Dr. Davis,

I continue to be amazed at how much value you are providing all the time to those of us deeply concerned about heart disease.

Whether it's at this blog, at LEF.org, at your TrackYourPlaque.com site, or in your Track Your Plaque book, your contribution is pretty astounding.

I only found your work in the last 2-3 weeks and already it has made a deep impression on me and I'm getting clearer about what I need to do to combat heart disease in myself and in family members.

Thanks for all you're doing!

Wow!

Thanks for the feedback. I'm glad it's helping you. It is wonderful to hear back about the impact the program is having.

Excellent article!  I especially liked the tie-in to poor kidney function.

Dr. Davis: In your excellent LEF article, I found your reference to a fascinating statement about statins and vitamin D by Dr. David Grimes of the UK. For those interested, here is the Lancet source article (reprinting for educational purposes):

The Lancet 2006; 368:83-86
DOI:10.1016/S0140-6736(06)68971-X

Are statins analogues of vitamin D?
David S Grimes MD, Blackburn Royal Infirmary, Blackburn, Lancashire BB6 8HE, UK

Summary

There are many reasons why the dietary-heart-cholesterol hypothesis should be questioned, and why statins might be acting in some other way to reduce the risk of coronary heart disease. Here, I propose that rather than being cholesterol-lowering drugs per se, statins act as vitamin D analogues, and explain why. This proposition is based on published observations that the unexpected and unexplained clinical benefits produced by statins have also been shown to be properties of vitamin D. It seems likely that statins activate vitamin D receptors.
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During the late 19th century, conventional wisdom held that masturbation was the cause of epilepsy, a more plausible explanation than the previous notion that epilepsy was the result of possession by the devil, and illness in general the result of divine interference. Since bromide was thought to reduce sexual desire, it became the logical treatment. Although reasonably successful, bromide worked for reasons that are different from the theory on which it was based. Can the same be said of statins for heart disease?

The emergence of coronary heart disease (CHD) in the 20th century required an explanation. Some had noted that cholesterol accumulated in the walls of the arteries, and a process of accretion was hence described as the major mechanism. Cholesterol was assumed to originate from diet, and the diet-cholesterol-heart hypothesis was established. The logical treatment was to reduce dietary and serum cholesterol concentrations.

Many inconsistencies in this hypothesis have emerged and been disregarded. In the London banking and transport study,1 for example, men with the highest dietary cholesterol intake had the lowest incidence of CHD. Furthermore, the results of the Framingham study2 showed that raised concentrations of serum cholesterol were predictive of CHD only in men younger than age 55 years. Findings of studies from Honolulu3 and Paris4 suggest a protective effect of high serum cholesterol concentrations, and the Leningrad paradox5 indicates that those exposed to famine subsequently have a high incidence of CHD, the opposite of what is expected. In Europe, populations that consume a large amount of dietary fat and cholesterol have a low incidence of CHD (the French paradox),6 and the lowest incidence of CHD is seen in European nations with the lowest consumption of wine and the most socioeconomic deprivation (the Albanian paradox).7

Initial treatments to reduce serum cholesterol were not effective. When introduced, however, statins did greatly reduce serum cholesterol concentrations by interfering with its synthesis; the beneficial effects of statins in CHD have been assumed to be the result of cholesterol-lowering, an assumption that I believe is a serious mistake.

Statins and the heart

The first statin trial was the Scandinavian Simvastatin Survival Study (4S),8 and its findings indicated a significant clinical benefit from simvastatin. The results of the West of Scotland Coronary Prevention Study (WOSCOPS)9 also showed clinical benefit from statins (pravastatin) and of a greater magnitude than expected; the mortality reduction was about 35%, whereas the reduction in cholesterol concentrations predicted a mortality reduction of only 25%. WOSCOPS9 showed no association between cholesterol-lowering and clinical benefit,10 indicating that cholesterol-lowering was not the mechanism by which pravastatin reduced coronary events.

In WOSCOPS, statins lowered serum cholesterol concentrations, but also raised concentrations of HDL cholesterol and lowered those of serum triglyceride, indicating that inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase was not the only metabolic action. The clinical experiment of cholesterol-lowering was thus intrinsically flawed, and what must be understood is that 4S and WOSCOPS were trials of statin therapy and not trials of cholesterol-lowering.

Unexpected benefits of statins

It is noteworthy that the participants treated with pravastatin in WOSCOPS had a reduced incidence of diabetes compared with controls.11 Additionally, when pravastatin was given to recipients of heart transplants in an attempt to reduce the likelihood of CHD, a reduction in the rate of rejection and an increase in overall survival was noted, irrespective of CHD status.12 The same pattern was seen in recipients of kidney transplants.13 Clinical benefits of statins have also been noted in a placebo-controlled trial14 of atorvastatin for rheumatoid arthritis. Furthermore, simvastatin has been used successfully to treat patients with multiple sclerosis.15 As with CHD, diabetes, rheumatoid arthritis, and transplant rejection, the benefit noted with respect to multiple sclerosis is independent of any effect on serum cholesterol.
Statins also have an effect on bone, and women who take statins have a greater bone density than those who do not.16 Moreover, the findings of the 10-year follow-up study of participants in 4S17 indicate a significantly reduced risk of cancer, particularly colorectal, lung, and prostate cancer, in those who received simvastatin. Results of a population study from Israel18 also show a greatly reduced risk of colorectal cancer in those taking statins.

In 1974,19 a group of illustrious diet-cholesterol-heart researchers studied the association between cholesterol and cancer. They noted that high serum cholesterol concentrations conferred protection against colon cancer. The effects of statins mentioned above hence present a major paradox: how can a drug that lowers serum cholesterol concentrations reduce the risk of colon cancer when high serum cholesterol concentrations are, in fact, protective?

A drug can act as a poison by blocking normal metabolic processes, but to produce a beneficial effect (other than antibacterial) we should assume that it is switching on or enhancing a normal metabolic process. I therefore suggest that statins mimic many of the actions of vitamin D and can be considered analogues of vitamin D.

Sunlight and vitamin D

Heart disease

In Europe, there is a higher rate of mortality from CHD in the northern than in the southern countries, with the lowest rates noted along the Mediterranean coast.20 This pattern suggests that susceptibility to CHD is affected by duration of exposure to sunlight. This notion is supported by findings from the USA21,22 that the higher the altitude of residence, and hence the greater the sunlight intensity, the lower the risk of heart disease.

Furthermore, the only dietary change that consistently protects against CHD is an increase in consumption of oily fish and fish oil, which contain large amounts of vitamin D.23 In the Netherlands, mortality from CHD was more than 50% lower in men who consumed at least 30 g of fish per day than in those who did not eat fish.24 A similar result was reported in women from a 16-year follow-up study in the USA.25

Multiple sclerosis

Multiple sclerosis also shows a latitude gradient in Europe, with the world's highest incidence reported in Scotland.26 The risk of developing the disease is reduced by a third by regular supplementation with vitamin D.27

Cancer

The risk of breast cancer and colon cancer is high in northwest Europe and much lower in the Mediterranean countries.28 And, in the UK, people die more readily from cancer in the north than in the south of the country. After being diagnosed, 34% of men with cancer and resident in Oxfordshire survive for 5 years compared with 26% of those who live in the northwest and Yorkshire. Men with stomach cancer who live in London survive on average twice as long as those who live in the northwest of England; the same applies to bladder cancer.29 Patients with colon cancer also have a greater chance of survival if they live in the south of England rather than in the north.30 The benefits of sunshine and vitamin D would explain these associations.
Results of a study31 done in 1941 in the USA and Canada showed that the cancer death rates among residents of the most northern cities were two and a half times those of the most southern cities. An extensive study32 of more than 5000 locations in the USA has shown that incidence rates of cancer are lowest where ultraviolet light exposure is greatest. Bladder, breast, colon, kidney, oesophageal, ovarian, prostate, rectal, stomach, and uterine cancers, and non-Hodgkin lymphoma are associated with low exposure to ultraviolet light.32

In the USA, cancer of the prostate has an increasing incidence with distance from the equator, suggesting a protective effect of sunshine. The incidence is highest in the eastern states and lowest in the west.33 This is exactly the same as with CHD, and is probably the result of a high altitude being protective because of greater ultraviolet light exposure. The association between prostate cancer and insufficient access to ultraviolet light has also been noted in the UK,34 with men exposed to low levels of ultraviolet light developing cancer at a younger age than those exposed to high levels (median age 67•7 years vs 72•1 years).

In a study35 of 456 people with early-stage lung cancer who had undergone surgery, those diagnosed and operated on in the summer, spring, or autumn had a significantly higher 5-year survival rate than those diagnosed and operated on in the winter. The survival rate was 29% in those who took no vitamin D supplements and had treatment in the winter compared with 72% in those who took vitamin D supplements and were treated in the summer.35


Diabetes

The international distribution of diabetes in children is very similar to that of CHD, with incidence increasing with distance from the equator,36 again suggesting a protective effect of sunlight and vitamin D. Furthermore, children of women who do, compared with those who do not, take cod liver oil during pregnancy have a reduced incidence of type 1 diabetes.37 The findings of a retrospective study,38 undertaken in Finland and involving 10 821 children born in 1966, indicate that the incidence of diabetes in adulthood is almost ten times higher in those who do not, compared with those who do, take vitamin D supplements in childhood. The benefit of vitamin D supplementation during infancy has been further strengthened by the findings of a large study undertaken in Norway.39

Rhematoid arthritis

Kröger and colleagues40 noted that 16% of 143 women with rheumatoid arthritis, compared with the general population, had very low concentrations of serum calcidiol. During the winter, 73% had levels of calcitriol below the seasonally adjusted normal range and the lowest levels were in patients with very active disease. In another study,41 of 19 patients with rheumatoid arthritis given vitamin D supplements, nine reported a complete remission of symptoms, and eight a satisfactory response. Inflammatory markers also improved: the mean erythrocyte sedimentation rate fell by 43% and the mean concentrations of C-reactive protein by 52%. This study is a small one but although far from conclusive the results conform to a pattern that should not be ignored.


Testing of my hypothesis

In view of the above, there is a striking similarity between the benefits of vitamin D and the benefits of statin therapy. I believe that the unexpected and unexplained beneficial effects of statin therapy might be mediated by activation of vitamin D receptors by this group of drugs. This hypothesis is, in theory, easy to test.
A prospective study should be undertaken in cancer treatment and prevention, with a factorial design, so that patients receive statins, vitamin D, a combination of statins and vitamin D, or placebo. A similar outcome in the three treatment groups would lend support to the suggestion of statins acting via vitamin D receptors. If vitamin D and statins are activating the same receptors, then if both are given in sub-maximum doses, the two together would have a greater effect than each individually. Intervention studies should also be undertaken to look at the relapse rates of established illnesses, including CHD, multiple sclerosis, and rheumatoid arthritis, comparing statins and vitamin D.

The difficulty in doing these studies is that we know only the minimum dose of vitamin D necessary to prevent and heal rickets: we do not know the dose necessary to increase to a maximum the other effects, especially those that enhance immune competence. The same applies to statins: their effect on serum cholesterol concentrations is easy to measure, but we do not know what to measure as a biochemical surrogate for the other effects, again probably those enhancing immune competence. As such, a range of treatment doses of vitamin D and statins need to be investigated. Additionally, clinical trials of established treatments—eg, statins for CHD—are difficult to design because of the ethics of not giving an established medication (a statin), but in place a trial medication (vitamin D). Comparisons with vitamin D supplements could be undertaken, but only once the optimum dose of vitamin D has been established.

Colonic mucosa and colonic cancer cells contain vitamin D receptors,42 strengthening my suggestion that vitamin D is biologically active in these tissues. Furthermore, vitamin D has an inhibitory effect on colonic carcinoma cell lines.43 Do statins have a similar effect? In-vitro experiments are one way that the effects of statins on vitamin D receptors could be investigated directly.

Conclusion

Anomalous results, such as the unexpected benefits of statins detailed here, lead to the advancement of science. Such an opportunity for research should not be overlooked. Statins should be looked at objectively and the diet-cholesterol-heart hypothesis on which the treatment was based disregarded. Statins have been described as wonder drugs because of their unexpected benefits; my hypothesis gives an opportunity for new thinking. The explanation of statins as analogues of vitamin D, if correct, would be reassuring to the millions of people who take them every day. Finally, sunlight and vitamin D might at last be recognised for their widespread health benefits.

Conflict of interest statement
I declare that I have no conflict of interest.


References

1. Morris JN, Marr JW, Clayton DG. Diet and heart: a postscript. BMJ 1977; 2: 1307-1314.
2. Kannel WB, Castelli WP, Gordon T. Cholesterol in the prediction of atherosclerotic disease: new perspectives based on the Framingham study. Ann Intern Med 1979; 90: 85-91. MEDLINE
3. Schatz IJ, Masaki K, Yano K, Chen R, Rodriguez BL, Curb JD. Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study. Lancet 2001; 358: 351-355. Abstract | Full Text | PDF (82 KB) | MEDLINE | CrossRef
4. Forette B, Tortrat D, Wolmark Y. Cholesterol as risk factor for mortality in elderly women. Lancet 1989; 333: 868-870. CrossRef
5. Sparén P, Vågerö D, Shestov DB, et al. Long term mortality after severe starvation during the siege of Leningrad: prospective cohort study. BMJ 2004; 328: 11-14. CrossRef
6. Renaud S, De Lorgeril M. Wine, alcohol, platelets, and the French paradox for coronary heart disease. Lancet 1992; 339: 1523-1526. MEDLINE | CrossRef
7. Gjonça A, Bobak M. Albanian paradox, another example of protective effect of Mediterranean lifestyle?. Lancet 1997; 350: 1815-1817. Abstract | Full Text | PDF (68 KB) | MEDLINE | CrossRef
8. Scandinavian Simvastatin Survival Study Group. Randomised controlled trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344: 1383-1389. MEDLINE
9. Shepherd J, Cobbe SM, Ford I, et alfor the West of Scotland Coronary Prevention Study Group. Prevention of coronary heart disease with pravastatin in men with hypercholesterolaemia. N Engl J Med 1995; 333: 1301-1307. MEDLINE | CrossRef
10. Packard CJfor West of Scotland Coronary Prevention Group. Influence of pravastatin and plasma lipids on clinical events in the west of Scotland coronary prevention study (WOSCOPS). Circulation 1998; 97: 1440-1445. MEDLINE
11. Freeman DJ, Norrie J, Sattar N, et al. Pravastatin and the development of diabetes mellitus; evidence for a protective treatment effect in the west of Scotland coronary prevention study. Circulation 2001; 103: 357-362.
12. Kobashigawa JA, Katznelson S, Laks H, et al. Effect of pravastatin on outcomes after cardiac transplantation. N Engl J Med 1995; 333: 621-627. MEDLINE | CrossRef
13. Katznelson S, Wilkinson AH, Kobashigawa JA, et al. The effect of pravastatin on acute rejection after kidney transplantation: a pilot study. Transplantation 1996; 61: 1469-1474. MEDLINE
14. McCarey DW, McInnes IB, Madhok R, et al. Trial of atorvastatin in rheumatoid arthritis (TARA): double-blind, randomised placebo-controlled trial. Lancet 2004; 363: 2015-2021. Abstract | Full Text | PDF (101 KB) | CrossRef
15. Vollmer T, Key L, Durkalski V, et al. Oral simvastatin treatment in relapsing-remitting multiple sclerosis. Lancet 2004; 363: 1607-1608. Abstract | Full Text | PDF (59 KB) | CrossRef
16. Edwards CJ, Hart DJ, Spector TD. Oral statins and increased bone-mineral density in postmenopausal women. Lancet 2000; 355: 2218-2219. Abstract | Full Text | PDF (59 KB) | MEDLINE | CrossRef
17. Strandberg TE, Pyörälä K, Cook TJ, et alfor the 4S group. Mortality and incidence of cancer during 10-year follow-up of the Scandinavian Simvastatin Survival Study. Lancet 2004; 364: 771-777. Abstract | Full Text | PDF (101 KB) | CrossRef
18. Poytner JN, Gruber SB, Higgins PDR, et al. Statins and risk of colorectal cancer. N Engl J Med 2005; 352: 2184-2192. CrossRef
19. Rose G, Blackburn H, Keys A, et al. Colon cancer and cholesterol. Lancet 1974; 1: 181-183. MEDLINE | CrossRef
20. Grimes DS, Hindle E, Dyer T. Sunlight, cholesterol and coronary heart disease. Q J Med 1996; 89: 579-589.
21. Mortimer EA, Monson RR, MacMahon B. Reduction in mortality from coronary heart disease in men residing at high altitude. N Engl J Med 1977; 296: 581-585. MEDLINE
22. Voors AW, Johnson WD. Altitude and arteriosclerotic heart disease mortality of white residents of 99 of the 100 largest cities in the United States. J Chronic Dis 1979; 32: 157-162. MEDLINE | CrossRef
23. Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet 1989; 3342: 757-761.
24. Kromhout D, Bosschieter EB, Coulander C de L. The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med 1985; 312: 1205-1209. MEDLINE
25. Hu FB, Bronner L, Willett WC, et al. Fish and omega-e fatty acid intake and risk of coronary heart disease in women. JAMA 2002; 287: 1815-1821. MEDLINE | CrossRef
26. Kurtzke JF. A reassessment of the distribution of multiple sclerosis. Acta Neurologica Scand 1975; 51: 137-157.
27. Munger KL, Zhang SM, O'Reilly E, et al. Vitamin D intake and incidence of multiple sclerosis. Neurology 2004; 62: 60-65.
28. Parkin DM, Whelan SL, Ferlay J, Teppo L, Thomas DB. Cancer in five continents VIII. International Association of Cancer Registries (IACR). Scientific publication number 155. Lyon: IACR, 2002:.
29. Silman AJ, Evans SJW. Regional differences in survival from cancer. Community Med 1991; 3: 291-297. MEDLINE
30. Coleman MP, Babb P, Damiecki P, et al. Cancer survival trends in England and Wales, 1971–1995: deprivation and NHS region. London: Stationery Office, 1999:.
31. Apperly FL. The relationship of solar radiation to cancer mortality in North America. Cancer Res 1941; 1: 191-195.
32. Grant WB. An estimate of premature cancer mortality in the US due to inadequate doses of solar ultraviolet-B radiation. Cancer 2002; 94: 1867-1875. MEDLINE | CrossRef
33. Hanchette CL, Schwartz GG. Geographical patterns of prostate cancer mortality: evidence for a protective effect of ultraviolet radiation. Cancer 1992; 70: 2861-2869. MEDLINE | CrossRef
34. Luscombe CJ, Fryer AA, French ME, et al. Exposure to ultraviolet radiation: association with susceptibility and age at presentation with prostate cancer. Lancet 2001; 358: 641-642. Abstract | Full Text | PDF (61 KB) | MEDLINE | CrossRef
35. Zhou W, Suk R, Liu G, et al. Vitamin D predicts overall survival in early stage non-small cell lung cancer patients. American Association for Cancer Research April 16–20, 2005, abstract LB-231.
36. Matthews DR, Spivey RS, Kennedy I. Coffee consumption as trigger for diabetes in childhood. BMJ 1990; 300: 1012. MEDLINE
37. Stene LC, Ulriksen J, Magnus P, Joner G. Use of cod liver oil during pregnancy associated with lower risk of type 1 diabetes in the offspring. Diabetologia 2000; 43: 1093-1098. MEDLINE | CrossRef
38. Hyppönen E, Läärä E, Reunanen A, Järvelin M-R, Virtanen SM. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet 2001; 358: 1500-1503. Abstract | Full Text | PDF (77 KB) | MEDLINE | CrossRef
39. Stene LC, Joner Gfor the Norwegian Childhood Diabetes Study Group. Use of cod liver oil during the first year of life is associated with lower risk of childhood-onset type 1 diabetes: a large population-based case-control trial. Am J Clin Nutr 2003; 78: 1128-1134. MEDLINE
40. Kröger H, Penttila IM, Alhava EM. Low serum vitamin D metabolites in women with rheumatoid arthritis. Scand J Rheumatol 1993; 22: 172-177. MEDLINE
41. Andjelovic Z, Vojinovic J, Pejnovic N, et al. Disease modifying and immunomodulatory effects of high dose 1α (OH) D3 in rheumatoid arthritis patients. Clin Exp Rheumatol 1999; 17: 452-456.
42. Kane KF, Langman MJS, Williams GR. Vitamin D3 and retinoid X receptor mRNAs are expressed in human colorectal mucosa and neoplasms. Gut 1994; 35 (suppl): S2.
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Affiliations

a. Blackburn Royal Infirmary, Blackburn, Lancashire BB6 8HE, UK

Also, a full-length booklet that contains just about everything you want to know about vitamin D (or at least a right-this-moment summary of what is known about it) will be available to Track Your Plaque Members for free before the end of the year.

The Graphs are too small to read even when clicked on.

It's not solely the fault of de novo lipogenesis, as even on a high fructose meal with radio-nucleotide labeled carbon in the fructose, only like 20 % of the triglycerides in the blood are from DNL.  Glucose consumption doesn't seem to result in DNL unless the liver is already full of glycogen.

Insulin is known to down-regulate acylation stimulating peptide (ASP), which is the paracrine hormone that regulates uptake of lipoprotein (i.e. "cholesterol") micelles into fat cells.

Dr. Mike Eades wrote a while back that fats, especially saturated fats go into the lymph system after digestion, and not immediately into the bloodstream.

Why is it then that "since fat must be absorbed via chylomicrons into the bloodstream" is an "accepted" notion?  You implied it was wrong, without actually saying so...Do most medical practioners really not know how fat is absorbed into the body?

You MUST look at this in context!  Excess dietary fat, especially saturated fat, causes insulin resistance.  It takes about 2 weeks of consistently eating approx 10% calories from fat, not more and not cheating, to remove that huge component of insulin resistance.  If the study were done in that context the results would be quite different.  How do I know?  I have done it several times on myself!!!

oops, forget to request email follow-ups. So now I have.

@ darnoconrad
Dr Davis did say "full-text here hoping people would follow the link, download the PDF, and have their own copy to enlarge as required.

Hi Dr. Davis,

Thanks for posting this.  It answered a question I've had for a while now.  The palmitate is interesting as well.

Very interesting and kind of scary, with family members of mine with heart disease pounding down the carbs and cutting the fat.  

I'm a bit confused by the Track Your Plaque Program, though.  In some of the info on the main site, saturated fats are described as inflammatory and something to be avoided.  But you seem to consider them okay - am I right?  And Dr. B G at AnimalPharm, who says she is counseling her clients with the TYP program, is big on saturated fats.  Can you explain the discrepancy?

Hi, Helen--

The Track Your Plaque program stand on a number of issues, including saturated fat, has evolved over the years. We now do not restrict them, but nor do we suggest a carte blanche  approach, since we do continue to maintain rather strict LDL targets for plaque reversal.

I believe that Dr. BG was expressing her own opinion in the Animal Pharm blog. While she's got plenty of great thoughts on this issue, it does not represent the "official" stand of the program.

Is it possible that the higher fat diet hit an optimum fat/carb mixture, where carbs were low enough to keep fasting TGs low and fats weren't high enough to spike post-prandial TGs?

Hi, Nigel--

Good question. Stay tuned--plenty more on this conversation to come.

The entire world of postprandial metabolism is truly a fascinating, though complex area, that is only beginning to yield to investigation. The Oxford group has made enormous contributions to this understanding.

Thanks for this, Gretchen, that's a lot of work!

It's interesting that my husband's endocrinologist, whom he is seeing for high blood pressure, insists on non-fasting labs.  He has my husband get his tests (blood and urine) one hour after a meal.  He says the fasting tests are very misleading.

Another question on saturated fats.  I know they raise LDL, and lately I've been reading that they raise the benign kind, not the vLDL.  But I have read in many places (including the Track Your Plaque article I mentioned) that they are "inflammatory."

Is that a false accusation, confusing saturated fats with trans-fats (since hydrogenated fats were used in some experiments regarding saturated fats)?

Or is it one of those things that depends - on other dietary factors or disease states, such as diabetes, etc.?  Or is it unknown?

It's hard for me to believe that nature would only want us to eat monounsaturated and omega-3 fats (as omega-6's are inflammatory, too).  That would seem fairly limiting for an omnivore.  Of course, it could be a proportion thing, too.

Helen wrote:
"Another question on saturated fats. I know they raise LDL"

The above may not be true. There may be a small near term rise, but long term I don't believe they have no impact or even lower LDL. You might find this blog entry interesting.

Rather interesting site you've got here. Thank you for it. I like such themes and anything that is connected to this matter. BTW, try to add some images .

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

Consequently, one of the advantages of glucose and other carbohydrates is that they can enter into the oxidation process much more quickly and provide energy more rapidly.

how do you treat a very low level?non prescripton D3? how much ? I was taught to gve 50000 unts for 8 weeks.

Could you please explain why gelcaps or drops only, not tablets? I could probably guess why, but for the benefit of the audience can you tell us?

Of course, gelcap or drops only, NEVER tablets.

Could you elaborate this point?  Is this a general recommendation (e.g. ease of digestion) or are there vit. D-specific reasons?

I have a large supply of D tablets and, after reading this, am trying to make a decision regarding replacing them.

What's wrong with tablets?

I have been told that some UK Doctors correcting Vitamin D status of elderly people in care homes use ANNUAL injections of about 300,000iu/D2.

The graph in Heaney's paper from Dr Davis's blog shows roughly how long 50,000iu/D2 lasts, unfortunately because the half life of Vitamin d is only around 21days, six times Heaney's amount will not last six times as long.

If daily/weekly or even monthly supplements are not practicable then surely injections every 2 months using D3 would be a be the least worst option.

Any longer interval than 2 months for an elderly person without access to sunlight surely cannot be in the patients best interests.

Anyone.
Why the emphasis on not using tablets?
Tks.

Had a friend get all excited b/c her doctor finally ordered a 25(OH) D level on her....which came back at 16 ng/mL.

She ended her email with, "yea, so I've got to pick up the RX for the D after work today."

I immediately wrote her back and said, " did he also tell you to eat more fruits and veggies? If so, don't forget to pick up a single blueberry to eat. You need your fruits and veggies!"

Taking D2 in an effort to raise you 25OH is like eating a single blueberry in an effort to get more fruits in your diet. Its not nearly enough, it doesn't work well and it's not worth the effort, as far as I am concerned.

Then I went on to tell her about D2 being the FOREIGN source of D in humans and how it's 1/3 less effective than D3 which is the natural form of D in humans.

Why would you settle for a foreign substance when you can get the natural form and it's more effective?

In our practice, we haven't experienced any negative issues with using the bio-pharm mini-capsules of D3. In our experience, they raise blood levels consistently and adequately.

I recently had my 25hyroxy D level checked (finger stick test recommended on this site)after 2 months of 5000/day tablets and the level was 80, so perhaps some tablets are better formulated/absorbed now.

While I am not a medical professional, it is my opinion from my use and study of nutritional supplements that the most bio-available form of anything is best. D3 is a hormone and the oil/softgel form is the best way to maintain the integrity of the supplement so the body can absorb it.  A tablet is processed, dried, things are added, etc.  This changes the action of the substance in the body and you can lose the benefit.

For those asking about why one shouldn't use the tablet-based Vitamin D, but rather the oil-based Vitamin D, he has answered this before a number of times in previous blog posts. Do a quick look under his Vitamin D posts. But here is one of the relevant posts: http://heartscanblog.blogspot.com/2006/11/oil-based-vitamin-d.html

Why not tablets? Because D is fat soluble and needs to be taken with some fat for best absorption.

I keep meeting people who are put on the prescription vitamin D for 2-3 months and then they are told to stop taking it. Some of these people have told me their doctor retested and told them they now had a "normal" level. Others were told to discontinue the D after a few months with no further testing.

Two people have been off and on vitamin D 3 times. They said their doctor cannot figure out why their vitamin D test keeps dropping after they stop taking the supplement.

Not only is the wrong D being prescribed by many physicians, but it seems that many don't understand that D supplementation needs to be maintained.

It's weird how most doctors don't know how to treat vitamin D deficiencies. When I was first tested, like 2 years ago, my family doctor came out and said she had no idea what the proper treatment was. She looked it up in her little medical PDA thing, said she'd write a prescription for 50K of D2.

I declined, saying I'd use D3 instead. She didn't seem so keen on the idea, and made a point that if D3 didn't raise my levels, she wanted me to use the prescription. She also didn't seem to think they sold D3 in anything higher than RDA levels.

So... basically saying... most doctors are clueless here. But what I don't understand is, can't doctors simply look up information the same way patients can? Just because they were trained in medical school a certain way, I assume doctors would want to learn and keep up-to-date with recent treatments and such.

As for gel/drops vs tablets, it's because vitamin D is fat soluble. Take your tablets at the same time as you take your fish oil -- when you run out, get gels or drops instead.

"D3, or cholecalciferol, yields confident increases in blood levels. It is inexpensive, safe, and an exact copy of the human form of vitamin D. (Of course, gelcap or drops only, NEVER tablets.)"

I started using 5 grams of D3 because I'd read it can help syptoms of S.A.D.  I take generic D3 with dietary fat: fish oil caps and nuts mainly.  I haven't had my levels tested but having done nothing else, this has been one of the easiest winters for me to survive.  I believe D3 requires fat for absorption.  Generic D3 is cheap, dietary fat is cheap, those D3 gelcaps are not.  Plus, living in rural Wyoming I'd have to drive for three hours to the nearest place that sells them.  

kevin

here is the best video on D3. it is an hour long and will work in IE only i guess.
http://www.uvadvantage.org/portals/0/pres/

"Plus, living in rural Wyoming I'd have to drive for three hours to the nearest place that sells them. "

Well, there must be internet access in Wyoming.  Lots of reputable online shops sell vitamins, including host of D3 options at very competitive prices, (ordinary drug stores usually have the worst selection of D doses/options at the highest prices, too.  

Doesn't compute that sourcing Vit D would require that long of a drive.  No mail delivery?  The only other barrier I can think of is no c/c or debit card for non-cash purchases.

What about capsules, or is that covered under tablets too?

As I understand it Vitamin D is metabolised in the body from cholesterol derivatives. Since statins reduce cholesterol I take it they will also reduce Vit D as well as CoQ10, dolichols  selenoproteins and hormones and steroids that are also derived from cholesterol.

Since Vit D and other molecules (eg CoQ10) tend to be depleted in the elderly, the use of statins would increase the risk of defiencies. Statins also deplete the anti-oxidant capacity.
But when prescribed statins, no replacement for the depleted items is ever prescribed. The Canadian authorities do require a black box warning on the data sheet for statins but neither the FDA or the MHRA do so despite the known depletion. This was known in 1988 when Merck registered two patents for their statins incorporating CoQ10.
In short, the trivial gains in cardiac attacks are one thing but the adverse effects of statins are another. Given the infomercials  claiming minimal adverse reactions (having excluded all possible reactors as in the HPS study and JUPITER) doctors blieve that they do not happen and do not report patients complaints. A study has shown that only 1 to 10% of doctors actually report adverse reactions.

In the case of simvastatin, the MHRA has recorded 66 deaths in their Drug Analysis Print for this statin. This represents, then between 660 and 6600 deaths.

You're preaching to the choir here...

I am a weight loss surgery post-op.  I had a biliopancreatic diversion with duodenalswitch nearly 7 years ago.  I had already been diagnosed with osteoporosis at that time - and had never been directed to do *anything* to address it.

Fast forward nearly 7 years.  I've lost 210 pounds, a wheelchair, diabetes, hypertension, congestive heart failure, sleep apnea, high cholesterol and triglycerides - to name a few.

It wasn't until I was a post-op - who malabsorbs fats significantly, meaning fat stored vites A, D, E, and K - that I found I not only *could* do something - but should.

Today I take boatloads of calcium citrate, dry forms of A, D, E, K1, and K2 - to name a few, and have a diagnosis of osteopenia - no longer osteoporosis.  And everything is trending in the right direction.

I hope you don't mind - I enducate patients now - and I've sent a bunch of people a link to your blog to read this info about Vitamin D.  It's so important for my community to know this!

THANK YOU!

My D level was 20 when my doc prescribed 50,000 iu D2 1x per week.  After 1 month, my D levels went down to 14.  She increased me to 50,000 iu D2 3x per week.  After another month, my D level is now 7.  Why is the D2 depleting my D level?  help!!

In my view, this is the knuckleheaded thinking of the conventional practitioner: “Don’t bother me until you’re really sick.” Prevention is a practice that has become fashionable only because of the push of the drug industry. Nutrition is an afterthought, a message conceived through consensus of “experts” with suspect motivations and allegiances.

So what if you blood sugar before a  whole-wheat cereal is < 90, and an hour later it's 115?  

Didn't reach the 168 mark, nor did it stay below 100...   based on those numbers, should the cereal be avoided for weight loss?

QUOTE:
"My favorite method to restrict carbohydrates is to eliminate wheat and minimize exposure to other carbohydrates, such as oats, cornstarch, and sugars. All these foods, wheat products worst of all, cause blood sugar and insulin to skyrocket."

I have diabetes, and I have belatedly started cutting way back on all those foods. And I sure hate to give up my sandwiches, but the bread has become a disaster for me.

Jim

ReliOn by WalMart $12, 50 test strips $20, my choice.

A small portion of oatmeal hardly raises my blood sugar but a big portion raises it a lot.  For me the portion size of carbohydrate seem to be more important than what the carb is.

Comical. Hiding from carbs isn't going to make your blood sugar problems go away.

sorry but I'm Scottish

"The Scots developed a deep love for oats, and it shows in their traditional recipes handed down through the generations.

Porridge, oatcakes, fish fried in oatmeal and many other particularly Scottish recipes have the humble oat at the centre.
Oats are extremely nutritious, containing more protein and unsaturated fat than any other cereal grain and for many years right up and including the present day, Scottish soldiers are considered to be tougher and stronger than their English counterparts, thanks to a daily diet of oats."

"Celts ate like most other Europeans, subsisting mostly on grains supplemented by meats, fruits, and vegetables. Exactly what they ate varied by area, and Celts grew local crops. Scottish highlanders were famous for supposedly subsisting almost entirely on oats, though this was not entirely true. However, oats remain the favorite grain of Scotland, and Scottish cuisine is full of them."

My mother has found that certain other things can raise her blood sugar as well--mostly stress and Xanex.

For the past few months, I've gotten after her every day to lay off starchy foods. It helps keep her blood sugar down, but mostly, I think she sticks with it because she feels better. She has a better mood and more get-up-and-go than I've ever seen in her.

@Matt Stone:

Comical, yes, I agree.

Sorry, but Dr. Davis appears to sincerely believe that:
carbs => insulin => fat

Remember, you're talking to someone who claims to have tried an Ornish type of low-fat diet and yet gained 31 lbs and had "skyrocketed" triglycerides.

http://heartscanblog.blogspot.com/2007/07/ornish-diet-made-me-fat.html


I wonder how those Asians eating white rice stayed so thin.  The "it's genetic" cop-out won't work, as those same populations gain weight when they come to the USA and adopt more SAD-like diets.

What would explain Dr. Davis' 31 lb weight gain on a low-fat diet?  I wonder where those extra calories came from?  31 lbs * 3500 calories/lb = 10,8500 excess calories.  

I wonder where those excess calories came from.

I think the thing with Asians I have known is although they eat a lot of white rice, they also eat a lot of veggies and meat and they do not eat much desert or other sources of carbs.  Most do not eat much wheat and no sodas.  Many do not even have bread in the house other than an occasional piece of 'bao.'  I suspect, compared to Americans, their overall carb/sugar intake is likely less.  Most food is prepared fresh, not canned or out of boxes.  And many lowcarbers think that sugar (fructose) and wheat are probably worse culprits than rice when it comes to glucose control.

As for oatmeal, you might want to research how much phytic acid and lectins are in that stuff.  Phytic acid leaches nutrients out of your system and lectins damage the intestinal tissues.  PLus there is the already mentioned issue of high insulin response.  Maybe the Scots are just tough because they are tough with a tough attitude and oats were eaten simply because they were available and people were hungry.

Another vote for the ReliOn meter. Crazy cheap (apart from the strips) but wicked easy to use.

I forgot to mention, people might want to do a bit of research on glucometer accuracy before purchasing one.  Many are wildly inaccurate and erratic, even the more expensive ones.  Some of the most accurate have often been cheap ones.  Back when I bought mine (my dog at the time was Type 1 diabetic and I needed to track his BGs), I found that a simple $20.00 one had excellent accuracy ratings.  SOmetimes you can even find free glucometer offers, but again, make sure you get a well rated one.  Some of those are so bad that to me they should be illegal.  Manufacturers are happy to provide the less wealthy with lowcost glucometers cuz they figure they will get you later when you buy the expensive matching test strips.  On the flip side, many who want the best wrongly assume the expensive glucometers are better.

Also, for those who want to do a glucose tolerance test for diabetes like they do at the hospital, you can do a reasonably accurate facimile of the test using 26 jelly beans and your own glucometer instead of the gross sugar syrup they feed you at the hospital.

It is broadly know what drives insulin. You can look it up everywhere. So why spend money on devices and test strips and put pins in your finger? Furthermore the measurements will depend on the state of Insulin Resistance you are in.

I agree with Eva - people need to see studies and results first before purchasing a glucometer, or at least be educated with the gravity of the disease before resorting to self-help equipments.  Diabetes assessment is not a walk-on-a-park.  It should be treated with utmost consideration to how your body would possibly react to certain medications / equipments, because we all know its fatal if we do otherwise.

Thought you might want to know your post was accompanied by an ad from joybauer.com telling us that a diet of pineapples and apples will cure our diabetes.

If you are going to use google ads you have to put some time into reviewing which ads come up and blocking them in your adsense account. Otherwise your visitors will be wafted to sites promising miracle cures and promoting all the foods you are warning them about. I check my ads on a daily basis. There's always one or two to weed out.

Even more comical is a bloated, doughy, carb-binging Matt Stone thinking he's somehow not a prime example of why Dr. Davis recommends laying off the carbs.

Dr. Davis,
Isn't a "blanket" target of 100mg/dl a bit unrealistic? I have witnessed some people never go above 90 even after having lots of carbs. I myself am very thin, but there's no way I could stay under 100 an hour after eating, even with almost zero carbs.

I don't know Matt Stone, but the question he raises seems like a good one.  Does lowering your blood sugar lead to less insulin resistance?  If anybody knows, I would be interested.

What Matt Stone said was " Hiding from carbs isn't going to make your blood sugar problems go away.", different to "Does lowering your blood sugar lead to less insulin resistance?".

In my case I have a personal problem with insulin resistance, fasting blood glucose 110, but no  postprandial, below 100 after almost any meal.

Can anybody ad some insight as to what may be the problem, or how to understand it?

"Even more comical is a bloated, doughy, carb-binging Matt Stone thinking he's somehow not a prime example of why Dr. Davis recommends laying off the carbs."

ROFLOL. EXACTLY.

"Even more comical is a bloated, doughy, carb-binging Matt Stone thinking he's somehow not a prime example of why Dr. Davis recommends laying off the carbs."

FAIL.  Nobody explained how Dr. Davis managed to gain 31 lbs on a low fat diet?  You can't manage that on rice and potatoes.  Maybe he indulged a bit too much on "low fat" refined sugar products, "low-fat-by-serving-but-still-fat" products, and oils.  That weight gain came from a calorie excess not possible by unprocessed starches, that's for sure.  Unless you think Dr. Davis could eat upwards of 20 potatoes a day...


Double FAIL for ignoring the thin Asians who eat carbs, yet when they quit their high carb diet for a SAD-like diet, they gain weight.

Wavesense Presto, also available
at Walmart - Test strips $17.87/50
in my store.

It does'nt hurt that the meter is
noticeably more accurate than many
(I take insulin, so it matters...)

Jack

My BG starts at 99, so eating a meal and keeping it at 99 would require me to eat no carbs.

So is it reasonable for me to try to keep my GB under 115 after a meal or should I stop eating all carbs?

Thanks

Steve

Related to this topic, I just returned from North America after several months in Japan and I saw a television show where they implemented an eating program for four people with high blood sugar. The diet program consisted mainly of eating all meals by chewing the food thirty times for each food bite as well as eating some type of vegetable fiber in this manner first.   The show monitored the people for three weeks, during which, the average blood sugar reading went from above on average 120 down to  88 when properly and slowing chewing the food. I could barely believe what I saw.

Dr. Davis, you will love the linked post below, an exhaustive analysis of the raw China Study data which completely ratifies your prescient beliefs about wheat (to a degree that may amaze even you):

The China Study: Fact or Fallacy?

Matt Stone, you are fat.

Matt Stone -- if that's him in that picture, is not fat. At all. Don't belittle people just because you don't agree with their opinions.

As for his statement of "Hiding from carbs isn't going to make your blood sugar problems go away." I'm not sure what that means. Where do you get "blood sugar" problems if not from carbs?

Regarding China, everyone just assumes they gorge on sticky white rice all day. In reality, the Chinese eat way more meat (especially fish), some vegetables and then finish the meal with rice. Visit China, they eat a lot less rice than the average person thinks. Also there is an "iodine theory" for as why they don't get fat off white rice. Plus just because white rice is a staple for them, doesn't mean it is anywhere equal to an american/SAD diet of french fries, bread, cereal etc.

@Peter
Yes, if your blood sugar stays at normal levels you're less likely to become insulin resistant. Insulin resistance happens when your blood sugar is elevated for long amounts of time.

The weight I gained years ago on an Ornish-like 10% fat diet, I believe, was from whole wheat bread products mostly, but also oat meal, oat bran, and some low-fat snacks like low-fat ice cream.

I'm going to make a prediction: controlling the excursions of postprandial blood sugars is going to prove to be among the most powerful youth-preserving, antiaging strategies known.

Does this also apply to athletes who go through strenuous physical exertion and training? Or, does the 100 mg/dl apply to the typical couch potato who goes for an occasional walk?

-- Boris

ALTERNATIVE WAYS TO LOWER POST-PRANDIAL GLUCOSE

Slowing gastric emptying should lower the post-prandial insulin spike.  

--Fiber: ?guar gum or pectin
--vinegar
--protein
--Fat

I disagree with Linda. I don't think you need an expert to figure out if your blood sugar responses are bad or not.  Try to get your fasting bgs around 80 or at least under 100  (80 is better).  Try to keep your post eating sugars from jumping all over the place, not too high but neither should they drop super low either.  There are tons of example charts on the net about what the govt considers normal/acceptable and you can assume you want to do way better than those.  There is disagreement about how low it really should be, but I don't see anyone arguing that you want those numbers to be high, that is for sure.  My point was only, when testing this, make sure you don't by a crappy inaccurate glucometer.  Informed type 1 diabetics are typically the most knowledgeable crowd on glucometers simply because their life depends on knowing their blood glucose (even in the short term) and so they are highly motivated.

Post-prandial at one hour under 100? I thought the target was under 120 at 2 hours post-prandial.  Why the sudden stricter number?  The rate of digestion is affected by many factors such as fiber and fat content of a meal.  Therefore -- one may not see their true blood glucose peak for 3 hours after a meal.  Also, those with hypothyroid conditions have delayed stomach emptying.  I think Dr. Bernstein and/or Dr. Michael Eades wrote that 1 gram of carb raises blood sugar 5 points -- this is an approximation -- so even a very small amount of carb could raise sugar over 100.  Say if I have small portion of meat, plus 2 cups of veggies, plus 1/4 cup nuts and 10 blueberries for dessert -- sugar hit from the blueberries may be delayed for hours because of the nuts.  Ditto for small amounts of very dark chocolate (85%+) -- chocolate slows stomach emptying.  This is why Dr. B does not believe in ever adding "fun foods" and restricts all fruit and sugar -- forever -- no small amounts added back.  His plan is 6 carbs in the morning, 12 at lunch and 12 at dinner. If I was a diabetic, I would do this - but for those of us that do not have diabetes and who are normal weight -- I don't thinks such strict measures are necessary for health or longevity.  As an aside -- my husband has the same supposedly ideal triglycerides as me -- 30s or lower -- yet he lives on whole wheat and grains -- seriously -- eats it at every meal plus desserts.  Yet his HDL is high for a man and LDL is low. He does exercise vigorously (lifelong athelete) and has an active job (no a desk jockey) -- plus both parents are active and near 90 -- no diabetes in either of them though both eat mixed carb rich diets.  I believe differing genotypes may explain this. Everyone's looking for a one size fits all holy grail to diet and I think we have to find what works for each of us.  Some people find fruit -- even low carb berries - makes blood sugar skyrocket yet can handle small amounts of tubers or whole grains.  I think testing gives one information on how to optimize one's diet but I am dubious of the 100 post-prandial target after only 60 minutes.  I have also noticed that when I am at my slimmest summer weight, the same carb portions make my blood sugar higher than when I am at my slightly heaview 5-6 pound heaview winter weight.  Drastic seasonal changes suck for weight control.

One of the best info sources I've read regarding diabetes/heart/low glycemic load.  Thank you.  I'm the only true non-diabetic in my family and have other complicated genetic medical issues going on.  I have learned to ignore much of what I've read about diabetes since my family followed the traditional diet without success.  What has worked for me best has simply been finger sticking and paying attention to everything and every reaction.  No oatmeal, no wheat, no rice/potatoes, small and frequent meals, moderation in all things, exercise, and I'm still amazed when people say "I can't do this".  It is not easy to change your habits but when your life depends on it, you just have to.  Watching our own reactions to food and lifestyle should always be the measure we follow. We all need to be our own health advocates, or at least I need to be.  I'll be reading "you" to follow the info you are providing.  Thank you so much.  Enlightening.

Hi, Jackie--

Your experience is similar to what I am witnessing: Knowledge of your postprandial blood sugars tell you what foods are screwing up metabolism. It tells you which foods, what portion sizes, and what other factors (like exercise, macronutrient mix, and liquids) affect glucose excursions.

There is a lot of help to control sugar these days.The instruments that can test sugar at home helps.Diet and exercise still stay at the top being the controlling factors for the disease.

I am losing weight like crazy on this diet.  If you wanted to get a lot of attention for it you could call it Dr Davis's Prick Diet and before you know it you'd have it in the Huffington Post.

Decided to try this - bought a one touch meter at wally world this afternoon - $11.75 for the meter, and $55 for 50 strips.

I hadn't had anything to eat for around 20 hours. Glucose shows 106. Had a Wendy's chicken club sandwich + diet coke - 2 hours later, glucose is 107. Had curried chicken for dinner with 1 1/2 cups of basmati rice and 20-25 rainier cherries, and 2 hours later - 157. Prediabetic?

My hand is sore too.

the level of insulin secretion doesn't necessarily correlate with blood sugar level.

Alfredo,

It might not be insulin resistance causing your high fasting sugars.  With insulin resistance, usually your post-prandial numbers decline before your fasting levels do.

I am in the process of trying to get tested for MODY 2, a type of usually mild diabetes marked by elevated fasting glucose, which can be accompanied by anything from a normal A1c (glucose control over time) to a moderately elevated one.  It has varying degrees of severity - often it is subclinical.  A person with MODY 2 may become insulin resistant, like anyone else, however.  In fact, the elevated fasting sugars and moderately impaired glucose tolerance might lead to insulin resistance in some people with this mutation.

Fortunately, people with this mutation tend to have low triglycerides, unlike most people with diabetes.  

You very well might not have this - it's supposedly rare - but I was in your boat for many years, and later developed gestational diabetes and now have "mild" diabetes.  

Read more about MODY types of diabetes at
http://www.phlaunt.com/diabetes/14047009.php
(Diabetes Update Blog by Jenny Ruhl.)  

As for people questioning how Dr. Davis got fat and diabetic on the Dean Ornish diet - I do think some people are less carb tolerant than others.  If you can eat all the carbs you want and not get elevated post-prandials and/or not become insulin resistant, kiss your genes, your pancreas, and your liver, and keep your fingers crossed.  Not everyone is built the same.  They really aren't.

The first few nights I kept dreaming about brown rice and steel cut oats, but now I am back to dreaming about women.

I've been doing this for a month and a half and I'm wondering about trade-offs.  My fasting glucose is normal for the first time in years but my measured LDL is way up, and my small particles are high too (835).

A lot of people are dying to lose weight. Most of them tried programs but eventually go back and gain more pounds. My wife got bigger after our first child. She went through so many things to get her size back. The safest and healthiest program she underwent was rejuvenating with an infrared sauna. Dealer made a great explanation about the health benefits. It detoxifies the entire body, removes dead skin and burn calories.

It is sometimes difficult for some individuals to lose weight. This article explains that you can lose weight by developing your mind and will power with behavior strategies that help you change the way you think about weight loss. It is exciting; and it is really the best way to lose weight.Buy Calorad.Thanks a lot for sharing this.

Carbs are just one element but if you want a more complete approach, you can try other methods to get rid of those unwanted fats.

Losing weight can improve your health in many ways. Just losing 10% of your current weight can make a difference in the way you feel on a daily basis.

medsheaven.net to help me lose weight fast, it works like a charm, I lost a lot of fat weight without doing any hardcore exercises!

May I ask, what is the optimal serum range for Vit D.  What do you consider too high and what are the undesirable consequences of too much vitamin D?
Thank you kindly -- fantastic blog !

I wonder- do you have a general rule of thumb for a starting dose based on how much the person weighs? I've found that 1,000 IU per 25 lbs of bodyweight seems to generally get it in the ballpark.

The "1000 units per 25 lbs body weight" that Dr. John Cannell suggests does indeed work well, though there is still great variation among individuals.

For that reason, we aim to maintain blood levels of 25-hydroxy vitamin D of 60-70 ng/ml.

can supplementing with D3 negatively impact TSH thyroid levels, causing TSH to increase? I have seen this stated on another blog.  Suggested remedy was to lower intake of D3.  Thanks.

With daily effort your endurance will continue to increase. In no time at all you will be able to sustain 30 minutes of continued activity. Now as you begin to get into better shape you will be on your way to experiencing fast weight loss.

Great article, I'd never known how vitamin D was related to weight loss until now.

But, with all supplements for weight loss it would need to be combined with exercise for best results

I have the same question as Steve: Can increased D3 affect TSH or thyroid in general. I have hashimotos thyroid autoimmune, and have increased my D3 for osteoporosis reasons, but it seems to be affecting my TSH---need less medication to have same levels of normal TSH.  I read that D is good for autoimmune disease.
Thanks for your response!
Kate

Awesome! really very nice article.

I wanted to take more than 4,000iu because I'm obese (11-17-08 level was 64, 8-3-09 level is 55), but my PCP said not to for fear of kidney problems?  I just upped it to 8,000iu.  We'll see - I sure could use help in the weight loss arena.

Though the levels of vitamin d and weight loss seem to be correlated, is it always true.

Dr. Davis
(Probably not the right forum to post this comment but I just had to send this to you)

Not many weeks ago a colleague of mine (let’s call him Eric) asked me if I knew the difference between D2 and D3 and I told Eric that D2 comes from irradiated mushrooms and D3 comes from the wool. In other words D3 is the same kind of vitamin as humans get from the sun. Humans just don’t get enough and we can’t produce it on our own, like the sheep can. (D3 is natural for humans, D2 is not just like you have said)

After telling Eric this, he asked me how he would know what he is taking and I gave him the medical definitions of them both (D2 = Ergocalciferol; D3 = Cholecaliciferol). Since I was aware of that he had gotten his Vitamin D by prescription I told him “I am 99.9% sure that you are taking D2, but I would be thrilled to find out I am wrong”.

Eric called his pharmacy right away and got the answer I was expecting: Ergocalciferol. When confronting the person Eric was talking to the answer he got back was that Ergocalciferol is the only Vitamin D they are giving out.

A week later, Eric had a new appointment with his doctor and decided to ask him about the D2/D3 issue. The doctor said he knew that there was a difference in them both, but could not say what, not even the basic facts I mentioned above. But the doctor stamped a post-it with what he had sent to the pharmacy just to show Eric… “Vitamin D3; 50,000IU tab” is what the stamp said.

Eric, off course, got confused and was starting to believe that the Pharmacy had made a mistake by giving him Ergocalciferol (D2) since the doctor had given him D3, or at least that is what was stamped on the little note he had.

Today, after getting a refill of his Vitamin D he also got and kept all his paperwork that came along with it. Still in believe about that stamp the doctor had given Eric earlier he asked me to double and triple check that my definition of D2 and D3 was correct. I did, just for my own sanity, and I was still right.

One of the sheets Eric brought me today was the “Patient Education Monograph” sheet stating the drugs and how to use it and so on… The thing the jumped out the most to me was this:

Generic Name: Vitamin D – Oral
Common Brand name(s): Drisdol, Maximum D3
Identification: PA140 Green Oval Capsule

This is the Drug Eric was given: Vitamin D 1.25 MG softgel; Generic name: Ergocalciferol

My researching mind went into high concentration mood and I started to dig. And this is what I found:

The brand name Drisdol is Ergocalciferol (D2), not D3. The Brand name Maximum D3 seems to be hard to find out there in cyber space as a brand name. But the ones I found that was called Maximum D3 seems to be the real stuff, however none of them required a prescription.

When trying to find out through the identification number on the pills (PA140) I now know for sure that Eric is taking Vitamin D2 and not the preferably Vitamin D3. The Brand Name Drisdol had the identification W on one side and D92 on the other, but it is still Ergocalciferol.

The only conclusion I can draw from all this is that the medical industry does not know or care about the difference in D2 and D3 – it is all same to them. And as long as the pharmacies only give out D2 it does not matter what the doctor prescribe anyway.

I knew that people are most likely to be prescribed a D2 pill than to be told to buy over the counter D3. But it was almost heart breaking to see the letter D and number 3 right next to the drug Drisdol as we know is a D2 vitamin. It just didn’t make sense to me that they can be labeled as the same type of medication, when we know it is not!

I love your blog, and I just wanted you to know that I am passing on your information to as many as I can. If you are interesten in seeing any of the documents that I have from this story you can just email me at helena.mathis@hotmail.com

moderator

shouldn't you take helena mathis' email off the blog post ?

This looks interesting.

Good point! I suppose this is true of anything fat-soluble, if you reduce the fat deposit then the concentration will increase?

wow..excelent post, thanks for sharing

thanks for this - with all sorts of info available on the net - this one gives me a greater understanding on vitamin D in relation to my weight loss level. More posts like this

I take calcium with my vitmain D3.  The vitmain D3 I take has olive oil with it.  It is highly advised to take calcium when taking more than 1000 UI daily.  You should get tested for vitamin D3 levels in your blood.  You can get a private lab or do it through a doctor.  I take 1000 UI for every 25 lbs.  I tried taking it a few days that way and I lost 4 lbs in a few days.
You shouldn't take more the recommend amount on the bottle more than a few months.

Thanks Every body for sharing information ....

You really need to consult a doctor if you have any plans to lose weight. Ask for a prescription of the right dosage of Vitamin D and eat nutritious foods as well. Don't forget to exercise too, its helpful.

In my case, I created my own – FatBlasters. It’s essential that you not feel alone, and reaching out to friends (new or old) is typically a smart move. I just heard about PeetTrainer, but didn’t know about it when I began down the road to weight loss. You have to know that others are out there for moral support – they know things that you couldn’t possibly know, and they’ve probably been “in your shoes” at some point in the past (or present). Share stories, laughter, tears, successes, and failures – share them. There are thousands of communities out there, so keep looking until you find the one that fits you.

Nice post on the Vitamin D and weight loss. Overweight is one of the major problem in the world. People do lot of things for losing the weight.

What is suggested here is that if you start out with an inadequate vitamin D level, it’s possible that this might inhibit or impede your ability to lose weight on a reduced caloric diet?

yes my dear friend ,definitely you lose weight on a reduced caloric diet, HCG diet , thanks

There is many more information on this post about how to reduce our weight loss and also there is plenty of information about the functions of vitamin D in weight loss.Office plugin Its really a helpful information to all of us.

This is a common phenomenon with substantial weight loss: lose weight and the need for vitamin D is reduced. The reduction in dose is roughly proportion to the weight lost. Vitamin D should therefore be reassessed with any substantial change in weight of, say, 10 lbs or more, either up or down, because of the influence of fat on vitamin D blood levels.

Vitamin D is good for weight loss.

I am now on a weight loss program and I can say that I am getting a very good result. I never thought that vitamin D can really affect my weight loss program.

Thanks for sharing the importance of vitamin D in loosing the weight. keep posting such a nice post....



Smith ALan

Dr. Davis, would like your thoughts on the Trader Joe's brand Omega-3 Fatty Acids:
1200 mg Fish Oil
400mg EPA
200 DHA
Thanks,
Chris O

I use Pharmax Finest Pure Fish Oil with Essential Oil of Orange from the TYP Marketplace.  I take 1 tablespoon per day to help reduce Lp(a).  Is it better to take this dose at one time or divide it through the day?

In Iceland where I come from we have a really high quality fish oil called Lysi.

In my opinion liquid form is the only real way to take it, with caps you have to take a ridiculous amount to reach the same amount as in a tablespoon.

Plus you have no way of knowing if the fish oil caps are spoiled except to chew them, often they're not even refridgerated in the supermarket.

I remember from an earlier thread that spacing the dose out over the day works better than a big dose once daily. That makes sense, given that you are trying to alter some liver metabolism that goes on around the clock. I've been using the Life Extension capsules, six a day, for several years with pretty good results. It gets my TG from 400+ to about 170. I'm hoping the gram a day of regular niacin I've been taking for a few months helps further and gets my HDL out of the sewer (27). I'll know that in a few days...

Nice tasting Liquid fish oil brand, 1 teaspoon=
1,500 mg EPA
+ 750 mg DHA
----
= 2,250 mg EPA + DHA
+   380 mg other Omega 3
-------
= 2,630 mg. Omega 3/teaspoon
(out of a total fish oil content of 4,400 mg./tsp.)

Canada made "Natural Factors",
"Dr. Michael Murray recommended pharmaceutical grade" says label; extracted
from anchovy/sardine/mackerel;
1 teaspoon stateside cost works out to less than US$1 a teaspoon; each teaspoon has 40 calories, 15 mg cholesterol, total fat 4.5 gr. (being 3.5 gr. polyunsaturated), natural vitamin E and natural orange flavor, no heavy metals/environmental toxins ... I've no financial interest in the product.

What about Carlson's?



http://www.amazon.com/Carlson-Finest-Liquid-Omega-3-Orange/dp/B001LF39S8/ref=wl_it_dp_o?ie=UTF8&coliid=I27QWKFK5P760T&colid=1J0P20X13IM7F

What are your thoughts on Chris Masterjohn's research regarding very low requirements of polyunsaturated fats in the human diet?  High amounts of fish oil would certainly contravene this hypothesis.  I am referring to his position paper, How Essential Are The Essential Fatty Acids?

The best fish oils should be, as expected, in fish. Eat more fish!!!;))

"1 teaspoon Pharmax fish oil, for example, provides an equivalent quantity of omega-3 fatty acids as 6 standard fish oil capsules on a milligram for milligram basis, but more like 8 to 9 capsules when absorption efficiency is factored in."

Color me confused, Dr D. At the moment, I ingest 6 (3, 2x/day) Sam's Club Omega 3 capsules (the ones you recommended in a long-ago post) to obtain the 6 Grams of total DHA and EPA/day. Does your comment I quote above mean that, with the liquid form, I can take less than the equivalent of 6G/day  because of its absorption efficiency? And how much, if yes?

Really, I am sufficiently befuddled that I think even my question is not clear...

Help!

Where can I check if the fish oil is trigyleride form?

uh.. off topic.. when I clicked on my bookmark, to the Heart Scan Blog all of the website except these comments are in what looks like Russian!!  nothing else on my computer is corrupted...anyone else?.. and how do I fix this?  I am on an IMac.

Thanks,
Jeanne

Fixed it!  funny that it was only this website.

on topic- I am very intolerant to anchovies, will Krill oil help me?  can't take ANY fish oil with anchovy.

Thanks

Seeing some confusion here: the ideal active ingredients in fish oil are the EPA mg. & DHA mg. omega 3's. Lables indicate there are other omega 3 oils, plus other non-omega 3 oils in all products and together these are the mg of "fish oil" (product may specify yet another blending oil). Companies make their EPA mg. & DHA mg. concentrations different, incur production costs to make it higher doseage and our purchase price reflects that.

If you have a theraputic goal for intake: it is not so much how much fish oil, but how much you need to take of any one specific product a day to meet your target for total EPA mg. & DHA mg. Omega 3 fatty acids. For a name brand product Doc recommended and gave his daily dose (whether capsule or liquid)he apparently did the math.

Unfortunately I am illergic to fish oils and react badly to them. Not a good way for me to get my omegas so I need an alternative.

Udo' Oil does do a 369 oil that has no fish oils. So far that is the only one I have been able to find I can handle.

best fish oil is no fish oil. Certainly if anyone knew how fish oils were made , they would not take them. It's interesting how dr. Davis says fish oil with no odor are best but those are simply sterilized and deodorized and for a reason so that the taste of smell would not be repulsed. Trust your own gut instead of anyone else I guess. Ray Peat has chronicled data and science behind the dangers and lipid peroxidation of fish oils. Brian Peskin makes a case that these derivative oils are a huge burden for the cells and should never be taken. Naturally such oils are protected by vitamin E and saturated fat but not in these fish oils. Most other literature documents effects of omega 3 on cancer metastasis, just google it.

Now Foods Omega-3 Fish Oil 16.9 fl. oz.
Serving Size: 1 tsp (5 ml)
Servings Per Container: 100
EPA: 740 mg
DHA: 475 mg
Other Omega-3 Fatty Acids: 185 mg
Total Omega-3 Fatty Acids: 1,400 mg

Cost: $19

100% triglyceride form **

** Now Foods 16.9 fl. oz. is the brand I use and I can confirm this is the TG form after a polystyrene test.  (Take a styrofoam cup, place a small amount of fish oil at the bottom of the cup, wait ten minutes, and if it eats through the bottom it's the EE form.)  

I can also attest that I do not suffer from "fish burps" that the EE form is known to cause.

Anonymous about Lp(a)--

We have no formal data on dosing regimens, but I have been advising dividing dose in two, a.m. and p.m. This appears to be working well.

David--

You may be confusing fish oil dose with dose of EPA+ DHA.

Check your label to see EPA + DHA content. This is what you use to dose your fish oil.

Readers

Is Carlsons fish oil the Triglyceride form one?

SVinay:  Carlsons Super Omega-3 Fish Oil is the ethy ester form.

I am currently taking Heart Health Omega-3 1000mg by Swiss Natural Sources.EPA 300 and DHA 200.  I take three capsules daily.  I have also purchased Jamieson's Omega-3 Select with the same EPA DHA content as the Swiss.  The Jamieson's is less fishy smelling and I will switch back to it when I finish the Swiss.  
Canned boneless herring fillets are usually a part of my lunch.  Omega-3 2g.  I also found some canned cod liver.  I'll try it in an egg bake.

For the poster who had a question about Carlson's... the liquid and low-dose caps are natural triglyceride. Their higher concentrate capsules are ethyl ester.

I currently like Barlean's, as it's triglyceride and relatively inexpensive. Their higher concentrates are ethyl ester though, so go for the lower conc. ones if you want the trig form.

I do disagree with Dr. Davis as far as preferring liquid however, due to oxidation issues. I'd recommend the caps instead, and simply chew them, if swallowing capsules bothers you. The caps do offer some extra oxidation protection.

Hi Vlado,
I think so-called
"pharmaceutical" grade fish oil is distilled to seperate out concentrated gradients of "x"% DHA & "x" % EPA in a product. Yes, fish scraps that the oil is extracted from first gets heated, but so is cooked fish. Solvent residues concievably might be in some products; you can inform me of other compounds resistant to purifying out.

1 teaspoon oil = 5 mL. = 200 pharmaceutical size droplets = 4.54 grams .... I, for example, weigh 79,379 grams (175 pounds/79.4 Kg.) and assume a daily teaspoon dose of 4.5 grams fish oil can be metabolized safely. If you've details on how the omega 3's are noxious when added into the diet please explain.

Is my fish oil already peroxidized and/or are ingested omega 3 lipids peroxidized to my detriment at this level? My math shows that one teaspoon for me is 5.7 hundred-thousandths of my body weight; multiplying 0.000057 x 79379 grams that I weigh = 4.5 grams in teaspoon of oil.

Is there any data guiding recommendations on the ratio of EPAHA? I've never come across any primary data on the subject. To the best of my knowledge, the ideal intake and ratio of EPA and DHA remain unknown and a point of contention. I've noticed many fish oils have a 3:2 ratio of EPAHA, but I don't know where that is coming from. I'd love to know your thoughts, Dr. Davis.

I love the brand from www.strongerfasterhealthier.com
They make 5 flavors with zero fish oil taste. My kids ask for it, so it's a big win in our house. The concentration of EPA and DHA towered over even barleans.

Carlson's Super DHA Gems and EPA Gems concentrate capsules are TG form.

Dear Dr Davis

I am looking for a Kosher liquid omega 3 fis oils
I find nutri supreme research
Calories   40

Calories from Fat   40

Total Fat   4.5g    7%**

Cholesterol   18mg   6%**

EPA   950 mg   *

DHA   475 mg   *

Other Omega 3   325 mg   *

Total Omega 3 Fatty Acids   1750 mg

is this ok? or there is something Kosher better?---------------------------------------------

Check out Ascenta! All their fish oil is in triglyceride form.

ascentahealth.com

What is your opinion of Krill Oil?

Dr. Williams, I am wondering what you think of only taking high doses of EPA? See the following article:
http://igennus-hn.com/omega-3-epa-treatment-for-a-heart-condition-news-release/

As I have M.E. (post viral fatigue syndrome) as well as astronomical total cholesterol (great tryglycerides), I''m interested in trying this protocol. Would love your input.