact, the opposite occurred: The largest epidemic of obesity and diabetes in world history. You could get angry from this failed experiment . . . or you could learn from it, take what lessons we can and improve on it.

Step back for a moment and consider: In what other age could we even have this discussion?

If we lived in a world where you were hungry, your children were hungry, and you didn't know where the day's food was to be found, we would have no need whatsoever for this conversation: You would take whatever you could find, kill, or steal.

Say you woke up this morning and your cabinets and refrigerator were empty. The stores were far away or non-existent. You and your family would have to improvise, to forage or hunt your day's food. It would require hours. You wouldn't fuss about glycemic index, or saturated fat, or whether or not sugar or wheat was present. You would just eat whatever you could get your hands on. When caloric deprivation threatens, we take what is available.

But we live in a world of plenty--of enormous excess--that allows us choices. It is a world that encourages eating more than is required for existence, a world tailored more to indulgence than to simple satiety or sustenance. That's when distinctions among food types and quality make a difference. But it is a dilemma born of riches.

Starvation and caloric deprivation would settle the argument for us very quickly. It doesn't mean that we shouldn't continue to debate the finer points of diet. But don't do it with anger or frustration. Do it GRATEFULLY, recognizing that we are lucky to be able to have such a conversation in the first place.


Image courtesy Food and Agriculture Organization of the United Nations.

HDL for Dummies

I frequently peruse conventional health websites to keep track of their message. One painfully conventional (read "drug company-supported") website that echoes the standard advice on heart disease and heart health is Everyday Health .

Since I subscribe to the newsletters for many conventional sites, I received an e-mail that took me to this Q & A about HDL cholesterol:

Q: I'm 36 years old and my good cholesterol is too low. What can I do?
– Nilsa, Florida

Dr. Lori Mosca of New York-Presbyterian Hospital responds:

A: A woman's HDL goal should be greater than 50 mg/dL (greater than 40 mg/dL in men). You can raise your HDL levels by eating a diet low in saturated fat and trans fat but high in monounsaturated fats. Lose weight if you need to and get at least 30 minutes of moderate-intensity exercise on a minimum of four days per week. If you smoke, quit. Despite positive lifestyle changes, though, some individuals may still be candidates for HDL-raising drug therapy because they are at increased risk for cardiovascular disease. Discuss your options with your health care provider.


Are you satisified with that answer? I certainly am not.

First of all, is this something you've never heard before? "Eat right, exercise, cut your unhealthy fats." Then why do people who follow this sort of conventional advice often still fail? Is the next step always medication?

Here's the part that Dr. Mosca and other conventional, drug-minded "authorities" have left out:

To raise HDL powerfully--not to 40 mg/dl for males or 50 mg/dl for females, but to 60, 70 or 80 mg/dl--think about the following strategies:

--Eliminate wheat and cornstarch products. I have droned on endlessly about this concept, but it is enormously effective. While the weight loss that inevitably follows elimination of these foods adds to the HDL-raising effect, there is also an independent effect, as well.

--Fish oil--The omega-3 fatty acids in fish oil reduce triglycerides. Triglycerides accelerate the destruction of HDL. Remove triglycerides, HDL goes up. (Though krill oil may share, even surpass this effect, we need more data than the single manufacturer-sponsored study.) Of course, this requires real doses, not the namby-pamby doses you often read about.

--Vitamin D--Achieving normal levels of 25(OH) vitamin D raises HDL with power I have never witnessed from any other strategy before, barring weight loss of 30+ lbs. Readers of the Heart Scan Blog know that just taking vitamin D is not enough. Verification with blood levels is an absolute necessity, particularly if raising HDL maximally is among your goals.

--Adding back saturated fat. I say "adding back" since most of us (including myself) went too far down the "saturated fat is bad" path over the past few years. While I do not advocate a carte blanche approach to saturated fat, I believe that adding back eggs (preferably free-range and/or omega-3 rich), lean meats, and hard cheeses is a good idea. The saturated fat in these foods raise HDL 5 or more mg/dl.

--Dark chocolate--Or other cocoa prepartions. What a cool way to raise HDL! Reach for the lowest-sugar, highest cocoa preparations.

--Alcoholic beverages--I am partial to the red wine/flavonoid-rich concept, being a wine drinker. Although all alcoholic beverages raise HDL due to the ethanol content, for benefits beyond alcohol (as well as to avoid wheat-based drinks like beer), I do believe that the bulk of data argue for flavonoid-rich red wines from southern France, Italy, and California.

--Achieve ideal weight--The toughest of all. But eliminating wheat and cornstarch makes it far easier.


Follow the conventional advice of those like Dr. Lori Mosca, and the majority of people will fail. ("It just so happens that I have a prescription drug just for that purpose!")

Buck the conventional advice, adopt strategies that won't be found in the drug ads, nor be provided by the conventionally-thinking, and you can succeed to heights you never thought possible.


Copyright 2008 William Davis, MD

"I gained 30 lbs from one cracker"


Let me tell you a story, a tale of a woman who gained 30 lbs by eating one cracker.

At age 50, Claire's health was a disaster. Her initial lipoprotein patterns were a mess, including HDL 36 mg/dl, triglycerides 297 mg/dl, blood sugar 122 mg/dl (pre-diabetic range), blood pressure 155/99. Small LDL comprised over 90% of all LDL particles.

At 5 feet 3 inches, she weighed 210 lbs--90 lbs over her ideal weight. Her face was flushed and red, her eyes swollen and weighted down with bags, her eyes dull. While interested in hearing about how to improve her health, I would hardly call her enthusiastic.

We talked about how removing wheat products entirely from her diet could result in weight loss--enormous weight loss--yet with reduced appetite, increased energy, less daytime sleepiness and fogginess, improved sleep quality. Removing wheat would also allow substantial correction of her lipoprotein patterns with minimal medication.

At first, she seemed confused by this advice. After all, it ran directly opposite to what she'd been told by her family doctor, not to mention the advice from TV, food ads, and food packages.

To my surprise, Claire did it. She didn't return to the office for another 5 months. But she came in, a big beaming smile on her face.

Even at 167 lbs--still overweight--Claire looked great. She glowed. She'd already dropped nearly 2 1/2 inches from her waist. She felt lighter on her feet, discovered energy she thought she'd lost 10 years earlier. Her blood results matched, with dramatic shifts in each and every pattern.

I quizzed Claire on her diet, and she had indeed made substantial changes. In addition to eliminating all foods made of wheat flour, she also eliminated foods made with cornstarch, rice flour, snacks, and other sweets. She ate her fill of vegetables, fruits, raw nuts, lean meats, and healthy oils. She was less hungry while eating less. Even her husband, skeptical at first, joined Claire after the first two months and her initial 20 lbs of weight loss. He, too, was well on his way to dropping to ideal weight.

But a dinner party invitation came. In the few that Claire and her husband had gone to over the few months, she had religiously stuck to her program, choosing cheese, pickles, olives, vegetables that she dipped, but avoided the pretzels, breads, Doritos, potato chips, and others.

This time, a tray of whole wheat crackers was laid on the buffet table, covered with some sort of sweetened cheese. She had just one. She savored the taste that she'd missed. "Maybe one more. I'll be extra good this weekend,'" she told herself.

Now Claire was hungry. The bruschetta covered with tomatoes and mozzarella looked awfully good. "It's got some good things on it, too!" she thought. She had three.

The floodgates opened. I saw Claire three months later, weighing just shy of 200 lbs. "I almost cancelled this appointment," she whispered quietly, tears at the corner of her eyes. "I don't know what happened. I just lost control. After losing all that weight and feeling so good, I blew it!"

I've seen it before: Fabulous success eliminating the foods that created the situation--the insatiable appetite, the endless cycle of hunger, brief satiety, the rolling, rumbling hunger--followed by temptation, then disaster. The weight lost comes right back.

It's experiences like Claire's that have absolutely, positively convinced me: Wheat products are addictive. It's not true for everybody, but it's true for many people, certainly most people who have weight struggles. It triggers some sort of appetite button, a signal to eat more . . . and more, and more. Keep it up long enough, and you have drops in HDL, increases in triglycerides, upward jumps in blood sugar and blood pressure, diabetes, etc. It doesn't matter if it's whole grain, 7-grain, or 12-grain. Yes, the whole grains contain more fiber and more B vitamins. But they all share one characteristic: They trigger a desire for more.

So that's the story of how one whole wheat cracker caused one woman to gain 30 lbs.


Next week's story:

California woman claims: My children are aliens!


Just kidding.


Copyright 2008 William Davis, MD

Wheat-free is not gluten-free

Eliminate wheat from your diet and wonderful things happen:

--Lose 15-20 lbs, sometimes in the first 1-3 months. (More or less, depending on your prior dietary habits, weight, age, etc.)
--HDL cholesterol goes up, triglycerides go down
--Blood sugar drops
--Small LDL is reduced
--C-reactive protein is reduced
--Pre-diabetics often convert to non-diabetics
--Diabetics gain far better control over blood glucose. Some even become non-diabetic (as long as they maintain the wheat-free, low-glycemic index diet and weight control).
--You feel better: Less mental fogginess, more energy, better sleep.
--Appetite shrinks dramatically.


(Many diet programs makes lots of money promising similar results. Prescription medications like the pre-diabetes drugs, Actos and Avandia, and the fibrates, Tricor and Lopid, nearly--nearly--reproduce the effects of eliminating wheat. Of course, these medications do not lead to weight loss or make you feel better. In fact, Actos and Avandia usually trigger a weight gain of 8 lbs in the first year of use.)


All of these wonderful effects develop with elimination of wheat. . . unless you confuse wheat-free with gluten-free. There's a difference.

Remove wheat from your diet, but discover the world of gluten-free products made for people with celiac disease, or gluten enteropathy, and you can regain the weight and recreate many of the phenomena associated with wheat. I've talked about this in past, but it trips up so many people that it's worth talking about again.

The concept that I am advocating is really low-glycemic index (or low glycemic load, actually). Foods that trigger a substantial rise in blood sugar, whether immediate (like whole wheat crackers) or delayed (like whole wheat pasta) are the culprits. The same effects develop with candy, cookies, fruit drinks, pizza, chips, table sugar, and other junk foods.

However, I pick on wheat specifically because it so dominates the American diet. It has grown to fill so many processed food products. It is also a food ingredient that is falsely advertised as healthy. In reality, pretzels, whole wheat crackers, whole grain bread, high-fiber cereals, etc. exert the same effect on blood sugar as candy or white table sugar. They also generate all the "downstream" phenomena listed above.

But wheat is hardly the only food that makes us fat, diabetic, and unhealthy. This is true for foods made with cornstarch (taco shells, cornbread, tortillas, chips, breakfast cereals); rice flour, puffed rice, and polished rice; and potatoes, particularly pulverized potato starch (potato chips). There are others.

These are the gluten-free products that are marketed to the gluten enteropathy (celiac disease) market. Yes, you can make muffins with cornstarch and no wheat gluten, but is it good for you?

No. It is nearly as bad as wheat. It can still skyrocket blood sugar, drop HDL, raise triglycerides, create small LDL, heighten inflammation, etc.

Ground flaxseed, oat bran, barley, quinoa, are some of the alternatives that do not create these effects. But not the majority of gluten-free products on the market.




Ingredients: Potato starch, rice flour, modified corn starch, olive oil, yeast, vegetable protein(lupine), corn syrup, sugar, salt, hydroxypropyl methylcellulose, sodium bicarbonate, ammonium bicarbonate, diacetyltataric acid esters of mono- and diglycerides of edible fats, natural flavor.

". . . only naturally gluten-free and wheat-free ingredients and adhere to the strictest quality processes, testing every batch for gluten using the ELISA assay."

NUTRITION FACTS
Serving Size 7 bread sticks (31g)
Servings per container 5

Calories 120 Calories from fat 25
Amount per serving
Total Fat 2.5g
Saturated Fat 0.5g
Trans Fat 0g
Cholesterol 0mg
Sodium 310mg
Total Carb 24g
Dietary Fiber 1g
Sugars less than 1g
Protein less than 1g

Death to chelation?


Does chelation work?

It's a question I get asked fairly frequently. Although I have never performed chelation, IV or oral, and therefore have no direct experience, my concerns for this purported therapy have included:

1) The concept of extracting calcium from atherosclerotic plaque by removing it first from the blood is absurd. Early chelationists believed that this was the means by which EDTA might reverse coronary atherosclerosis. However, removing calcium from blood would more likely lead to osteoporosis or calcium extraction from bone, since bone is a more ready repository for calcium. Blood calcium levels are also tightly and narrowly controlled; any significant reduction in calcium ("hypocalcemia") can be life-threatening. And, indeed, there have been deaths from hypocalcemia in people receiving chelation.

More recently, chelationists have argued that removal of heavy metals like lead and mercury are responsible for the purported benefits of chelation. And, indeed, blood levels of these heavy metals can be reduced by chelation. That alone may be a benefit. But to then make the leap to say that it also regresses atherosclerotic plaque by the same mechanism has no basis in science.

2) Practitioners associated with chelation tend to be shady. I have seen homeopathic therapies (among THE most ridiculous of concepts), "energy balance" therapies, desiccated organ extracts ("applied kinesiology"), and a variety of other fringe treatments offered by practitioners offering chelation. This doesn't necessarily mean, of course, that chelation is also fringe or suspect, but it tends to be offered by practitioners who engage in generally unscientific, unfounded practices.


The few people I've seen go through multiple courses of chelation (usually 30 or so infusions) have shown no impact on heart scan scores or any other measure of heart disease.

In response to the many questions I receive on chelation, I had been answering that, if we would simply wait for the publication of the NIH-sponsored trial of IV chelation therapy, perhaps we'd know once and for all.

However, in a lengthy criticism, four expert authors argue that the TACT trial to assess chelation study is doomed to failure for an entire list of reasons and should therefore be abandoned. The discussion is available on Medscape Cardiology. (Free sign-in required.)



Why the NIH Trial to Assess Chelation Therapy (TACT) Should Be Abandoned
We investigated the social and the scientific histories of chelation therapy beginning in the 1950s. We examined TACT protocols and consent forms, which, in response to Freedom of Information Act (FOIA) requests, the NIH provided to us with curious redactions. We examined the existing RCTs and the numerous case series cited by the TACT protocols. We examined evidence for risks, including information that is not in the standard medical literature. We examined various hypotheses that advocates have offered to explain how chelation "works."

We present our findings in 4 parts. First, we provide a brief history of the use of disodium EDTA as a treatment for CAD. Next, we describe the origin and nature of the TACT. Next, we discuss the evidence for chelation as a treatment for CAD and for atherosclerosis in general, and place it in the context of other proposed treatments that have been ineffective after an initial period of enthusiasm. Finally, we discuss the risks. For each topic, we contrast our findings with relevant statements in the TACT literature, to the extent that such statements exist.



Among the highlights:

--Since the mid-1970s, court documents and newspapers have reported at least 30 deaths associated with IV disodium EDTA, most of it administered by ACAM members.

--Early chelation investigators had chosen the disodium salt of EDTA, reasoning that if it could remove calcium from atherosclerotic plaques, it might shrink them. That notion was soon demonstrated to be invalid. It has largely been replaced by a "toxic heavy metals" antioxidant hypothesis, which is based on the potential for metal ions to produce free radical damage. Chelationists now cite "removing heavy metals" as the basis for their claim that chelation is effective for approximately 70 conditions, ranging from schizophrenia and autism to cancer. This provides them with numerous reasons to ignore any trial that finds chelation ineffective for CAD.

--Biochemical literature, either not cited or misrepresented in the TACT protocols, has demonstrated that the heavy metals hypothesis is implausible. Antithetically, it also demonstrates that the chelation mixture used in the TACT has pro-oxidant effects in vitro.

--In our opinion, TACT literature -- including 2 versions of the protocol, the consent form, information posted on the NCCAM Web site, and 2 editorials co-authored by the PI -- has misrepresented chelation, its risks, and the facts of the study. It has exaggerated the value of supportive case series, not only by ignoring evidence of bias and incompetence, but by misrepresenting citations and reporting erroneous data. It has minimized the dangers, both by understatements and by omissions of specific, published complications. It has not acknowledged the deaths mentioned above. It has repeatedly conflated disodium EDTA and a different drug, calcium-sodium EDTA.

--The TACT includes nearly 100 "chelation site" co-investigators who, in our opinion, are unsuitable to care for human subjects or to report trial data. Most espouse implausible health claims while denigrating proven methods; several have been disciplined, for substandard practices, by state medical boards; several have been involved in insurance fraud; at least 3 are convicted felons. Several were members of the ACAM or GLACM IRBs mentioned above. Few appear to have real expertise, required by TACT literature, in treating patients with CAD or in conducting clinical trials. Most continue to promote chelation while the TACT is in progress, contrary to good science, to human studies ethics, and to US Federal Code.


While the criticism itself does not prove the point one way or another, as a clinical trial should, anyone contemplating chelation therapy would be well-advised to read the document first. Another reference: EDTA chelation therapy for cardiovascular disease: a systematic review.


The authors of the exhaustive discussion are:
Kimball C. Atwood IV, MD, Anesthesiologist, Newton-Wellesley Hospital, Newton, Massachusetts; Assistant Clinical Professor, Tufts University School of Medicine, Boston, Massachusetts; Associate Editor, Scientific Review of Alternative Medicine
Author's email: katwood@partners.org

Elizabeth Woeckner, AB, MA, President, CIRCARE (Citizens for Responsible Care and Research), Columbia, Maryland

Robert S. Baratz, MD, DDS, PhD, Medical Director, South Shore Health Center, Inc., Braintree, Massachusetts; Assistant Clinical Professor of Medicine, Boston University School of Medicine, Boston, Massachusetts; President, National Council Against Health Fraud, Inc.

Wallace I. Sampson, MD, Clinical Professor of Medicine (Emeritus), Stanford University, Stanford, California; Senior Attending Physician and formerly Chief of Medical Oncology, Santa Clara Valley Medical Center, San Jose, California; Editor-in-Chief, Scientific Review of Alternative Medicine



The authors provided the following disclosures:


Disclosure: Kimball C. Atwood IV, MD, has disclosed no relevant financial relationships in addition to his employment.

Disclosure: Elizabeth Woeckner, AB, MA, has disclosed that she has received compensation for consulting in civil litigation and professional disciplinary actions.

Disclosure: Robert S. Baratz, MD, DDS, PhD, has disclosed that he has been retained by state licensing boards, the Office of the US Attorney, and plaintiff counsel as an expert in disciplinary proceedings and litigation with regard to chelation therapy and associated matters. He is compensated only for his time and has no commercial interest in the outcome of the proceedings or litigation.

Disclosure: Wallace I. Sampson, MD, has disclosed no relevant financial relationships in addition to his employment.

American Diabetes Association


These are actual quotes from the American Diabetes Association website:


Myth #2 (from list of Diabetes Myths): People with diabetes can't eat sweets or chocolate.
If eaten as part of a healthy meal plan, or combined with exercise, sweets and desserts can be eaten by people with diabetes. They are no more “off limits” to people with diabetes, than they are to people without diabetes.



Myth #5: If you have diabetes, you should only eat small amounts of starchy foods, such as bread, potatoes and pasta.
Starchy foods are part of a healthy meal plan. What is important is the portion size. Whole grain breads, cereals, pasta, rice and starchy vegetables like potatoes, yams, peas and corn can be included in your meals and snacks. The key is portions. For most people with diabetes, having 3-4 servings of carbohydrate-containing foods is about right. Whole grain starchy foods are also a good source of fiber, which helps keep your gut healthy.





How can I have sweets and still keep my blood glucose on target?
The key to keeping your blood glucose on target is to substitute small portions of sweets for other carb-containing foods in your meals and snacks. Carb-containing foods include bread, tortillas, rice, crackers, cereal, fruit, juice, milk, yogurt, potatoes, corn, and peas. For many people, having about 45 to 60 grams at meals is about right. Serving sizes make a difference. To include sweets in your meal, you can cut back on the other carb foods at the same meal.

For example, you’d like to have cookies with your lunch. Your lunch is a turkey sandwich with two slices of bread. Your first step is to identify the carb foods in your meal. Bread is a carb. You decide to swap two slices of bread for two slices of low-calorie bread and have the cookies -- it’s an even trade. Your total amount of carbohydrate remains the same for the meal.



Can I eat foods with sugar in them?
For almost every person with diabetes, the answer is yes! Eating a piece of cake made with sugar will raise your blood glucose level. So will eating corn on the cob, a tomato sandwich, or lima beans. The truth is that sugar has gotten a bad reputation. People with diabetes can and do eat sugar. In your body, it becomes glucose, but so do the other foods mentioned above. With sugary foods, the rule is moderation. Eat too much, and 1) you'll send your blood glucose level up higher than you expected; 2) you'll fill up but without the nutrients that come with vegetables and grains; and 3) you'll gain weight. So, don't pass up a slice of birthday cake. Instead, eat a little less bread or potato, and replace it with the cake. Taking a brisk walk to burn some calories is also always helpful.


Or take a look at the recipes for breads, muffins, cakes, pies, cookies, and pizza.


My point? As I often say, while the "official" organizations like the American Diabetes Association, the American heart Association, and the USDA dominate the message provided to mainstream Americans, to those of us who know better, they have become irrelevant. You can see how obviously boneheaded their advice is. I'd go so far as to say that, if you want diabetes, follow the American Diabetes Association diet. If you have diabetes, and you'd like to accelerate complications like kidney disease, heart disease, and neuropathy, then follow the American Diabetes Association diet.

I'm going to bet that American Diabetes Association sponsors like Lilly, Novo Nordisk, Merck, Pfizer, Abbott ($1 million or more annual contributions) and Cadbury Schweppes (3-year, multi-million dollar support for Weight Loss Matters program) will continue to charge full-speed ahead to maintain the status quo. Cadbury Schweppes are the proud makers of Dr. Pepper, Hawaiian Punch, Snapple, Motts' Apple Juice, and Hires Root Beer--you know, the foods and drinks that you can have as long as you adjust your insulin dose or talk to your doctor about adjusting your diabetes medications. And if you gain, say, 30 or 40 lbs eating these foods. . . well, we've got a treatment for that. Merck's Januvia , for instance, can help you out for only about $200 a month!

Looking at the facts this way, and it seems like some cheap conspiracy theory: They're all out to get us. Dispense information that virtually guarantees propagation of the disease, and all your friends and cronies profit. I don't know if it is or it isn't, but it sure smells like it sometimes.
All posts by william-davis

Lipoprotein(a) Research Foundation

There is no longer any doubt that lipoprotein(a) is a major causal factor in heart disease:

Meta-analysis (combined re-analysis) of 27 prospective studies:
Danesh J et al. Lipoprotein(a) and Coronary Heart Disease: Meta-Analysis of Prospective Studies


Lp(a) and "subclinical" atherosclerosis
Brown SA et al. The relation of lipoprotein[a] concentrations and apolipoprotein[a] phenotypes with asymptomatic atherosclerosis in subjects of the Atherosclerosis Risk in Communities (ARIC) Study.

Lp(a) and oxidized LDL
Tsimikas S et al. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease.

Lp(a) predicts peripheral vascular disease
Valentine RJ et al. Lp(a) lipoprotein is an independent, discriminating risk factor for premature peripheral atherosclerosis among white men.

Peltier M et al.Elevated serum lipoprotein(a) level is an independent marker of severity of thoracic aortic atherosclerosis.


Lp(a) across various populations
Gambhir JK et al. Association between lipoprotein(a) levels, apo(a) isoforms and family history of premature CAD in young Asian Indians.

Weber M et al. Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians.



Lp(a) and stroke risk
Jurgens G et al. Lipoprotein(a) serum concentration and apolipoprotein(a) phenotype correlate with severity and presence of ischemic cerebrovascular disease.

Willeit J et al. Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.




From just about any direction, Lp(a) has been conclusively associated with atherosclerotic disease. We have more than enough data proving association.

But there are two areas of desperate need:

1) Data on effective treatments.

2) Raising awareness of this widely unknown (among the public) and ignored (among health professionals) genetic condition.

Treatment remains a real struggle. In a recent detailed Track Your Plaque Special Report, Unique Treatment Strategies for Lipoprotein(a) Reduction, we summarized the treatment approaches that have some power to reduce Lp(a) and/or its potential for causing heart disease. But, even armed with an appreciation for the world's scientific literature on this genetic condition, full control remains difficult for many people.

Track Your Plaque's HeartHawk has Lp(a) and he has struggled with this pattern for the last several years. He details some of his thoughts in a recent blog post.

More research and clinical studies are required and we need it soon if we hope to gain better control over this genetic pattern that affects up to 20% of people with coronary or vascular disease. Much of the needed research is sophisticated, background work similar to that being done by Dr. Santico Marcovina at University of Washington, Dr. Angelo Scanu at the University of Chicago, and Dr. Sally McCormick in New Zealand.

However, much of the needed research also consists of brief clinical experiences that detail whether or not there is an effect of various potential agents. Larger experiences, for instance, with potential treatment agents such as various phospholipid fractions, acetylcysteine, antibiotic regimens, some hormonal treatments, etc. could be performed quickly and simply. These studies would not require the $20 or $30 million typically spent by a drug company for a study, nor the several hundred million dollars to gain FDA approval of a new agent. They would simply be examinations of existing agents. These studies still cost money, require expertise, staff, and equipment. But the cost is a tiny fraction of the drug industry's investment in research. But it also means that investment return is nil from a drug manufacturer's perspective. Yet there are literally dozens, perhaps hundreds, of agents that hold some promise but have not been thoroughly studied.

For instance, if a specific modification of the phosphatidylcholine molecule were to generate a substantial Lp(a) reducing effect, Merck, Pfizer, and AstraZeneca would yawn--it is non-patent protectable, cannot be protected from competitors through the costly FDA approval process, and therefore is simply not worth their investment--regardless of whether it works or not.

(This is yet another example of how the drug industry, as well as hospitals and many health professionals, have lost sight of their real mission: to alleviate disease, not to profit from sickness.)

HeartHawk and I have discussed on a number of occasions whether a Lipoprotein(a) Research Foundation should be formed, an organization that seeks to fund the smaller research efforts that may accelerate productive research in Lp(a) and perhaps yield useful strategies faster than hoping for somebody to simply stumble on a treatment, or wait for the drug industry to create a unique, patentable entity that returns billions.

I'd like to propose that our Track Your Plaque program begin to fund such an effort. But a lot more help will be needed, particularly to generate the money to fund genuine, high-quality research from high-quality researchers.

If any readers of the Heart Scan Blog have any thoughts or insights into this process of creating a foundation, we'd appreciate your input.

More on ASTEROID

Since we are on the topic of the ASTEROID trial and rosuvastatin, I'd make one more point before I start to sound like I'm plugging this drug (which I definitely am not).

In an informative Roundtable Discussion (open to subscribers to the American Journal of Cardiology; sorry) amongst Dr. Steve Nissen, principal investigator behind ASTEROID; and Drs. Vincent Friedewald, Christie Ballantyne, P. Shah, and William Roberts, Dr. Nissen made some interesting comments:


Dr. Shah: In ASTEROID, was the magnitude of atheroma volume change seen across different levels of LDL-C and HDL-C?

Dr. Nissen: No. There was no plaque regression seen in the 17 persons with LDL-Cs >/= 100 mg/dl, and there was little change in persons with LDL-Cs of 70 to 100 mg/dl. Only in persons with LDLs less than or equal to 70 mg/dl was there significant regression. The study was not powered to look for an HDL-C(which increased by 14.7%)-raising effect.



Interesting. In other words, ASTEROID, in a fairly internally consistent way, suggests that the lower the LDL is reduced, the more likely plaque regression is obtained. This is consistent with the Track Your Plaque experience, in which we've advocated reducing (calculated) LDL cholesterol to 60 mg/dl for the past several years.

Unfortunately, the message that the ASTEROID Trial sponsors, AstraZeneca, as well as the roundtable discussion panel (later in the discussion) try to make is that there is something magical about Crestor, that it yields benefits superior to other statin agents or other means of reducing LDL.

I disagree with this message. In the Track Your Plaque experience, we do aim for a similar LDL target. But we also employ a number of other strategies. We have also succeeded in regressing plaque without use of any statin drugs (though, admittedly, many people do require statin drugs to obtain LDLs in this range). We also witness magnitudes of reversal that often far exceed that seen in ASTEROID.

The Rountable Discussion is unfortunately tainted, as is the ASTEROID Trial itself, with deep drug industry financial involvement of the Roundtable participants. In fact, the discussion begins with a listing of the financial disclosures of the participants, a listing that occupies a full column of a two-column page. The potential biases of the participants doesn't necessarily invalidate the arguments, but to me suggests that participants are more likely to argue in favor of the sponsor's drug, or that participants were chosen because of these biases.

Why bother to even mention the ASTEROID Trial in a venue (the Heart Scan Blog, that is) that purports to seek unvarnished, unbiased truth in coronary plaque reversal? Because useful information can sometimes be found in unlikely places. Just like the four-year old child who blurts out an unexpected pearl of wisdom, so it can happen with the gobbledy-gook that emerges from the drug industry.

Every once in a while, they are worth paying attention to.

LDL cholesterol, statins, and plaque regression

The ASTEROID Trial reported in 2006 examined the effects of LDL cholesterol reduction using the statin drug, rosuvastatin (Crestor), with coronary atherosclerosis quantified and tracked with intracoronary ultrasound. The Track Your Plaque report, New study confirms: LDL of 60 mg reverses plaque, on the ASTEROID Trial provides commentary on the results.


Though I remain skeptical that a statin-only treatment strategy can reverse coronary plaque in the majority of people, I do believe that the AstraZeneca-sponsored ASTEROID Trial does add to the wisdom on heart disease management. More importantly, it has served to raise awareness among both the public and my physician colleagues that atherosclerosis is indeed a potentially reversible condition.


Specifically, the ASTEROID results confirm that, either directly or indirectly, LDL cholesterol reduction achieved with statin agents does correspond to increasing degrees of plaque reversal. The mean (calculated) LDL cholesterol achieved in ASTEROID was 60 mg/dl, the same as the Track Your Plaque suggested LDL target.

Though the ASTEROID Trial is not news, I stumbled on a chart posted on the ASTEROID Trial website that clearly highlights how a number of other studies beyond ASTEROID have fallen into this pattern:





The graph reveals a linear relationship: The greater the reduction in LDL cholesterol with statin drugs, the greater the plaque regression ("change in percent atheroma volume"). (Several other studies not included in the graph also cluster into the same linear relationship.)

I am no supporter of drug companies, nor a defender of their policies and practices. But I do believe that their data can serve to teach us a few lessons. For instance, here is an (cherry-picked, to be sure) example of intracoronary ultrasound cross-sectional images before and after two years of rosuvastatin, 40 mg daily:





The color-coded/outlined atherosclerotic coronary plaque is shown shrinking, while the "lumen," or the path for blood to flow, enlarges. The reduction in coronary plaque is irrefutable. (The small circle within the lumen with the white halo surrounding it is the ultrasound catheter.)

If you and I were to choose a single treatment approach to coronary disease reversal, then 40 mg of rosuvastatin is probably at the top of the list. However, in the Track Your Plaque program, we do not advocate a single treatment strategy. While the Crestor-only approach is relatively straightforward--one pill a day--few people, in my experience, can tolerate this dose for any length of time. Patients invariably have to stop the drug or reduce the dose severely due to muscle aches when I've had patients try it. Contrary to the ASTEROID results, in my experience the majority of people, perhaps all, eventually give up with this improbable "one-size-fits-all" scheme.

The Track Your Plaque approach, while more complicated and involves several nutritional supplements and strategies, in my view addresses more causes of coronary plaque, is better tolerated, and provides health benefits outside of just LDL cholesterol reduction. It also minimizes or eliminates the need for prescription medication.



Studies cited in graph:

1.Nissen S et al. N Engl J Med 2006;354:1253-1263.
2 Tardif J et al. Circulation 2004;110:3372-3377.
3 Nissen S et al. JAMA 2006;295 (13):1556-1565
4 Nissen S et al. JAMA 2004;292: 2217–2225.
5 Nissen S et al. JAMA 2004; 291:1071–1080

When is a calorie not a calorie?

One ounce of raw almonds (about 23 nuts) contains:


6 grams protein

14 grams fat

6 grams carbohydrate

3.5 grams fiber

For a total of 163 calories per ounce.


(From the USDA Nutrient Database)


Calorie content of foods is determined by summing up the calories from each constituent: 1 gram of fat = 9 calories; 1 gram protein = 4 calories; 1 gram carbohydrate = 4 calories. Calorie content can also be directly measured using a device called a burn calorimeter, in which the amount of energy released from a specific food is measured by literally burning it and gauging precisely how much energy is released.


The problem with both of these methods is that it is assumed that all foods are digested with equal efficiency. That is, it assumes that a potato chip is as readily digested and absorbed as energy from table sugar, a pretzel, oatmeal, a piece of steak, or a handful of nuts. In real life, of course this is not true. Different foods are absorbed with varying efficiency.

For a long time I've suspected that some foods are very inefficiently absorbed. I've particularly suspected that raw nuts are relatively poorly absorbed and thus yield only a fraction of the calories ingested.

Among the studies recently reported at the Federation of the Association of Societies for Experimental Biology (FASEB) meetings I attended in San Diego this past week were several devoted to almonds.

One study, to my surprise, documented this phenomenon. In Manipulation of lipid bioaccessibility of almonds influences postprandial lipemia in healthy human subjects, it was determined that, of 100 calories ingested from the fat fraction of almonds, only about half was actually absorbed. The remaining half passed out in the stool. (They did this by collecting stool samples and comparing the fat composition after eating the different almonds prepartions. This is not discussed in the limited text of the abstract.) In addition, postprandial (after-eating) surges in triglycerides were much less with whole almonds compared to the oil separated from the nut (i.e., broken down into almond oil + defatted almond flour). The researchers attributed the difference to the inhibitory effects of the almond nut's "food matrix," or the structural properties of chewed foods.

Add to this the fact that, of 6 grams of carbohydrate per ounce of whole almonds, 3.5 grams are indigestible fibers. This means that 6 - 3.5 = 2.5 grams of digestible carbohydrates are present per ounce (assuming 100% release).

If we follow the reasoning that only about half the fat fraction of almonds are absorbed, and assume that the protein and carbohydrate (minus the indigestible fibers) are absorbed efficiently (100%), then we would re-calculate the calorie content of almonds to be 97 calories per ounce, or 40% less than calories calculated by composition or measured with a calorimeter.

If we were to assume that protein and carbohydrates were, like fats, inefficiently absorbed because of the effects of the food matrix, then one ounce of almonds yields 88 calories per ounce, or 46% less. This is, in fact, a likely scenario, since the food matrix is largely created by the cell wall and should impede digestive access to fat, protein, and carbohydrate equally.

My point? Almonds and other nuts at first appear to be calorically dense due to fat composition. However, this simplistic view of nuts is misleading because of the confounding effects of the food matrix. Stated differently: Whole foods yield less calories. And, judging by the postprandial triglyceride effects: Whole foods yield less undesirable effects, such as postprandial rises in triglycerides.

Some other observations with almonds included:

The effect of almonds on plasma lipids in persons with prediabetes This study confirmed the LDL-reducing and modest HDL-raising effects of almonds.

Almonds (Amygdalus communis L.) as a possible source of prebiotic functional food This curious observation suggests that almonds modify the bacterial flora of the intestinal tract in a positive way (like the cultures in yogurts).



Copyright 2008 William Davis, MD

Track Your Plaque data abstract

An extraordinary thing happened about 2 1/2 years ago.

While we have been following the Track Your Plaque program for coronary plaque regression for nearly 10 years, about 2 1/2 years ago we witnessed an extraordinary surge in success--bigger, faster, and more frequent drops in heart scan scores.

Up until then, we did witness significant reversal of coronary plaque by heart scan scores. We were planning to publish the data to validate this approach, but then . . .

Heart scan scores starting dropping not just 2%, or 8% . . . but 24%, 30%, 50% and more. Why? I attribute the surge in success to the addition of vitamin D.

Unfortunately, it also meant that the preceding 8 or so years of data lacked experience with supplementing vitamin D. The hundreds of participants in the Track Your Plaque program had not, until then, included vitamin D in their program.

So I decided to start from scratch (from the standpoint of data collection, not for the participants). That also meant that the preceding years of experience went unreported, though even that data far exceeded the results of what is achieved in conventional heart disease prevention.

Thus, the data I presented at the Experimental Biology Proceedings (FASEB 2008) in San Diego this week included only experiences in the group of participants that included vitamin D in their program, with data collected until mid-2007. The number of experiences is therefore modest.

However, the Track Your Plaque experience, as reported, far exceeds any prior experience in coronary plaque regression.

The full abstract will be published in the Track Your Plaque website.


Copyright 2008 William Davis, MD

Small fish oil capsules

Many people complain about the size of fish oil capsules. Let's face it: They're usually big and kind of smelly.

Women in particular struggle with big capsules. This becomes a real problem when somebody requires high-dose fish oil for treatment of post-prandial (after-eating) abnormalities, high triglycerides, or lipoprotein(a), when 6 or more--occasionally up to the equivalent of 20--standard fish oil capsules are required.

I came across a small capsule alternative for people who struggle with the big capsules. It's a product called Learn from PharmaOmega, a source of super purified fish oil.

The Learn product is actually made for children, since omega-3 fatty acid supplementation has been linked with improved intellectual performance. But the small capsule size is convenient for women and other people who would like to avoid the big standard-sized capsules.

Each capsule is about 60% of the size of a standard fish oil capsule (the smaller capsule in the photo, next to a standard size fish oil capsule), yet contains 375 mg EPA + DHA per capsule, 25% more than standard capsules (which contain 300 mg per capsule). The ratio of of EPA:DHA is a little more heavily weighted towards EPA with a 5:2 ration, compared to 3:1 of standard capsules. The capsules are also faintly orange flavored and non-fishy.





Disclosure: I receive no compensation for discussing or promoting this product.


Copyright 2008 William Davis, MD

Low-carb eating for diabetes

Jenny provided permission to reprint her very excellent introduction to low-carbohydrate eating for people with diabetes. You can also view the original version on her Diabetes 101 website.

Jenny is a stickler for monitoring the effects of blood sugar. We might take some lessons from her experiences for improving management of people with metabolic syndrome or borderline blood sugars. In other words, monitoring the blood sugar-raising effects of various foods and food portions can provide great feedback on what foods are preferable, what undesirable, given your physiology.

Even if you are not a diabetic, Jenny's discussion is must reading to gain a better understanding of food choices, particularly carbohydrates. Along with seizing control of health, she has also gained deep wisdom in how to best manage this disease and its physiology.


Introduction to low-carb nutrition for diabetics

It's carbohydrates that raise blood sugar.

Sugars and starches, not the fats that dietitians have been warning you about for so long. If you've been testing your blood sugar after meals, you've probably noticed that already and you are starting to understand why a healthy diabetes diet will have to be one that limits carbohydrates to an amount that doesn't push your blood sugar up over the level where you are damaging your body.

But if your previous experience with restricting carbohydrates involved doing a weight loss diet like Atkins or Protein Power, which worked well for you until you crashed off it entirely and gained back all the weight you'd lost, you may be hesitant to embark on another course of dieting that requires some carb restriction.

I've been there myself. I've done the extremely low carb diet Dr. Richard Bernstein recommends for months on end. I did Protein Power for 3 years. And I've gone on the "Eat all the carbs you didn't eat over the past three years all at once" diet, too. The following observations grew out of my 8 years of experience with learning how to make carb restriction work long-term.

Unlike much of what you've read before, there are no scholarly references for this section. It's based entirely on my own observations and the experience of many dozens of people who have participated in online discussion groups devoted to low carb dieting and diabetes.


Weight Loss Diets Usually Fail but Diabetes Diets Can't Afford To Fail

People who adopt a low carb diet to lose weight tend to start out with great enthusiasm, adapt extreme dieting strategies, swear they will never eat another piece of bread or french fry for the rest of their lives, lose some weight, stall out, burn out, and slink back to their old diets, where they gain back all the weight they lost and more.

This is not a surprise. People on any diet, including low calorie and low fat, do the same thing. The body is very resistant to weight loss and deeply buried instincts in our brains do everything they can to maintain our weights, no matter how unhealthy they might be.

But while this pattern of dieting may be tolerable for those who are dieting to shed a few pounds before their class reunion, it spells disaster for those who must change their diet in order to prevent the high blood sugars that result in amputation, blindness, kidney failure and heart attack death.

Low carbing for diabetes means low carbing for life, long after the thrill has worn off of eating that runny brie and steak. Despite the hype in the diet books, it is not easy, simple, and fun. I know only a handful of people who have been able to sustain a low carb lifestyle for more than five years. And that is after years of online participation in low carb groups.

What you'll find below is what I've found works for me. I used a low carb diet to control my blood sugar for more than five years and have gone through the whole cycle, from enthusiasm, to boredom, to burnout, to saying "To hell with it, we've all got to die some time!" to starting all over again determined to avoid the mistakes that sent me round the bend the first time.


How Many Grams of Carbs to Eat? As Many as Allow You to Reach Your Blood Sugar Targets

When people think about adopting a lower carb diet, their first question is almost always, "How many grams of carbs can I eat at each meal?" Most of the diet books will answer that question with a hard and fast number. Atkins, for example, tells you to start out with 20 grams a day. Protein Power starts you at 30 grams. And Dr. Bernstein suggests 6 grams for breakfast and snacks and 12 grams at lunch and dinner.

Adopting these very low carbohydrate limits will control your blood sugar very nicely. But over time, many people find that sticking to a diet this low in carbohydrate becomes impossible. That's why I'm going to ask you to throw away all those diet books and try a new approach to restricting carbs.

What you will do is to try the strategy used by the people from the alt.support-diabetes newsgroup who informally call themselves "The 5% Club" because their A1c test results fall in the 5% range which doctors consider normal: use your blood sugar meter after each meal to determine how many grams of carbs you can eat and still meet a healthy blood sugar target.

You will start out by measuring your blood sugar one and two hours after each meal. Write down what you ate and observe what it did to your blood sugar. If a meal allows you to reach your blood sugar targets, try eating it again on a different day and test it test again, possibly at a later time, to make sure that your good numbers weren't just a result of slow digestion.

If you end up too high after a meal, the next time you eat it, cut back on the portion size of the carbohydrate elements in the meal and test again. Do this until you can hit your targets, or flag the carbohydrate-containing foods in that meal as ones your body can't handle.

What you're doing here is creating what newsgroup activist Alan S. calls, "a low spike diet" rather than a low carb diet. He can achieve normal post meal blood sugars by eating as many as 30 or 40 grams of carbohydrates at a meal. Others will find that they need to eat a lot less than that amount to hit safe post-meal blood sugar targets.

Usually how much carbohydrate you can manage has something to do with your body size. The more you weigh, the less each gram of carbohydrate you eat will raise your blood sugar. Those of us whose weight is less than 150 lbs often find that we can eat between 12 and 20 grams of carbohydrate and still reach normal blood sugar targets without the help of medications, and that we can add perhaps another 10 or 20 grams more, with medications. People who are much heavier can often eat 30 or 40 grams per meal and still reach their blood sugar targets. In general, men can eat more carbohydrates and still reach their targets than can women, again, because of their larger body size.


How to Learn How Much Carbohydrate is in Your Food

To make this system work, it helps if you start to learn how many grams of carbohydrate are in the foods you eat. That way you won't have to test hundreds of foods once you've learned how a representative sample affect you.

The best way to learn how many grams of carbohydrates are in the different foods you eat is to read food labels carefully, invest in a nutritional guide like one of Connie Netzer's books of nutritional information, download nutrition software like LifeForm (http://www.lifeform.com) or use online calculators like Fit Day (http://www.fitday.com). Software and online sites will compute the amount of carbohydrates and other nutrients in your meal for you as long as you know the portion size.


Learn about Portion Sizes!
This brings up an important point: When you estimate how many grams of carbohydrate there are in a portion of food, it is very important to find out if the amount of food on your plate corresponds to the amount in the "one serving" listed on a label, in a book, or in your software.

The best way to do this is to invest in an electronic food scale and to weigh your foods for a few weeks until you get the hang of estimating portion size. You can get a good food scale at a gourmet kitchen shop for $25 to $40 dollars. This food scale may be the best nutritional investment you'll ever make.

Once you start using your scale, you will find that the muffin you bought at the coffee shop weighs 8 ounces, which is fully four times the 2 ounces that most food databases give as "one serving" of a muffin. When you read that a mythical 2 ounce portion of muffin contains 27 grams of carbohydrate you will realize why that 8 ounce coffee shop muffin with its 108 grams of carbohydrates sends your blood sugar into the psycho zone!

With ice cream, when you weigh your ice cream on a food scale, you'll quickly see that the "one portion" listed on the package turns out to be only a few teaspoons' worth. That bowl you've been considering as one portion of ice cream weighs in as four servings or 72 grams of carbohydrate and 600 calories, which may explain its damaging effect on both your blood sugar and your waistline.

This may sound like a lot of work, and when you first start, it is. But after you do it for a few weeks you'll find you have memorized the carbohydrate gram counts and the portion sizes for the foods you usually eat, and once you have tested your blood after eating these portion sizes, you won't have to test every time you eat a favorite meal, because you will know what it is going to do to your blood sugar.


Eating Away from Home

The biggest challenge you'll encounter as you start learning what you can eat will be eating away from home. You aren't going to be able to weigh restaurant foods nor can you look up the nutritional values of many restaurant offerings--though many of the common fast food outlets do provide nutritional information online--though often without listing portion sizes.

That makes it a very good idea to avoid starchy or sugary restaurant foods or, if you do eat them, to eat only a small portion of what you are offered. Measure your blood sugar an hour or two hours after eating if you aren't sure about how a restaurant food will affect you.


Fat and Carbs Eaten Together will Digest Slowly

Foods with a lot of fat in them take longer to digest than those without a lot of fat. This is why pizza and ice cream often give deceptively good readings on your meter. If you test a meal and see a reading that is too good to be true, be sure you test at 3 or four hours after eating.


The Truth About Pasta

Pasta was long recommended to people with diabetes as a food that would not raise blood sugar and you will still see it starring in many cookbooks and magazines intended for people with diabetes.

However, if you test pasta 4 or 5 hours after eating, you may get an unpleasant surprise. This is true with the so-called "low carb" pastas, too. These foods give you excellent readings at one and two hours because they are resistant to digestion so they don't turn into glucose right away. But five hours later, they do break down into glucose and when they do, the 52 grams of carbohydrates found in each 2 ounce serving of pasta will hit your blood stream with a nasty wallop. (Not to mention that you almost need a microscope to see a 2 ounce portion of pasta. Most people's idea of a portion of pasta is closer to 6 ounces--and 156 grams of carbohydrate!)

If you have pasta for dinner and don't see a peak 3 hours later, be sure to check your fasting blood sugar the next morning. You may see the blood sugar rise there, too.


Sugar Alcohol and "Sugar Free" Foods

The sugar alcohol used in so-called "sugar free" foods can also show up in your blood sugar an hour or two after you'd expect to see them, especially the maltitol used in "sugar-free" candy. At least half of the sugar in Maltitol does turn into glucose in your blood stream and it can raise your blood sugar, but the rise is delayed so you may miss it on testing. So if a "sugar free" food seems to be kind to your blood sugar, try testing it an hour or two after your first tests. Erythritol is the one sugar alcohol that usually does not show up in your blood sugar.


Dealing with Limited Blood Testing Supplies

In in ideal world, we'd all have all the testing supplies we needed to control our blood sugar, but in real life blood sugar test strips are very expensive and many insurers sharply limit the number of strips people with Type 2 diabetes can get each month.

Here are some strategies that can help you if your access to strips is limited.

If you only have 50 strips to get you through a month, plan out what you are going to test ahead of time. Pick one of your favorite meals, and test at 1 hour after eating the first time you eat it and 2 hours after eating the second. Do this with a couple different meals and see if there's a pattern as to when you see the highest reading--whether it is at one hour or two. Then choose another meal and test it at the time when you saw the highest reading in the earlier meal. If you ever get a surprisingly low reading, try testing an hour later or earlier, to make sure you aren't missing the peak.

Make the goal of your testing be learning how many grams of carbs you can tolerate in one meal. If you learn that 30 grams is your upper limit, use software and your scale to find portions of other foods that will also clock in at 30 grams or less. Test one or two of these, and if you see the result you expect, you don't have to test every time you eat these foods again.

Wal-mart sells a cheap and effective blood sugar meter with strips that cost one half as much as other vendors. Some drug stores also sell store brand meters with cheaper strips. If you need more strips, consider the $50 you pay for another 100 strips an investment in your health. It's far better to spend that $50 now, than to spend it on expensive doctor bills caused by complications you don't need to develop!


Keep the focus on Achieving your Blood Sugar Goals

By testing after meals, you'll learn how many grams of carbohydrate your own, unique, body can handle. And more importantly, you'll also be able to decide if you are going to be able to control through diet alone, of whether it is time to talk to your doctor about supplementing dietary control with drugs.

Many people are so excited to learn that they can achieve normal blood sugars by cutting way back on carbohydrates that they become zealots for low carb dieting. I've been there and I've done that. But it's important not to get too carried away with a "Carbs are Evil" mentality which makes it a matter of religious zeal never to let evil carbs cross your lips again. Like all conversions this one tends to fade out in time. And as we said at the start of this chapter, your ultimate goal is to maintain your blood sugar targets for the rest of your life. So the safest approach is to get the most blood sugar benefit you can out of restricting carbohydrates, but restrict them to a level you can maintain year in and year out.

Most importantly, I have learned it is best to treat carb restriction as a strategy, one of many, which used in combination with other strategies including medications if needed, can give you normal blood sugars, rather than the One and Only True Way. If you can be flexible and find more than one tool to help you meet your blood sugar targets, you are more likely to be able to maintain those excellent blood sugars for years to come.


Eliminate "Habit Carbs" and Concentrate on "Value Carbs"
When people think about restricting their carb intake they assume this means never eating any of their favorite foods again.

But for many of us, this doesn't have to be true. Why? Because a quick look at your daily carb intake will often reveal that the bulk of the carbohydrates you are eating are what I call "habit carbs." These are the carbs you eat without a second thought because they are there. Not because they taste good. Not because you couldn't live without them. Just because you're in the habit of eating them.

Here is a list of some prime "habit carbs."

Steam table mashed potatoes

Limp french fries

Squashy hamburger buns

Cardboard toast

Cold home fries

Stale boxed cookies


How many of these flavorless, starchy foods are you consuming everyday just because they're there? Probably more than you realize. So before you lift that fork-full to your mouth, ask yourself, "Is this food thrilling me?" If not, put it down. This should go a long way towards getting your carb intake down.

What I'd call "value carbs" are those carb-rich foods that really do mean something to you. I'm not going to lie to you. You are not going to be able to make them the mainstays of your diabetes diet. But by using the strategies describe below, you should be able to eat enough of these foods to keep yourself from feeling deprived--without destroying your health.


Don't Create "Forbidden Foods!"

If you are one of those people who could live happily on Purina People Chow, you can skip what follows. But if food has been important to you, and if you have hitherto had a long and emotionally satisfying relationship with food, or if, like me, baking from scratch was one of your favorite ways to show love and express creativity, restricting your carbohydrate input will mean that a whole lot of what you've been eating (and baking) up until now is suddenly, completely, off limits. I can't eat cake and get a healthy blood sugar level. Even with two different diabetes drugs in my system. I can't eat cake even with an insulin shot before I eat it. I love cake but there is no way I can eat more than a bite or two without seeing very high blood sugars and there is no way I can eat two bites of cake and be happy. The same goes for french fries and Thai noodles.

During the first enthusiastic weeks of exploring carb restriction most people deal with this kind of discovery by coming up with new recipes and finding new, delicious and healthy things they can substitute for old, high carb standards. They appreciate the way cutting way back on carbohydrates curbs their hunger and makes food much more manageable. This is good and it is why long term low carbing is possible. But our old favorite foods do not go away that easily.

If you decide that some food you have been eating and enjoying all your life will never again cross your lips, it is almost 100% guaranteed that you'll end up pigging out on that very same food at some time in the future, hating yourself, and even beginning a binge that can throw you completely off your diet for months.

It might not happen the first month you are restricting your carb intake or even the first year. It took me three years of low carbing to get to where I crashed off my stringent low carb diet. But eventually it happens, and because after almost a decade of counting my carbs I've learned that I will never lose my love for certain foods that don't love me, I've put a lot of time into finding a way of restricting my carbohydrate intake in a way that avoids the buildup those feelings of deprivation that eventually lead to long periods of unwise eating.

The key, for me, is to build safety valves into my diet. I don't call them "cheats" or "bad foods" for reasons I'll get into later. I call them "off plan" foods because they are not food I can make an ongoing part of my daily food plan. Because my goal is life-long blood sugar control, I accept that I will occasional eat "off plan" and that this is okay as long as I am meeting my blood sugar targets most of the time. "Good enough" control that I can adhere to year in and year out beats a few months of perfection followed by crashing off the diet entirely and ruining my health. Here is one way to approach doing this:

Do the Diet Straight for a Month or Two Before You Try Off-Plan Goodies

As you learn what foods raise your blood sugar and what foods don't, you will almost certainly find that there are a lot of foods you used to love that don't work for you anymore. Waffles for breakfast, coffee cake at coffee break, three slices of pizza with crust, a burger with a bun and a side of fries are just a few of the foods that it is almost certain will not allow you to meet your post-meal blood sugar targets.

As you keep using your meter to test what you eat, if you are like most people with diabetes you'll also learn that some of the so-called "low glycemic" foods and the supposedly "healthy" whole grains that nutritionists recommend for people with diabetes won't work either. Oatmeal and whole wheat bagels raise my blood sugar far too high, so does cracked whole wheat, whole wheat bread, and brown rice.

If the dietician tells you a food is good for you, but your meter tells you it is raising your blood sugar to a level that is high enough to cause complications, you will have to listen to your meter. Your meter will tell you what is safe to eat and for the first couple of months while you are learning how to get your blood sugar under control and how bring those high blood sugars down to normal levels you will have to accept that you can only eat those foods that don't cause spikes.

If you attempt to add in off-plan foods before you are solidly on-plan you may never really get into the swing of eating a diet that controls your blood sugars and you may not get to where your body learns to enjoy the lower carb foods that don't give you blood sugar swings.

But after you've gotten your blood sugar under control, nothing horrible will happen if you make room for a small portion of some high carb treat every now and then.


How to Add Off-Plan Foods to the Plan

If you've avoided bread for a couple months, the humble roll in that restaurant bread basket may start to call out to you with an irresistible siren song. If you give in and eat it, with each bite you may find yourself feeling as if you are doing something incredibly sinful--the way you might have felt if you had eaten a whole box of chocolates in the past.

That feeling is the sign that you're heading for trouble. You've created a "forbidden fruit" and sooner or later that forbidden fruit is going to get you. You may find yourself thinking about that roll, craving another, sneaking off to eat one where nobody knows you, or, alternatively, you may declare that you will never again eat a roll ever--and then ruin your Thanksgiving holiday when you go to Aunt Glenda's and refuse to eat even a single one of those wonderful rolls of hers you've eaten every year of your life which say, "This is the family Thanksgiving" to you.

It is far better to make a bit of room in your diet for high carb treats so that they don't build up a charge. If you do this, you'll find that they almost never taste as good as you remembered, and you'll be able to leave them behind without turning them into an object of obsession.

Just knowing that you can eat some specific off-plan food at some future time, when it is scheduled, makes it that much easier to say, "No thanks" to it, and maintain your healthy blood sugar the rest of the time.


How Often Can You Eat Off-Plan?
How often you have an off-plan food depends a lot on your dietary goals, how high your blood sugar is before you eat carbs, and whether you are willing to exercise after eating. It also depends greatly on what medications you are taking for your diabetes. Whatever I eat, I try to keep my blood sugar below 120 mg/dl (6.7 mmol/l) at 2 hours after any meal.

Forty minutes of cardiovascular exercise will burn off a lot of extra carbs, so if you exercise regularly, try to eat your high carb treat before you head for the gym.

If you're trying to lose weight, you may have to keep off plan treats few and far between. When I was actively losing weight on a low carb diet without medications I ate one off-plan meal about once every two weeks.

Once I reached my weight loss goal I loosened up a bit but I found it best to cycle between weeks of eating a strict very low carb diet, and then a week of eating slightly more carbs--but I tried very hard not to ever anything that would cause my blood sugar to be over 120 mg/dl (6.7 mmol/L) at 2 hours after a meal because doing so makes me feel rotten.


Throw Away the Vocabulary of Self-Destructive Dieting

When you eat something with carbs in it, don't think of it as a "cheat." Cheating is what you do when faced with an authority figure--your 9th grade math teacher or the IRS. But you are the one in control of what you eat. So when you eat something that is off-plan, you should stop thinking of it as "getting away with something" and treat it instead as something you've decided to do--for a reason that should be clear to you while you do it.

If you keep eating things that were not what you had intended, rather than beating yourself up, it's time to reconsider your food plan and figure out why it isn't working. Are you having trouble finding foods in restaurants that don't raise your blood sugar? Maybe it's time to bring your lunch along to work for a while, or to find new place to dine.

Are you bored with what you have been eating? Google for good low carb recipes you can try at home. There are thousands of them. If you use the Google Groups search and look for messages in alt.support.diet.low-carb that start with "REC" you'll find a treasure trove of ideas to try.

Keep the vocabulary of sin and guilt for the confessional. You're going to eat a lot of things in the years to come that will mess up your blood sugar. But if you are kind to yourself and dust yourself off after you mess up and keep on going, doing the best you can to hit your blood sugar targets, you may very well end up healthier than many people who do not have diabetes. The important thing is to keep at it, doing the best you can and forgiving yourself when the best you can do isn't as good as you wish it was.


Know Your Limits
I've learned the hard way I can't eat half a blueberry muffin, so I don't even try portion control for that particular food. I know blueberry muffins are trouble and I also know that I will eventually eat one. That's just how it is, so every blue moon or so I eat a blueberry muffin, experience the miserable high blood sugars that follow, and then remember why I don't eat muffins every day any more. What I don't do is fool myself that I can buy a muffin and only eat half. Everyone has a few foods that fall into this category. Treat them with caution!


Eat Off-Plan Foods Out of the House
I've learned the hard way that if a big box of something full of carbs is in the fridge, bad things are going to happen. So I try to eat my off-plan foods away from home. I eat my muffins or cookies at a coffee house. I have a slice of pizza at a pizzeria. I don't buy a box of muffins or a whole pizza and bring them home.

Getting this strategy to work requires that your whole family understand what's at stake. It took me a couple years of harping on what "complications" means, but by now, my family understands that if my blood sugar is too high, I'm damaging my body. They want to keep me around for a while, so they understand that there are some foods that shouldn't be brought into the house--ever.

When other family members want to have treats at home, they are kind enough to buy things I don't like. For example, if someone wants Ben & Jerry's they buy the Chunky Monkey flavor that I find revolting, not the New York Fudge. By the same token, when my kids lived at home, I didn't buy them the brands of cookies I can't resist. There are plenty of others cookies they liked that don't tempt me at all, and those were the ones in the cupboard.

Over the years the nondiabetic members of my family learned that no one is doing themselves a favor scarfing down 300 grams of fast acting carbohydrate every day--particularly not people with a family history of diabetes and heart disease!


Medications Can Help

I'm not a big fan of medications because I've learned the hard way that drug companies lie about side effects and some of these side effects are permanent and can ruin your life. But I learned the hard way, too, that some of us (like, say me) can't get normal blood sugars no matter how low our carb intake. For us, adding a diabetic drug or two to our daily regimen may be the only way we can get normal blood sugars without a life of tormenting self-denial.

Drugs I have found useful over the years include metformin, precose, and post-meal insulin shots. The new incretin drugs, Januvia and Byetta help some people make dramatic improvements in their blood sugar, but the way that they work makes it necessary to eat a slightly higher amount of carbohydrates with them because they only work when your blood sugar rises over a certain threshold. Even with these drugs (including Januvia) I've never been able to eat more than 120 grams of carbohydrates a day, but after many years of eating an extremely low carb diet--which was the only diet that would control my blood sugars--120 grams of carbs a day feels like a completely normal diet!


Be Aware of Rising Insulin Resistance

Some people may find that eating a low carb diet is not enough to control their blood sugar because they are very insulin resistant. Perhaps they have been diagnosed with PCOS, or have to take a drug, like Prednisone that increases insulin resistance. The book, Dr. Bernstein's Diabetes Solution by Dr. Richard K. Bernstein, the distinguished diabetes doctor, recommends Metformin as an appropriate drug for patients on a low carb diet whose blood sugars are still not completely controlled. It isn't a cure by any means, just one more tool you can use to keep blood sugars under control, and if you limit your insulin resistance you may solve both weight and hunger problems that otherwise can derail your diet.

You can read more about the different drugs available to help control blood sugars HERE. Just remember that all these diabetes drugs work best when you combine them with some level of carbohydrate restriction. How much restriction? Test your meals one and two hours after eating, and your blood sugar meter will tell you exactly how much.


Top Medical Journal Publishes Landmark Study Showing Very Low Carb Diet Most Effective and Safest for Lipids etc.

In case you are still being given out-of-date medical or nutritional advice by people who tell you that a low carb/high fat diet will give you a heart attack, take a look at this recently published study, which appeared in the Journal of the American Medical Association.

This study found that an Atkins style low carb diet not only caused double the weight loss of the low fat diet at the end of one year, but it did not adversely affect cholesterol levels.

This finding, added to the Women's Health Initiative finding (after $40 million dollars of research) that low fat dieting does NOT prevent heart disease, should lay to rest any last fears you might have about the impact of cutting carbs on your health.

The findings of this study, are not news to anyone who has tried a low carb diet and stuck with it for any period of time, but they appear to amaze the entire medical community who continue to cling to their to the "Fat is Bad" religious belief long no matter what evidenced-based medical studies might come up with.

Bottom line: You can cut your carbs way down, replace carbs with fat, and await the better health this kind of eating will provide.

Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women: The A TO Z Weight Loss Study: A Randomized Trial.Christopher D. Gardner, PhD; Alexandre Kiazand, MD; Sofiya Alhassan, PhD; Soowon Kim, PhD; Randall S. Stafford, MD, PhD; Raymond R. Balise, PhD; Helena C. Kraemer, PhD; Abby C. King, PhD


Here's the summary of the WHI findings:

NIH News: News from the Women?s Health Initiative: Reducing Total Fat Intake May Have Small Effect on Risk of Breast Cancer, No Effect on Risk of Colorectal Cancer, Heart Disease, or Stroke


Here's a study that documents the effectiveness of lowering carbs and increasing fat and protein consumption for the control of blood sugar in the absense of weight loss:

Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition. Nutrition & Metabolism 2006, 3:16.


To Get More Help with Making a Low Carbohydrate Diet Work

My "Low Carb Facts and Figures" site, which now shares this server, has more information I collected back in the days when I used a low carb diet for both weight loss and blood sugar control.

You'll find articles there that address a few of the issues people run into while eating a very low carb diet,which are not answered in a completely honest fashion by the people who sell diet books promising you can lose weight easily while gorging on all your favorite foods--which, sadly, is 99% of all authors writing diet books.

Interview with an outspoken advocate of truth in diabetes

I stumbled onto Jenny Ruhl's Diabetes Update blog after I received several very insightful comments to this blog whenever I posted a discussion on diabetes or pre-diabetes/metabolic syndrome.

Who the heck was this commenter who clearly had deep insight into diabetic issues?

It turned out to be Jenny Ruhl, a woman who learned her lessons the hard way: by receiving a belated diagnosis of (an unusual form of) diabetes, then receiving plenty of mis-guided advice from physicians on diet and treatment. Reading her many blog posts and websites, you get the clear sense of how hard this individual worked to gain the depth of knowledge she's acquired, on a par or superior to most diabetes specialists.

And she minces no words in expressing her heartfelt and carefully considered opinions. But that's what I look for: people who are unafraid to voice opinions that may not be consistent with the flow of conventional thought, but ring true and prove effective.


Dr. Davis: From your blog and websites on diabetes, it is clear that you exceptionally knowledgeable in the world of diabetes, metabolic syndrome, and related disorders. Can you give us a little background on how you came to this quest?

Jenny: Though I was told I was a "classic type 2" [diabetic] by my doctors, nothing I read about diabetes corresponded to my own experience. I knew my diabetes had not been caused by obesity because I'd been a normal weight all my life until my blood sugars went out of control at which point I developed ravenous hunger and gained a lot of weight very quickly.

I also wondered at the huge gap between what Dr. Bernstein said was a normal blood sugar and what my doctors told me was a safe blood sugar for a person with diabetes. The people I met who followed Bernstein's very low carb diet had much better blood sugars and far fewer complications, but my doctors dismissed this as irrelevant. So I decided to do some research to find out who to believe. I plunged into the medical journal articles that had recently been made available on the web to see if I could answer two questions: What causes diabetes? and "What does science actually know about what blood sugar levels damage organs?"

The result was the information that became the basis for the Blood Sugar 101 site. Initially, I attempted to sell it as a book, but editors told me that though what I'd learned was "fascinating" it would be "over the head" of the typical health book buyer who wanted simple explanations and if possible, a simplistic slant towards "cure." Fortunately, the very strong response and high traffic volume to the web site proved that, as I had thought, there are a lot of people who do want more than an oversimplified overview and who, given the information they needed, were able to make huge positive changes in their health.


Dr. Davis: What do you think your life would be like if you hadn't pursued this unique course?

Jenny: Possibly a lot shorter.

People in my family die of heart attacks in their 50s, probably from undiagnosed high blood sugars. The pattern of the type of diabetes I have is to have a normal fasting blood sugar and an extremely high post-meal blood sugar after consuming very few grams of carbohydrate. When doctors diagnose using only the fasting blood test, they miss those highs, which research is now finding to be a primary cause of heart disease.

I also would have been a lot fatter. My doctors told me that I was packing on 20 lbs a year due to "normal menopausal changes" and that there was nothing I could do about it. Lowering my carbs significantly dropped all the weight I had gained and I still weigh a lot less now than I did in 1998.


Dr. Davis: You've been a keen observer of the diabetes scene for some years. Have you discerned any important trends in both the public's perception of diabetes as well as how diabetes is managed in the conventional world?

Jenny: The huge difference I see is that, over the last decade, the online diabetes community has learned the value of cutting back on carbohydrates and shooting for truly normal blood sugar levels. So people who put some time into researching diabetes online and talking with those of us who have succeeded in avoiding complications will learn that they do not have to settle for very high blood sugars and deterioration their doctors think inevitable.

Unfortunately, the media have put most of their energy into promoting the discredited idea that diabetes is caused by gluttony and sloth and to promoting the equally discredited idea that people with diabetes should eat a high carbohydrate diet and avoid fat.

So for now there is a huge divide in the quality of life of those people with diabetes who educated enough to go out on the web and educate themselves and those who get their diabetes information from doctors. Sadly most doctors still encourage patients to eat low fat/ high carb diets, and counter the very high blood sugars this diet produces with oral drugs of questionable efficacy, while assuring patients they will be safe if they maintain blood sugar levels that meet the American Diabetes Association's recommendations, though a mass of research shows these are high enough to produce every single diabetic complication possible.


Dr. Davis: I understand that you've released a new book, Blood Sugar 101. How is your book unique in the world of diabetes books? Who should read Blood Sugar 101?

Jenny: Blood Sugar 101: What They Don't Tell You About Diabetes differs from other books in that it gives the reader a much deeper understanding of what is really going on in their bodies as their blood sugar control breaks down and what sciences knows about how abnormal blood sugars cause complications. Then it gives the reader the tools they need to find what diet and/or drug regimen will brings their own, unique, blood sugars down to a truly safe level.

Unlike some books, this one does not present a one-size-fits-all solution, but recognizes that Type 2 diabetes is really a catch-all diagnosis that covers a lot of disorders that behave quite differently. That is why what works for one person with diabetes may not work for another.

Because this book provides details available nowhere else about the physiology of diabetes and the drugs available to treat it, readers will find the information they need to work with their doctors to craft a regimen that brings their blood sugar into the range that preserves and improves their health.


Dr. Davis: Before we close, tell us a little about yourself outside of your diabetes advocate role.

Jenny: I live in rural New England and am a passionate gardener. I've been online since 1980 when I was part of the team at IBM that developed the first commercial email program, PROFS. I got involved in online discussion groups in 1987 and have been messaging on bulletin boards ever since.

I was a professional singer/songwriter in Nashville in my youth and spent my middle years as a bestselling author of books about consulting. Right now a lot of my energy goes into managing the financial and software side of a family business that makes hand made pocket tools for collectors.


Dr. Davis: Thank you for your great insights, Jenny!

The Marshall Protocol and other fairy tales

True to form, Dr. John Cannell has published yet another wonderfully insightful Vitamin D Newsletter.

One item caught my eye, a response to a question about the Marshall Protocol. I, like Dr. Cannell, was inundated with questions about this so-called protocol, which amounts to little more than the unfounded speculations of a non-physician, actually someone not even involved in health care.

In all honesty, I blew the whole issue off after I read Dr. Marshall's rants. They smack of pure quackery, though from somebody who clearly has a command of scientific lingo. To Dr. Cannell's credit, he took the time and effort to construct a rational response in the latest issue of the newsletter. I reproduce his response here:



Dear Dr. Cannell:

I understand Dr. Marshall conducted a study and found vitamin D is bad for you. What kind of study did he do?

Mary, Minneapolis, Minnesota


Dear Mary:

I have been inundated with letters asking about Professor Marshall's recent "discovery." Some have written that to say they have stopped their vitamin D and are going to avoid the sun in order to begin the "Marshall protocol." The immediate cause of this angst is two publications, a press article in Science Daily about Professor Marshall's "study" (which is no study but simply an opinion) in BioEssays. Dr. Trevor Marshall has two degrees, both in electrical engineering. Before I begin, I want to again remind you that I am a psychiatrist who works at a state mental hospital. In my duty to full disclosure, I must say that I have known a lot of psychiatrists in my life and a few electrical engineers. If I knew nothing else of a disagreement between two people but their professions, I would believe the electrical engineer, not the psychiatrist.

In reading his two articles, Dr. Marshall's main hypotheses are simple. (1) Vitamin D from sunlight is different than vitamin D from supplements. (2) Vitamin D is immunosuppressive and the low blood levels of vitamin D found in many chronic diseases are the result of the disease and not the cause. (3) Taking vitamin D will harm you, that is, vitamin D will make many diseases worse, not better. If you read his blog, you discover that the essence of the Marshall protocol is: "An angiotensin II receptor blocker medication, Benicar, is taken, and sunlight, bright lights and foods and supplements with vitamin D are diligently avoided. This enables the body's immune system, with the help of small doses of antibiotics, to destroy the intracellular bacteria. It can take approximately one to three years to destroy all the bacteria." That is, Dr. Marshall has his "patients" become very vitamin D deficient.

Again, Dr. Marshall conducted no experiment and published no study. He wrote an essay. He presented no evidence for his first hypothesis (sunlight's vitamin D is different than supplements). From all that we know, cholecalciferol is cholecalciferol, regardless if it is made in the skin or put in the mouth. His second hypothesis is certainly possible and that is why all scientists who do association studies warn readers that they don't know what is causing what. Certainly, when low levels of vitamin D are found in certain disease states, it is possible that the low levels are the result, and not the cause, of the disease. Take patients with severe dementia bedridden in a nursing home. At least some of their low 25(OH)D levels are likely the result of confinement and lack of outdoor activity. However, did dementia cause the low vitamin D levels or did low 25 (OH)D contribute to the dementia? One way to look at that question is to look at early dementia, before the patient is placed in a nursing home. On the first day an older patient walks into a neurology clinic, before being confined to a nursing home, what is the relationship between vitamin D levels and dementia? The answer is clear, the lower your 25(OH)D levels the worse your cognition.

Wilkins CH, Sheline YI, Roe CM, Birge SJ, Morris JC. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatr Psychiatry. 2006 Dec;14(12):1032-40.

Przybelski RJ, Binkley NC. Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Arch Biochem Biophys. 2007 Apr 15;460(2):202-5. Epub 2007 Jan 8.


These studies suggest that the low 25(OH)D levels are contributing to the dementia but do not prove it. Only a randomized controlled trial will definitively answer the question, a trial that has not been done. So you will have to decide if vitamin D is good for your brain or not. Dr. Marshall seems to be saying demented patients should lower their 25(OH)D levels. Keep in mind, an entire chapter in Feldman's textbook is devoted to the ill effects low vitamin D levels have on brain function.

Brachet P, et al. Vitamin D, a neuroactive hormone: from brain development to pathological disorders. In Feldman D., Pike JW, Glorieux FH, eds. Vitamin D. San Diego : Elsevier, 2005.

It is true that in some diseases, high doses of vitamin D may be harmful. For example, in the early part of last century, the AMA specifically excluded pulmonary TB from the list of TB infections that ultraviolet light helps. They did so because many of the early pioneers of solariums reported that acutely high doses of sunlight caused some patients with severe pulmonary TB to bleed to death. Thus, these pioneers developed very conservative sun exposure regimes for pulmonary TB patients in which small areas of the skin were progressively exposed to longer and longer periods of sunlight. Using this method, sunlight helped pulmonary TB, often to the point of a cure. Furthermore, it is well known that sunlight can cause high blood calcium in patients with sarcoidosis. In fact, sarcoidosis is one of several granulomatous diseases with vitamin D hypersensitivity where the body loses its ability to regulate activated vitamin D production, causing hypercalcemia.

Cronin CC, et al. Precipitation of hypercalcaemia in sarcoidosis by foreign sun holidays: report of four cases. Postgrad Med J. 1990 Apr;66(774):307-9.

Furthermore, although medical science is not yet convinced, some common autoimmune diseases may have an infectious etiology. I recently spoke at length with a rheumatologist who suffers from swollen and painful joints whenever he sunbathes or takes high doses of vitamin D. As long as he limits his vitamin D input his joints are better. To the extent vitamin D upregulates naturally occurring antibiotics of innate immunity, sunlight or vitamin D supplements may cause the battlefield (the joints) to become hot spots. I know of no evidence this is the case but it is certainly possible.

However, If Dr. Marshall's principal hypothesis is correct, that low vitamin D levels are the result of disease, then he is saying that cancer causes low vitamin D levels, not the other way around. The problem is that Professor Joanne Lappe directly disproved that theory in a randomized controlled trial when she found that baseline vitamin D levels were strong and independent predictors of who would get cancer in the future. The lower your levels, the higher the risk. Furthermore, increasing baseline levels from 31 to 38 ng/ml reduced incident cancers by more than 60% over a four year period. Therefore, advising patients to become vitamin D deficient, as the Marshall protocol clearly does, will cause some patients to die from cancer.

Lappe JM, Travers-Gustafson D, Davies KM, Recker RR, Heaney RP. Vitamin D and calcium supplementation reduces cancer risk: results of a randomized trial. Am J Clin Nutr. 2007 Jun;85(6):1586-91.

I will not write again about Dr. Marshall's theories. No one in the vitamin D field takes him seriously. Personally, I admire anyone willing to swim against the tide and raise alternative theories. I have done the same with influenza and autism. However, I agree with the New York Times, An Oldie Vies for Nutrient of the Decade and Jane Brody's conclusion, "In the end, you will have to decide for yourself how much of this vital nutrient to consume each and every day and how to obtain it." I agree. You will have to decide for yourself.

John Cannell, MD
The Vitamin D Council

Breaking news from the American College of Cardiology meetings

The American Heart Association (AHA) was kind enough to send me an e-mail headlining the breaking news from the American College of Cardiology (ACC) meetings underway in Chicago:


ISAR-REACT 3
A Randomized, Double-Blind, Active-Controlled, Multi-Center Trial (ISAR-REACT 3) of Bivalirudin Versus Unfractionated Heparin in Troponin-Negative Patients Undergoing Percutaneous Coronary Interventions After Pre-Treatment With 600 mg of Clopidogrel

TRITON - TIMI 38 Stent Analysis
Prasugrel Compared to Clopidogrel in Patients With Acute Coronary Syndromes Undergoing PCI With Stenting: The TRITON - TIMI 38 Stent Analysis

Percutaneous Coronary Interventions in Facilities without On-Site Cardiac Surgery (NCDR)

(And four other similar reports)


Let's meld the ACC headlines with the financial headlines:

July 2, 2007
The Medicines Company announces reacquisition of all marketing rights to bivalirudin, anticoagulant growing in use for coronary angioplasty and related procedures. 2008 sales anticipated to be in the $15-20 million range, to grow to $90-110 million, a growth rate of 50% per year.


November 20, 2007
Drug manufacturing giant, Eli Lilly, vies for a portion of the $5 billion (annual revenues) oral anti-platelet market, now occupied by Plavix, with its newer, but questionably better, agent, prasugrel.


Growth of the coronary angioplasty (percutaneous coronary intervention, or PCI) doesn't ordinarily make headlines, but the performance of specific companies within the industry does. Angioplasty and cardiac device maker (inc. the drug-coated stent, Taxus), Boston Scientific, for instance, announced record sales of $8.537 billion for 2007, an increase of $536 million. How to grow this market? We could always hope for more people with heart attacks or other unstable symptoms. Or, we could . . . increase the number of hospitals capable of PCI! Brilliant.


The money behind this push for procedures is staggering. It drives enormous marketing efforts, pays Washington lobbyists, pays for many nice dinners and trips for doctors who engage in the system, and pays for very costly research.

And the AHA and ACC are kind enough to let us know about these great pieces of news.