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

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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.

Hi Dr Davis,
I am an apoe4 carrier. My trig=62, HDL=69; LDL-C=175 after 16 months on a carbohydrate restricted, gluten free diet. Wondering whether I need to also reduce my fat intake. But then what is left to eat? Making up the calorie difference with protein does not sound too healthy.

David

Hi, David--

I would urge you to NOT rely on the calculated LDL value, since on a low-carb diet with potential conversion of small to large LDL particles calculated LDL can substantially overestimate true LDL.

The best: LDL particle number through NMR lipoprotein analysis. The next best: apoprotein B, widely available from nearly all labs.

When you're armed with this information, then you can make an intelligent decision about diet changes.

Regarding Item 6

There was some traffic between Chris Kresser and Jimmy Moore on Twitter yesterday regarding whether low carb caused low T3 in susceptible individuals. Clearly bad news for heart health.

I am a treated hypothyroid and this was my recent experience - I had gone low carb and ended up with an abscess in the roof of my mouth that needed antibiotics.  When tested, my T3 had fallen from 5.5 to 3.8 (RR 4 - 6.8) - however, my TSH was 0.672 (RR 0.35-4.5).  In the UK, this low T3 would normally would have been missed as there is a TSH only testing policy here unless the TSH is found to be outside the reference range - I elected to pay privately for the T3 test.

I remain on low-carb (and wheat free of course) as it is the only approach which allows me to lose weight, and have increased my meds from 75T4+20T3 to 100T4+40T3.

I would query whether you consider hypothyroidism to be rare. I suspect it is very common.

Hi Dr. Davis:
What if the patient  followed the above diet, had a particle count of 2,100, but only 200 were small and HDL 69 and Trgs 66.  Would this be acceptable, and better than a particle count of 640, less than 90 small, HDL 64, Trgs 45, but on statin and Zetia?  Assume thyroid and D all normal, and Apo E3/3
Thanks for all the input

Hi Dr Davis,
This post really hit home with me (and ironically this is my first visit to your site).  I had a heart attack 2 years ago (34 years old, ate well or so I thought, in great physical condition at 5'9" 150 lbs).  My cardiologist advised the usual low fat diet and pravastatin, and while my lipids are better than they were, I'm still very concerned they are not near where they should be.

About 5 weeks ago I found the primal diet and began eating that diet.  Last week I had another lipid test and my numbers actually got worse (not by much).  Would you mind reviewing my numbers and if you have any suggestions I would appreciate it.

8/31/2009 heart attack
total chol 115
LDL 74
HDL 16
Triglycerides 126
VLDL 25

07/19/2010 checkup
total chol 138
LDL 64
HDL 33
Triglycerides 203
VLDL 41

03/21/2011 Healthfair
total chol 122
LDL 69
HDL 31
Triglycerides 111
VLDL 22

8/19/2011 walk in lab:
total chol 159
LDL 98
HDL 34
Triglycerides 135
VLDL 27

Glucose 97
hsCRP 1.2
A1c 5.5

Do you suggest giving the "primal" diet more time or do you suspect I may have another condition causing this?

Also in May of this year I had the following tests done at the cardiologists:
Date of service: May 13, 2011
CAT Scan MRI & NMR
Diagnostic Radiology X-Ray
Cardiovascular Stress Test

I was told everything was fine.

Track Your Plaque once gave a desirable level of ApoB  as under 70 mg.dl as surrogate marker for the desirable LDL particle number (which is less than 700 nm/l) if one only has ApoB testing.  Maybe some one else can recall the conversion ratio of ApoB into LDL particle numbers.

A cholesterol fractions normal transfer from HDL to ApoB is governed by  the cholesterol ester transfer protein (CETP). Genetic variants of CETP can cause differences in the numbers of  small LDL and sparse CETP can cause cholesterol to stay stuck in HDL  ( CETP has little impact on numerical % of HDL). So genetic variants of ApoB can influence the levels of cholesterol shunting around.

In  the liver ApoB normally gets it's lipids when ApoB goes into a cell's endoplasmic reticulum. And if the ApoB doesn't improperly degrade ( ApoB needs "enough" microsomal triglyceride transfer protein SREBP-1c, the sterol regulatory element binding protein, to avoid degrading) then ApoB can pick up triglycerides to form VLDL molecules. So, if there is not enough liver SREBP-1c  then lipids can't be transferred over to make triglyceride rich VLDL; conversely lots of liver SREBP-1c provokes extra VLDL.

Doc says carbohydrate related  post-prandial high glucose not only induces  more VLDL output  from the liver but that this is part of the mechanism whereby carbs can boost body fat. High carbohydrate intake causes extra lipo-genesis in the liver because a significant  reflex of high post -prandial liver insulin is a signal that upregulates SREBP-1c. Then SREBP-1c expression rises and that in turn activates genes for the lipogenic enzymes (ex: fatty acid synthesase & acetyl CoA carboxylase),

Rogue readings of VLDL may be due to viral hepatitis proteins, flavivirus and pestivirus, which can decrease VLDL formation and secretion while dropping levels of ApoB. Viral proteins "smear" onto lipids and this blocks SREBP-1c action and viral proteins can also "stick" on to the HDL protein fraction ApoA1 inside of the  liver cells' Golgi Apparatus. Thus in chronic liver disease and hepatitis circulating VLDL associated triglycerides eventually decreases so there are more non-VLDL  triglycerides in play.

Hi Dr. Davis,

I was just wondering, due to many healthy cultures including the kitava, okinawan's...etc, who indulge in rather high carb intakes and retain rather pristine health, is it possible that high trigs, low hdl..etc may just be a lipid profile reflecting high carb* intake rather than suggesting atherogenic buildup ?

*when based on safe starchy type carbs

Hi, Paul--
In the population I see, hypothyroidism is exceptionally common, both in people on low-carb but also in people prior to initiating their low-carb efforts. So, without a formal analysis, I'm skeptical that low-carb in and of itself causes free T3 to drop.
There are also numerous inhibitors of the 5'-deiodinase enzyme that converts T4 to T3, including perchlorate residues from fertilizers in vegetables and polyfluorooctanoic acid, the residue of non-stick cookware, just to name a couple.

This is the BIG unanswered question. Sadly, there are next to no data that speaks to this question.
My day to day answer has been to 1) eliminate small LDL, then 2) maintain LDL particle number 1500 nmol/L or less. But that is pure speculation on my part.

Hi, Chris--
Something doesn't compute: Every panel you list is the pattern of excessive carbohydrate consumption and/or sensitivity. So something is sneaking through. There is no question that a "primal" or low-carbohydrate approach works for this pattern.  

You might also have an Apo E2 gene that amplifies carbohydrate sensitivity.

Hi, Might--
As always, you are an incredible fountain of unique insights!

Sorry, Jack, I didn't understand your question. Could you rephrase?

Thanks.  I've only been eating primal/paleo for about five weeks, so only the last panel would reflect this (if thats enough time to be reflected in my lipid panel).  I will re-test after another few months.

Dr Davis. Jeez. This sounds similar to my story (Frustrated's #s). I have eaten Paleo for over a year now, I have done exceedingly well with body composition in that time. See my "Share You Paleo Before and After" here ---> http://paleohacks.com/questions/7058/share-your-paleo-before-and-after/28493#28493. But this only adds to the confusion for me (and others).

For some reason, my labs came back on July 8, 2011 with small dense LDL and pathetic HDL at 40, despite a diet rich in GF beef, pastured eggs, bacon, pasture butter, coconut oil, ghee, veggies, starch and fruits only for carb sources, etc etc. I spend mega money to eat well. We don't mess around. I posted my VAP panel results on PaleoHacks last month and it has resulted in a lot of attention on this very subject. Chris Masterjohn weighed in with his thoughts. Dr Kruse wrote a blog all about it.

http://paleohacks.com/questions/50347/hack-jack-kronks-vap-test-results

I will be retesting again in about a month, as I have made some changes, like eliminating bananas, less heavy cream and pasture butter, etc.

My lab said it's $390 just to do the ApoE test. Is this a normal price? If not, where do you recommend people get the testing done?

I'm genuinely confused. It's like my body is saying... "Yes Jack. Good job. I am very happy with what you are eating. I will continue to keep fat off and pack on muscle." But then my heart is saying "Nooooo. Stop!!"

How can this be?

I was questioning if your pathological interpretation of a blood lipid profile that exhibits low hdl and high triglycerides, could instead just be a reflection of a high carb diet rather than suggesting an increased risk for CVD. I was referencing a couple high carb cultures, such as the Okinawa and the kitava, who exhibit a similar lipid profile but have very small incidence of CVD. Compared to other cultures with similar lipid profiles, such as the Swedes and Americans, who have much higher rates of CVD would suggest it's more about quality of blood lipids rather than their certain partitioning. Hopefully that's a better re-phrasal?

This is the BIG unanswered question. Sadly, there are next to no data that speaks to this question.
My day to day answer has been to 1) eliminate small LDL, then 2) maintain LDL particle number 1500 nmol/L or less. But that is pure speculation on my part.

My understanding related to your above comment is that large LDL is nearly as athrogenic as small LDL and that you want the particle number low with mix between largle and small LDL taking secondary importance.  Of course, that is based on a diet that the avg american consumes,  and not on the low carb with wheat sugar and cornstarch elimination you advocate.
Am i under a correct understanding regarding large LDL being dangerous as well and therefore the need to minimize this even with your dietary recommendations?  Also, i thought you advocated a total LDL particle number to approach 600?  Is your 1500 number a revised viewpoint based on newer diet or clinical observations?
Thank you again.

Server error blocking me again ... testing after hour passed.

ApoE is crucial to VLDL & chylomicron formation. Variant ApoE 2 less efficient at transfering lipids to liver and is binding lipids up an extra +/- 2%; result is that lipids take longer to clear from circulation and more can go wrong. From my notes, here is the rate some ancestral populations have at least 1 copy of ApoE2: 2-4% of Mexican-american & American Indian, also  3-4% of Japanese & West African. There is 0% of South American Indians with ApoE2 and one wonders which variation of  ApoE  might be in Kitava melanesians. .
ApoE4 degrades easiest of all ApoE forms, leaving protein fragments in cell's cytosol which then can affect a mitochondria's lipid binding region impairing the performing of  tasks. In addition ApoE4 fragments diminish gene PPAR gamma expression; and this depresses the desirable bio-genesis of mitochondria. The affects on mitochondria may be why high levels of dietary fat is problematic for ApoE4 individuals; there may be too sparse output of viable mitochondria and mitochondria membranes are involved in how efficiently we burn fat or glucose.  .
In light of these ApoE4 nuances it is interesting to know that fasting raises free fatty acid levels (from fats in the body and not loose fats from recent food); and then those free fatty acids upregulate  gene for PPAR gamma in the liver. Fasting makes one put out ketones  because of the extra PPAR gamma programing and this ketogenesis is also one way that activating more PPAR gamma improves insulin sensitivity. This suggests to me that individuals with ApoE4 may (?) find some benefit from modified fasting; possibly something like decidedly fewer meals in a day and also simply not grazing on snacks (ie: in addition to just trying to select what foods to eat) between meals that are regularly spaced apart (ie: very early breakfast to let meal times spread put more evenly) .

Finally again from my notes, here is the rate some ancestral population have at least 1 copy of ApoE4: .14-19% Germans & Finns, also 7-12%  French & Italians. Of course America is one of the world's melting pots so an individual's propensity for ApoE 4 & ApoE 2 is hard to pin point.

This is fascintaing Might. I have been guilty of snacking too much. All healthy snacks, but still the concept of grabbing bites of delicious foods between meals might be messing with my liver. For my VAP test, I did not fast. Chris Masterjohn believes this was the reason (or at least the reason for dismissal) of my increase in triglycerides in the blood. I am most concerned about my low HDL, because if I raise my HDL, I believe my LDL will become more dominantly pattern A.

Thank you for the reply.  I would like to share a speculation.  Strict low carb means gluconeogenesis means an increased cortisol demand? OK in young fit Paleo men, but what about long-term un(der)treated hypothyroid individuals?

In "Safe Uses of Cortisol", Dr William Mck Jefferies (p. 183/4) observes that low dose (20mg/day) of hydrocortisone taken by a patient with hypothyroidism increases T3,  lowers T4 and improves patient energy levels suggesting such low dose cortisol enhances T4 to T3 conversion.

Could VLC, by putting demands on potentially weakened adrenals, have the opposite effect?

HDL molecules hold triglycerides (there are 45 different variations of triglycerides in circulation, which are based on what their esterified fatty acid component is), cholesterol esters (about 13 - 27% of the HDL surface particles), shingomyelins and glycerophospholipids. HDL's principle proteins are +/- 70% ApoA1 and +/- 20% ApoA2;  yet any changes in the ratio of ApoA2 from genetics (Kitavans?, I propose so) or drugs (ex:fibrates) can have effects.  

Usually people with low levels of  HDL have more trigs on their HDL surface (compared to those with high levels of HDL) and low HDL is associated with the passing of more cholesterol esters to VLDL & chylomicrons. Also, when HDL trig levels go up that makes it easier for the liver enzyme hepatic lipase to cleave off more ApoA1 for the kidneys to clear away; and that further tends to keep HDL levels low.  

In comparison people with high levels of HDL have more cholesterol esters on their HDL; which may be due in part to cholesterol esters affinity for ApoA1 in HDL. And statisticly high levels of HDL are usually associated with bigger ("large") HDL molecule size. Both large HDL and ApoA1 are considered to be more protective factors against atherosclerosis.

I suspect that Kitavan melanesians' low HDL fortuitously correlates with a geneticly higher than normal % of ApoA2; and ApoA2 configures more deeply nestled into the HDL complex than ApoA1. It (ApoA2) influences molecular  interactions all the way to the HDL surface and limits certain lipid dynamics.

ApoA2 holds ApoA1 off of mature HDL molecules and this results in a shunting of ApoA1 into forming up the pre-Beta HDL; these lipid poor ApoA1 configurations are great at doing reverse cholesterol transport that brings back cholesterol  to the liver for excreting as bile acids. Those pre-Beta HDL are small, yet notably excellent at taking cholesterol away from nefarious macrophage foam cells (the large HDL  molecule also picks cholesterol nicely from foam cells).

Experiments see that preceeding type of change with fibrate drug doses, which only minimally raise HDL & ApoA1 yet increase the ApoA2 amount in HDL by over 25%. Since fibrates are agonists activating the peroxisome proliferator activiated receptor PPAR alpha it might be instructive to see if anything in the Kitavan diet is a similar agonist, such as heirloom tuber roots derived from wild yam with high diosgenin content (diosgenin is well known to affect PPAR gamma).

Thanks for the excellent post! Bookmarked! Will come back again…

Hi, Steve--
There really is no final word on what the desired endpoint is when small LDl has been eliminated and you have pure large LDL. In a perfect world, I'd wish for a particle number of 600 nmol/L with pure large LDL. But I'm no longer entirely sure this is necessary. But this remains anecdotal. There are no formal data, nor do I have any formal analysis of our own data on this question.

Hi, Jack--
Don't know, since I've never seen any genuine lipoprotein data on these populations. Most of the data I've seen has been total cholesterol, which is far too crude to draw any conclusions from.

Have you seen lipoprotein data on these populations?

Might. Do you suspect that I have low HDL and highish Trigs/VLDL in the blood for this reason? I do take in a fair amount of protein (including a whey isolate daily). Also, plenty of eggs. Does dietary protein consumption have any actual affect on HDL's principle protein and/or surface cholesterol esters?

Yes Jack Kronk, it seems that you have low HDL and highish Trigs, I do also think.

Just wanted to comment. I've been a long time low carb person, gluten-free too. I also had my thyroid ablated with RAI many years ago. I have found, as have many low carbers, that my reverse T3 is very high and Free T3 is scraping the bottom or below the range.

Unfortunately this does seem to be a common side-effect of low carb eating. It's even documented in studies on the topic.

We had a low carb eater recently watching his LDL climb to very high levels after he began eating low carb. He started taking cytomel and his LDL is coming down very nicely.

Did he get a sudden onset of hypothyroidism that just coincided with low carb eating? I suppose that's possible, but I do think there's something more going on.

I'm taking Armour thyroid myself, but I still have the tendency to turn T4 into reverse T3 and I suppose that means the Free T3 can't get to the receptors. I'm going to experiment with raising my carbs a little higher and sticking to things like yams and squash for my carbs.

Dear dr. Davis,
I just attended the annual cardiology congress of the European Society of Cardiology. Amongst others, the new guidelines on dyslipidemia were presented and I had the opportunity to ask the working group the question you mention above in your first of opportunities : What about measuring lipids during an ongoing substantial weight loss? The were not able to give me a proper answer.
Do you have any scientific references saying that weight loss induce a temporary dyslipidemia or is it based on your experience?
I would be most thankful for your comment on this.
Best regards
Espen Rostrup, MD, PhD-fellow
Bergen, Norway

Dr. Rostrup--

Unfortunately, I know of no published data documenting this effect. However, I have seen it hundreds of times. It is, in fact, quite predictable: drop in HDL, rise in triglycerides, variable small LDL effects, increased blood glucose. It all subsides and improves over time.

It would indeed be an interesting study to chronicle the changes serially in a small number of people.

I am also seeing a heck of a lot of omega-6 intake there.  Also, the healthfulness of monounsaturated fats is a bit overstated.  I've heard of studies where they had 3 groups of people.  One got their normal saturated fat, one group replaced the saturated fat with olive oil and the third group replaced the sat-fat with corn oil.  The corn oil eaters did the worst in health outcomes, but the olive oil group wasn't great either--both groups that replaced the sat-fat did more poorly.  I've heard of other studies where lard was compared with olive oil and the lard-eaters turned out better.  Bottom line, the human body seems to like saturated fat best.  (Lard is not as saturated as butter, but it is more saturated than olive oil.)  If I were in a position to make medical recommendations (I'm not), I'd tell someone like this to ixnay on the plant oils for a while and see what happens.

It should be noted that one of the more dubious selling points of grass-finished meat is that it is lower in saturated fat.  To me, this is not a selling point.  If this person were only getting PUFAs from their grass-finished meat it would be one thing--at least then it'd be closer to a 1:1 omega-6/omega-3 ratio.  But that's not what's going on here.  If they were just eating the fish they might still be OK (depends on the fish--cold-water is better).  But they're adding in walnut oil and chicken consumption and those are going to add more omega-6, even if the chicken's pastured.

I'm curious what this person's inflammation markers are.  If they're off the map the LDL may still be high because the body's trying to repair the inflammation.  That would explain the low HDL too; LDL takes cholesterol out to the body from the liver, and HDL returns it to the liver.  If the cholesterol is *needed* elsewhere in the body then of course it won't be returned to the liver.

Even if inflammation markers are normal, this person's diet may not be meeting their needs for saturated fats in the cell membranes, which may mean they need more cholesterol in their cell membranes to try to make up the deficit.  Not an ideal situation.

Get the PUFA reduced, get the inflammation down if any, see what the lipids do and then we can talk about weird genes.  Absent the necessary DNA profile we really don't know, anyway.

"just eating the fish" = in addition to the pastured beef.  I would not drop beef in favor of fish, there's too much good nutrition a person would be giving up, but fish in addition to beef's not bad.  Chicken used to be a luxury food, you had it on Sundays if then.  Best that it's relegated to that role again.  The white meat is too dry and the dark meat's rife with PUFAs.  Other fowl are not much better.  A foray into the USDA's nutritional database is an eye-opener.

[...] Genetics: Dr. Davis has argued that some combinations of ApoE alleles may make a  person “unable to deal with fats and dietary cholesterol.” [...]

"As the scramble for heart patients intensifies, you are going to feel like you are being pulled closer and closer into the jaws of this hungry monster called the American cardiovascular healthcare machine."

I wish our primary care doc understood this.  When we expressed some reservations about a follow-up CT angiogram (and entering the CVD "machine" prematurely) after my husband's EBT heart scan score of 282 (and the recommendation for a statin Rx STAT without a chance to try diet, lifestyle and supplements), we were reprimanded in no uncertain terms and accused of distrusting Western medicine, and what we wanted to try (TYP) was malpractice if he agreed.  I really thought this PCP was one of the more enlightened PCPs in our system because he was informed on and recommended optimal Vit D levels, bioidentical hormones and compounded Rx, and EBT coronary artery calcium heart scans.

I take your point here and thank you for putting it so clearly. But I'm not sure that the system has "outgrown demand" in any absolute sense. As people conquer some kinds of illness, they live to grow old and encounter new kinds. Perhaps if switch resources are switched from procedures to preventive and geriatric medicine, hospitals can maintain their size?

Anna, welcome to the real world.

Nowdays, I just go to the doctor to have one or other test done and then to hear the results and the diagnosis. Then I choose my own path. Of course I say I need time to think things over and I will get back to him when I have decided.

Scary stuff. I do things the same way Vin does.

it is so ironic to see Google ads for major procedure-driven local heart centers and hospitals alongside your wonderfully insightful blog!

If anyone doubts the truth of this most recent Heart Scan Blog entry "Wag the Dog", just take a look at the targeted marketing Google slips in.  In my case it was ads for Houston areas gigantic Memorial-Hermann and Texas Heart Institute, your content may differ.

madcook

Hi, Mad--

You noticed?

All ad revenues, by the way--the modest amounts--go towards defraying the continuing development costs of the Track Your Plaque website. It does not go into my pocket.

It's even worse in Diabetes World. The ADA, Diabetes UK etc. sponsored by manufacturers of high carb foodlike substances and drug manufacturers, tell you to eat lots of carbs and offset their effect with lots of meds, thus providing a ready feed to the cardiovascular disease industry (The ACCORD effect)

It is absolutely ridiculous that doctors don't understand how to cure diabetes with a low-carb diet.

This is just really basic biochem 101, carbs release insulin, and prolonged excess insulin causes insulin resistance, then diabetes.

This seems so simple that almost anyone with any small knowledge of biology should understand it, yet the main diabetes experts in the world don't.

I sometimes wonder if the "experts" don't want to give out simple solutions, since then half of them will eventually be unemployed and they won't be experts anymore. Kind of like how the oil companies obviously don't want us to invent renewable energy sources.

Dr. Davis, just to nitpick for clarity,

I'm assuming in the second paragraph "reductions in weight loss and HbA1c" is really meant to read "reductions in weight and HbA1c".

Sadly, what the studies show is that when these low carb weight
loss studies are continued past six months, invariably the weight loss stops dead for most participants.

This is true even in studies where the researchers tested for ketones in urine to ensure that people were eating what they said they were eating. The six month prolonged (and often permanent) stall is a repeatable low carb diet phenomenon.

My own polls among the low carb community verify this finding. Most people with diabetes will report they easily drop 15-20% of starting weight on a low carb diet but after that weight loss often comes to a complete halt even in my sample population which was made up of people with diabetes who had continued to maintain A1cs in the 5% range.

There are some lucky people for whom this won't be true, but they are a minority and tend to be male.

Since they are enthusiastic and vocal you tend to run into them online. The people whose experience is more typical tend to blame themselves and keep quiet.  

The real benefit of low carb dieting is in how it controls blood sugar. That effect will persist.

But long term diets of all types, including the low carb diet, downregulate the metabolism in ways that make it progressively harder to lose weight.

The big problem with posts like this one is that they raise false expectations--if you do well the first six months, a year later wow! That kind of false expectations eventually lead to frustration, feelings of failure, self-blame and almost inevitably diet failure and regain.

I can't tell you how many people I've seen posting on online support groups who did well for those first six months but ended up crashing off their diets a year later because they couldn't lose any more weight.

So after 13 years of observing people dieting with the low carb diet, I'm convinced that it's best to start the diet because of the blood sugar benefits--not with the dream of reaching what is all too often an unrealistic weight goal.

Figure that you'll lose 15-20% of your starting weight (you'll lose more if you are very heavy). Maybe you will be one of the small number of lucky people who do much better, in which case it will be a lovely surprise.

That way, you won't end up blowing off the diet once weight loss stops at a level where you still are much heavier than you had hoped to be.

There's also Long term effects of ketogenic diet in obese subjects with high cholesterol level by Dashti et al. Serum TGs & Glucose dropped like a stone in the Met Syn group.

The economics are not right for doctors to cure diseases. Healthy people do not come back until the next disease. Such is life. Doctor should only be paid for cures, when one exists.

We need to take charge of our own health and stop eating sugar, grains, manufactured oils and eatable products. Get a bit of exercise most days, and live a bit.

but what do I know

My perception:  I live in the "Deep South", home of the most obese people in the world.  The frustration for many health care professionals is in the unwillingness of patients to significantly change their diet.  It seems culturally mandated for many people to eat a certain way.  I fear that most obese people in the south would rather take medications than adhere to a diet such as this.  We can hardly blame the health care industry for this.

But what about the normal weight relatively young (41) type two diabetic?  (BMI 24)  Could I lose 20 pounds to be model slim?  Yeah. And I do eat low carb, although not 10 gram low carb.  And I have gotten my Hba1c to 5.4.  But, my insulin is crazy high, I hit 90 at my last glucose challenge.  I think it would be a big help if we acknowledged that diabetes is a SYMPTOM of a variety of related but not identical diseases.  Not everyone ate their way to diabetes, and while diet can totally help control symptoms, for me neither maintaining a proper weight nor controlling my carbs has solved the underlying problem, which seems to be a severe insulin resistance.

Might Jenny's observation and Nigel's study reference be reconciled somewhat ? I'll tag on my disclaimer of being unqualified to judge low carb or specific diets; since I've never struggled with weight or diabetes, and am not a doctor.

The study Nigel linked was done with all Kuwaiti subjects. In that country co-sanguinity in marriage is practised by +/- 54.3 % of Kuwaitis. And 1 in 5 are reported to be diabetic.

The data is very admirable; my suggestion is that the data trend may not exactly transfer to a modern Caucasian population; which is essentially interbred from migration and war (rape). This may be why Jenny sees a +/- 6 month plateau among her respondents and the co-sanguine Kuwaitis saw changes continue for a year +.

Genetic poly-morphisms influence fasting glucose (GCK, G6PC2 and MTNR1B), are implicated in Hb1Ac, triglyceride levels, HDL levels & so on. That said, I personally would try the low carb approach if I was diabetic.

edit my previous text to read  "... cross-bred from migration ...." instead of inter-bred.

Just personal experience here, but I'm a postmenopausal female and have lost 35% of my starting weight by doing low-carb. I've maintained that loss for four years. My BMI is 21.0.

For me, the key to reaching goal was the realization that eventually calories start to count. Low-carb has a natural appetite-limiting effect, but it is not a perfect tool. For people like me who have rather robust appetites, it becomes necessary to keep track of carbs for health and calories for weight loss and weight maintenance.

I wish low-carb weight loss were as quick and easy as Dr. Atkins made it out to be, but it's not. Prescription drugs, thyroid issues and exercise all factor into the equation, but after a certain amount of weight has been lost on low-carb, the sad fact has to be faced: calories count.

I just read the article on the front page of the American Diabetic Association website where they compared the benefits of a low carb vs. low fat diet for diabetics, and they said the big advantage of the low carb diet was you can reduce or eliminate insulin.  It seems like this idea is getting more and more respect from mainstream medicine.

I agree with Jenny that it's cruel to promise people that their diabetes will be "cured" by ANY treatment, including drugs, diet, exercise, or a combination of the above.

It sets up unrealistic goals and is equivalent to the nurse who tells obese people that if they'd just lose 10 pounds their diabetes would "go away."

It's simply not true. Type 2 diabetes is caused by faulty insulin-producing beta cells as well as insulin resistance, and that is often genetic.

Some people in very early stages of diabetes, when they're still producing a lot of insulin, can return to near-normal blood sugar levels with various regimens. Low carbing is one.

But if those people resume eating carbs, their blood sugars will go into diabetic ranges. They're not cured. They're just well controlled.

I have type 2 and I'm on a LC diet to control blood sugar, but I also take metformin and inject a basal insulin once a day or my blood sugars will be higher (I'm not comfortable with fasting or premeal numbers over 100, which they can be without the insulin).

I was diagnosed in late stage of type 2, and nothing we know about today will bring my beta cells back.

Please don't promise people false cures.

Anon posted "But what about the normal weight relatively young (41) type two diabetic? (BMI 24) Could I lose 20 pounds to be model slim? Yeah. And I do eat low carb, although not 10 gram low carb. And I have gotten my Hba1c to 5.4. But, my insulin is crazy high, I hit 90 at my last glucose challenge."

Just sounds like insulin resistance to me.  Some causes are transient fat in blood stream from high fat meals (In my experience in my body, saturated fat is more of a culprit than unsaturated by a very large measure), excess body fat and lack of muscle (lots of people are what I call "skinny fat").  Low carb diet, in one sense bypasses the problem since w/ low carb you don't produce much blood sugar load at once so the insulin resistance makes little difference.

I had fairly high postprandial readings (175-180's at one hour) and rising A1c.  Low carb per Bernstein made me feel terrible and worse the longer I did it though it did lower my sugar readings dramatically.  Now I eat a very high carb diet and about 30% fat (from whole, raw, seeds and nuts) but all the carbs are in high fiber veg and fruits and beans (with their resistant starch component)(occasional starchy veg and rarely whole grains NOT flour) and my one hour postprandials are in low 120's to teens and my most recent A1c was 4.7

My mother is a type 2, overweight diabetic. She's been helped tremendously by Dr. Davis's advice to eat low-carb and avoid wheat. But even on a VLC diet, her fasting blood sugar is typically in the 120s. Her diabetes was uncontrolled for 20 years, and her blood sugar was wonky for probably most of her adult life. She's never going to be back to normal.

Excerpt, ' Experiments described in the medical literature have tested the effects of high-fat diets on insulin intolerance. In one study, healthy young medical students were fed a very high fat diet containing egg yolks, heavy cream, and butter, and within two days all of the students had blood sugar levels high enough to be labeled diabetic.1 Complex carbohydrates have been shown to have the opposite effect.

Again I am not saying that low fat diet will work for everyone, but I think it worth trying, expecially if low car dose not work.

Sorry my previous post was not posted so do it again,
I think what people dont understand, that fat reduces insulin sensitivity and effectiveness, so when glucose and fat present inthe blood stream need much more insulin to maintain glucose homeostasis, and in many people even hyperinsulinaemia cannot compensate. Listen a few interviews with Dr. Delgado, dr. McDougle they explain it more clearly. When you keep your fat intake under 10%, the insulin is much more sensitive , sure you need to eat whole grain, proper carbs, and not junk cereals, breatds etc.
However, low carb diet works when people restict carbs, so they are able to maintai low blood glucose,  but once they consume more carbs,  blood sugar goes sky high.

Moreover, in some studies, has been shown, that when people eat fat diet, even pure sugar does not cause glucose spikes, as it is immediately regulated by insulin. , here i do not advocate eating sugar.
Another study Hollenbeck C, Doner CC, Williams RA, Reaven GM. The effects of variations in percent of naturally occurring complex and simple carbohydrates on plasma glucose and insulin response in individuals with non-insulin dependent diabetes mellitus. Diabetes 1985; 34:151.

http://www.joe-cannon.com/home/wp/can-type-ii-diabetes-be-cured/comment-page-1/#comment-1394

"I make the bold statement that type II diabetes can be cured because I care and I desperately want people to know the facts about type II diabetes that few people appear to have ever been told. I want people to know:

"1. Type II diabetes will go away -and stay away – in most people who take care of their health.

"2. Most people don’t have to get type II diabetes. Most type II diabetes is environmental  (eating too much and exercising too little).

"3. Losing a little weight and getting some exercise every day – even 20 minutes a day – can make profound changes not only on type II diabetes, but how long that diabetic lives."

Apparently Joe Cannon, personal trainer, whom I quote, believes most type 2s can be cured. Through 12 years of diabetes, type 2, I have exercised by ass off. I went from the typical ADA advice which didn't work for several years, to following Protein Power which brought management, to Dr. Berstein, which brought more and better management but didn't cure it. Found Dr. Davis's web site about 2 years ago and have been reading every post, becoming increasing radical in my approach. Dropped the steel cuts oats, added niacin, fish oil, you name it, I did it. Just ordered Dr. Ron Rosedale Diet because he says  diabetes can be cured in most cases. Okay, which radical approach is going to cure diabetes? I am one of your readers that is taking your words in your blog as a personal challenge. And I'm taking the personal trainer to task as well. I expect to be cured in six months (and am devoting six months to do that!) I expect you to continue to give fabuous advice, and as your experiment of one, I expect this to happen. I now have adopted the theme: "Diabetes is the Terminator"--it canot be reasoned with, doesn't show pity, and absolutely will not stop until you are dead!" Sorry if I sound desperate, but some of us are taking your words to heart!

Type 2 diabetes will rise and rise until people stop overeating. I see it around me everyday. Obese friends/relatives. For the last 20 years I'v watched them live an unhealthy lifestyle. Now it is catching up on them. One relative, age 48 type 2 diabetic, and one friend diagnosed last year. Age 52. Both have not changed their diet since diagnosis. Each carries an average of 60 extra pounds.
They were given nutritional guidance from a dietician, and I gave them websites to check out. Neither is interested in changing their lifestyle.

They refuse to change. Period. I'm sure there are thousands more like them out there......

Fat is not all the same or always acting as we think. An unusual poly-petptide in the intestine is upregulated by fat; and it follows a diurnal rhythm (inactive at night).

After "fasting" in response to
the first meal the body synthesizes bile acids for digestion of fat intake. When their litocholic and chono-de-oxy-cholic acids hit the small intestine they
interact with bile's Farnesoid X Receptor. This  upregulates Fibroblast Growth Factor 19 (FGF 19) in the intestines.

FGF 19 cycle is at maximum 1.5 to 2 hours after the post-prandial bile production kicked off; and bile synthesis had largely came on and abated. If the breakfast had no fat content then FGF 19's "on" trigger of specific bile acids can be low.

FGF 19 for it's part acts somewhat like a hormone; it integrates into a feed back loop. Humans have at least 22 different types of FGF with distinct action.

FGF 19 acts in turn to upregulate the anti-diabetic protein Insulin-like Growth Factor BP2. So there is less insulin resistance and blood glucose levels drop.

FGF 19 accelerates adaptive thermogenesis by  upregulating Uncoupling Protein 1 (UCP 1); the mitochondria energy gets "spilled" as heat. This makes the metabolic rate go higher and fatty acids are oxidized for energy.

Weight gain from fat is, in this scenario, less; but mostly from less liver cell fat. There is increased fatty acid oxidation burning for useful energy, since the mitochondria energy supply shifted from ATP delivery.

"Carbohydrates cause diabetes; elimination of carbohydrates cures diabetes."

"Type 2 diabetes will rise and rise until people stop overeating."

Stupid slogans like the above just confuse what is already a complex issue. To reiterate what has been said so many time, we have plenty of evidence of societies where carbs make up 65% or more of daily calories, but those societies show little obesity, diabetes, or heart disease, and they show long-life expectancy. The Japanese are a fine example of a developed society which eats a carb-based diet, and refined carbs at that, but doesn't have a diabetes epidemic. Clearly, carbs is NOT the problem.

And just as clearly, plenty of fat type II diabetics want to lose weight, but they can't. It is perfectly realistic to ask people to suffer hunger for a few months while getting down to normal weight. What is not realistic is asking them to suffer for the rest of their lives. So the real question is, why is causing people to have such huge appetites? And that is not an easy question to answer.

I grew up in the 1960's and everyone then was eating plenty of refined wheat, sugar and partially-hydrogenated vegetable oils, but people weren't fat like they are nowadays. Perhaps the manufacturers of processed foods have simply gotten much better at arranging fat, sugar and salt so as to make food irresistible. Perhaps it is a cultural thing: the same media brainwashing that has everyone wanting to supersize their house (McMansions) and car (SUV's) has them wanting to supersize their bodies as well. Perhaps the tendency towards obesity started after WWII, when food finally became cheap, and it simply took several generations for people to get accustomed to the idea of eating as much as they want, instead of treating food like something valuable not to be wasted. (Ever heard the expression "puts meat on the table?" Yes, there really was a time when an hour of labor at minimum wage didn't buy that much meat.)

If there is a magic bullet to the diabetes epidemic, it will have to do with appetite suppression. My impression, based on my own experiences and observations of people around me, is that low-fat/high-carb is more effective in the long-run at curbing appetite than low-carb/high-fat, at least for most people. In other words, the convention wisdom is right.

Japan obesity (BMI > 30 kg/m2) in 1990 - 1994  was nationally 3%. Japan statistic then for the overweight (BMI = 25 - 29 kg/m2) was 24% of men and 20% of women.

Adults were over weight 4 times more than they were in 1960 statistics; and mostly in the rural population. The 1994 school children (age 6 to 14) had 5 - 11 % obesity.

Data is from my notes (source was a Japanese translation) and I haven't looked up current statistics. Those 1994 obese school kids are all adults now
of course.

A recent analysis suggests that the lowest rate of death in East Asians (Japan, China, Korea) is for those with BMI of 22.6 to 27.5. This is similar to the European Prospective Studies Collaboration data of BMI = 23 - 27 as having least death risk in Caucasians.  

In obese East Asians with BMI >35the risk of death was 1.5 times greater. However, those with a BMI of 15, or less, saw their risk factor go up by 2.8 times. In those with super low BMI the theory is underlying co-morbidity is involved, like respiratory disease.

Coconut (like Doc's header image) has a  long 12:0 chain of lauric acid in it's fat that contributes to food satiety. It upregulates Glucagon-like Peptide 1 (GLP 1) release in the intestines.

GLP1 is secreted in the endocrino-cyte "L" cells and is one of the hormone group called incretins; some GLP is also active in the brain. GLP 1 inhibits gastric secretion, gastric emptying and digestive secretion from the pancreas.

It does enhance the release of insulin, which in this scenario
(GLP 1 activated) occurs in the context of slowed digestion; so blood sugar drops in real time. GLP 1 also stymies the release of glycogen (stored liver glucose) and the body is driven to burn something else.

GLP 1 does not provoke hypo-glycemia; the body burns it's fatty acids to run on. In fact if the individual does NOT graze between meals the satiation potential of coconut oil can work for up to 1.5 days worth of meals.

It seems coconut's lauric acid fat works on GLP 1 with a timed phase that also kicks in +/- 3 hours after a meal. This has the affect of getting some insulin out to sweep away the blood glucose and force the body to burn fatty acids.

Coconut's effect was greater than that of other fats; like milk fat, linoleic acid,stearic acid and oleic acid. Palm oil is more similarly satiating to coconut oil than other those other fats.

I detail this as a suggestion how dieters can keep the weight they lost off. Read Doc's old posts and you will see his objection to "grazing" food between meals; it supplants the GLP 1 surge benefits.

Here is a closing observation to amplify what others have infered. When western packaged foods switched out of palm and coconut oil shoppers lost the strongest activators of GLP1. Obesity from over eating got worse as we snacked up calories that sneak up on the waistline.

It is normal for people to overeat when food is readily available. That is a biological characteristic that has aided survival. We live in a time of excess. We need to learn to live normal in a abnormal world.

I try to do that by avoiding sugar, grain, manufactured oils and other eatable products.

but what do I know

Might-o'chondri-AL, thanks for that mini-treatise on coconut oil. Lately I have been eating two tablespoons of coconut oil for breakfast as part of my weight maintenance program. I have noticed that the coconut oil is able to produce satiety as well as lower my blood sugar, but I had no idea why it worked.

Some folks are very sensitive.  Control is probably a better word than cure, but the message is the same.  Low carb helps many folks with their blood sugar which is what seems to be so damaging.  It almost seems as though some cannot see beyond their own world views ("it isn't anyone's fault other than some medical-industrial complex", paraphrasing) when presented with evidence that INDIVIDUALS can help themselves, though some choose not to.

"Cure" implies that you no longer have diabetes, that you can eat whatever whenever and maintain normal blood sugars.  For almost everyone diagnosed as diabetic, that's not ever going to happen.  

Diabetes -> High blood sugar -> complications

You cannot change condition one - if you're diabetic, you're diabetic.  You can't really do much with link two - high blood sugar is going to cause complications in everyone who isn't killed by something else first.  But many type 2 diabetics can break link 1 and maintain normal blood sugars by limiting (or effectively eliminating) the amount of carbohydrate in their diets.

But "cure" is definitely the wrong word to use.

Diabetic Cookery 1917 Rebecca Oppenheimer
Trouble is we forget what we once knew.

This is an interesting discussion.  Like "Anonymous" who is a young diabetic with a BMI of 24, I didn't eat my way into diabetes, and if I could eat my way out of it, I would have by now.  

To M-Al and proponents of both low-carb and low-fat approaches, my experience tells me that type II diabetes is definitely NOT one disease, and (I'm getting to be a broken record on this forum I'm afraid) therefore the best regimen for control won't be the same for each person.  I do believe that many diabetics benefit from low-carb, and some from low-fat.  I suspect you will find refugees from one diet in the forums of the other - e.g., people for whom one alternative didn't work.

One thing you probably can't do as a diabetic is eat both fats and carbs. And diabetes is so complex - a research article I read said that many diabetics seem to have disturbed lipid *and* carbohydrate metabolisms.  So where do you go from there?  Plus, you just dump sugar from your liver for no good reason, regardless.  This is why many diabetics (most?) will need to add medications to their diet and exercise routines.

To commenters saying things like, "I know why there's diabetes - everyone's eating too much":

Look at all of us: we're on a health blog.  We all have in common an unusual interest in health matters.  The fact that some people not reading this blog do not want to change their habits doesn't make it okay to blame diabetics for their disease.   Easy for you to say if it hasn't happened to you.

What people do not take into consideration is that blood glucose is not dependant solely on dietary intake.  The liver dumps glucose into the blood stream in response to catecholamines.  Beta cells do not respond to endogenously produced glucose.  Glucose not utilized by the brain and the skeletal muscles will circulate for long periods of time.

Hi Helen,
Me, for my part, am just trying to examine the science of what Doc says works. It intrigues me, as do your comments.

Whatever the causes of insulin resistance it starts unnoticed. The pancreas cells that should respond to circulating glucose go awry.

Beta cells don't polarize their
mitochondria membranes in the "normal" response to blood sugar (for many reasons, as you say).The Potassium ( K+) Channel is ruled by ATP and is unable to perform it's K+ channel function; it closes up for those people. (Mitochondria in other tissue can still be functioning normally.)

So that Beta cell's mitochondrial
Calcium ( Ca++) Channel gets a disorganized electrical charge. The Ca++ can't reach the triggering level the islet
cell needs to put out insulin.

A rhythmic swinging of Ca++ between the cell's mitochondria and that cell's cytoplasm (interior) is what sustains "normal" insulin activity. Why this happens, when and to whom is as you say  variable.

First comes that pancreatic
islet Beta cell mal-function, which instigates body's
insulin resistance and then that
individual shows symptom of hyper-glycemia (high blood sugar). If that kind of Beta cells' mitochondria mis-step (detailed above)is happening when someone's body tries
to respond to blood glucose Doc's carbohydrate restriction is logical (to me).

Insulin resistance apparently starts for adults long before blood glucose tests indicate
even "pre-diabetes"; by age 60 +/-  1 in 5 will become Type II diabetic in the U.S.A. It seems with age our Beta cell mitochondria get out of whack and what we got away with in youth is not going to last forever.

Genetic, epi-genetic and age are part of the disease progression; diabetes is a process, not a static condition over time. Abnormal Beta cell workings can lead to improper protein structure of the insulin molecule itself.

This afflicts the Endoplasmic Reticulum (ER)where proteins are supposed to be appropriately folded. The erroneous protein configurations trigger the cell to "opt" for pre-programmed death (apoptosis, kind of like cell "suicide").

That apoptosis is what eventually
causes the diminished number of Beta cells in Type II diabetes.
Early on Type II diabetics are not neccessarily suffering from dying Beta cells, or even always shrunken (atrophied) ones.

Once the Type II diabetic's Beta cells die, then they suffer irreversable insulin insufficiency. That person has no response to hyper-glycemia and again Doc's regimen makes sense (and,I think he alluded to
adding prescription diabetes drugs in certain individual cases).

Anon about typo: Thanks for catching that. Now fixed.

Hi, Jenny--

Thanks, as always, for your insights.

However, I am witnessing something different. I see 30, 40, 70, 80, 100 lbs of weight loss, followed by profound reversals of diabetes and all its associated measures.

I suspect that many of the people you are talking to are not really following the diet that has the potential, in most diabetics but not in all as you well know, to completely reverse diabetes. It is a matter of the intensity of diet, the long-term commitment, and knowing what feedback tools to monitor.

Just doing--

Well said!

Gretchen--

Same response as that to Jenny.

I was diabetic 20 years ago. No longer. I have a long list of former diabetics. It ain't that tough.

There are indeed people who are physiologically incapable of reversing or ending diabetes. Jenny's LADA, for instance, can only be minimized, not completely reversed.

But, as much as I respect the opinions of both of you very sophisticated ladies, I disagree with you on this issue. In fact, I would crudely estimate that 70-80% of all current diabetics, with the proper insight and information, can completely rid themselves of diabetes. This is no false hope.

Revelo--

You are venturing very close to my Zero Tolerance Policy for rude behavior. Nonetheless, you often have insightful comments, so I'll let this one pass.

Having done this in many patients, I can tell you it works in many, perhaps most, thought not all. There are too many paths to this place called diabetes, variable residual beta cell function, variable leptin status, variable adiponectin status, varying apo E status, etc. to allow 100% generalizations.

The important lesson here is that MANY people, me included, who can kiss diabetes goodbye.

Incidentally, I made myself diabetic 20 years ago eating low-fat, high- carb while jogging 5 miles a day.

Another typo? About the paper you link to, is about a "small experience" or a "small experiment"?

Just to be argumentative

Dr. Davis, if you are no longer diabetic, how could you start with a blood sugar of 84 mg/dl, eat 4 ounces of whole wheat bread, and then have a blood sugar of 167 mg/dl one hour later?

In search of wheat: Einkorn and blood sugar

I'm not a physician, but a postprandial blood sugar of 167 might indicate that your diabetes has not been cured.

after losing 70 lbs, even at 6:2 225 lbs, I was still in the Obese category.  I am not a bigbfan of one size fits all number ranges.  

btw:  funny how it is the last ten lbs as if the number is the same. most low crabbers lie about their REAL carb intake.. We forget how quickly they add up.  


Calories do NOT count.

better the last ten is harder than the first fifty.

GRAND control but no cure.

'I see 30, 40, 70, 80, 100 lbs of weight loss, followed by profound reversals of diabetes and all its associated measures."

Dr Davis, with all due respect, if I lost 100 pounds, I'd weigh 20 pounds, which doesn't sound very appealing to me.

As I noted, *people who are diagnosed in early stages of diabetes when they're still producing a lot of insulin* can go into remission with any kind of weight loss diet. These are the patients you're seeing.

But they're not CURED. If they regain the weight, they'll have the same problems again.

And people who aren't grossly overweight when diagnosed can't even go into remission by reducing carbs and giving up wheat. There are many many reports of this on the discussion boards and the anger the patients feel because medical people promised them something that didn't happen. They lose faith in doctors and try all kinds of alternative treatments, some of which could be dangerous.

I think it's fine to tell patients that they MAY find that the weight loss puts them into remission. But to tell them that any diet will cure their diabetes is cruel, IMHO.

If you had diabetes 20 years ago, then you still have it. Nondiabetics can be grossly overweight and maintain normal blood sugar levels. Some very obese people aren't even very insulin resistant.

Human physiology is complex, and simplistic slogans (it used to be "fat makes you fat") are misleading.

(BTW, Jenny is MODY, not LADA).

I thought of an analogy: Someone is alcoholic. He gets counseling and gives up alcohol. Is he no longer alcoholic?

I don't think so. Nonalcoholics can have one or two drinks and stop. He can't. He's controlled, but not cured.

A lot of this controversy involves definitions. If you define "diabetes" as an A1c in the 4s, which is found in truly healthy young people, then if you get your A1c down that low with diet, you're not diabetic.

But if you define diabetes as an inability to eat a lot of carbohydrate without going over 120 mg/dL, then you could have a low A1c on a low-carb diet and still be diabetic.

Here are some quotes from lists from people who tested nondiabetic relatives:

"My non-diabetic husband has never tested above 4.7 (85) and I've tested him a few times 1 and 2 hrs after amazing carb loads - 200g plus in 1 meal. Once after a Christmas dinner with 2 desserts (one dessert was sugar pie) and once after a pasta+white bread+dessert meal. After gigantic amounts of pancakes and gobs of maple syrup. He stays pretty much rock-steady."

"I took my glucometer down for Thanksgiving and tested everyone an hour and two hours after the big meal with potatoes and pies etc. My brother in law's BG was only 82!"  and "I did the same thing with my siblings...including a sister who is close to 400 pounds. She was 84, my other sis who is about 220 lb was 75 and my brother who is thin was 100."

It's not just weight.

I don't like to argue about this, because I think you're doing a lot of good by urging people to cut carbs. But I think we need to face facts. Weight is an important factor, but not the primary cause of diabetes.

I think that Grtchen's comment sums it up well. Dr Davis is a cardiologist. He also has a strong interest in nutrition and its impact on cardiovascular health. He is not an endocrinologist. And this shows in many of his comments regarding diabetes.

Stargazey,

  I'm not diabetic, neither my wife, both of use can get 170 mg/dl after a vegetable sandwich with white bread. So, from my perspective your comment does not make much sense.

Seems to me that low carb with elimination of grains and fructose would be a necessity for anybody with impaired glucose tolerance or diabetes.  Depending on how bad your insulin sensitivity is, you may have to switch from saturated fat to mono-unsaturated as well.  Add an hour a day of physical activity and I expect a significant percentage of diabetics/prediabetics will be off their meds.  The others will hopefully at least stabilize and not get worse.  Are they "cured"?  Not exactly...they still can't eat all that sugary stuff we all like to eat.
But here's how I look at it.  Maybe they were never "sick" to begin with.  Maybe they were just poisoning themselves with foods they were never adapted to eat. After prolonged and sustained exposure to these poisons they got sick. Remove the poison and they no longer have the "disease" of diabetes.  I wonder what percentage of diabetics this definition of "disease" might apply to?

@GeoffreyLevens
I would be interested in how much exercise you do along with your diet to keep your bloodsuger (and A1C) that low.

exercise has little positive effect on blood sugar in the short term, in fact, in early efforts to control my numbers without meds, exercise would increase BS numbers after excerise. But in the long term, as a means to repair the body, it is very positive with diet.

I find that exercise is a significant way to control blood sugar level. For me, a 30-min brisk walk (breathing hard at end) will reduce a 150+ blood sugar to under 125 mg/dL.
I have found that the time of day for exercise is important. Physiologically we release glucose from liver glycogen prior to and on wake-up, preping our metabolism for activity so to speak. With increasing insulin resistance blood sugar will rise from the released glucose. Blood sugar is controlled by the insulin release in nondiabetics. Diabetics and the insulin resistant, can verify this with a series of fasting morning sugar checks, say on rising every 20 mins for an hour. By the way, this is known as the "dawn effect". For diabetics, the effect seems to be compounded with rigorous morning exercise. Exercise later in the day does not seem cause a problem. I had to go low carb (reducing stored hepatic glycogen) to reduce this natural response.
This is my experience, and I am a DMT2. Be curious to hear about impact of exercise from you non-diabetic types.

semsons.group: You may not consider yourself a "diabetic" but hitting a one-hour postprandial blood sugar of 170 after eating a sandwich is not healthy. Increased postprandial blood sugar levels is a sign of possible insulin resistance and a prediabetic condition.
Continuous glucose monitoring studies show that for healthy individuals blood sugar rarely rises over 130 mg/dL and then only briefly during a 24-hour period. It is generally beleieved that blood sugar levels over 140 mg/dL are harmful.

I use the term "cure" loosely. "Latent" would be a better term.

Personally, I run HbA1cs of around 4.7%, fasting glucose below 90 mg/dl, and postprandial glucoses of less than 100 mg/dl. In other words, no diabetes.

However, if I have whole grain bread, cookies, and pretzels, I will be fully diabetic in short order, especially if I gain weight.

I've seen this played out many, many times.

Thanks, Dr. Davis. I suspected that might be the case.

On a related topic, semsons.group and his wife may wish to avoid vegetable sandwiches with white bread.

Dr Davis, thanks for clarifying your terminology. The reason I'm so adamant about avoiding the word "cure" is the following.

I knew a man who was Dx'd with type 2. He did all the right things and got his BGs into normal ranges. So he thought he was cured and stopped testing. Nondiabetics don't test, and he was cured and nondiabetic, right?

Then he had a piece of cake for his birthday. It was pretty good. Soon he was having cake every Sunday. Then every day. Then he forgot about the diet altogether. He was cured, right?

One day he noticed he was thirsty all the time and decided to test. His BG was in the 400s or 500s. He wasn't worried. He knew what to do and went back to the diet that "cured" him before.

Only this time it didn't work. He'd burned out his beta cells with high glucose. And he had to start injecting insulin.

If instead of being told he was cured, he'd been told he was in remission but still had to be careful, he might have tested and discovered the problems before they were irreversible.

This also illustrates the benefit of early diagnosis. If you wait too long, the condition may become irreversible no matter how strict your diet.

A difference between Dr. Davis's patients and typical low-carb dieters is that the patients may be taking more supplements of the right kind. There's a whole school of thought that overweight is caused by lack of nutrients, especially minerals. I believe that whacking out the empty, carby calories is important, but I also believe you need vitamins and minerals to metabolize fat--including your own fat. It's often forgotten that Dr. Atkins recommended supplements, and even wrote a book on the subject.

In some studies I've seen, low-carb dieters were allowed, over time, to go back to eating more and more carb. (I'm sure this happens sometimes in real life, too.) Naturally, they stopped losing weight.

Has anyone used supplements like lipoic acid ? (The R version is supposedly superior). It is used in Germany as a treatment in diabetes.

Revelo: No, my comments are not stupid. I have yet to see a Type 2 diabetic within their normal weight range, AND eating healthy. I am surrounded by fat relatives/co-workers who live on highly processed boxed packaged foods, morning, day, and night at home and work place.  

Myself and only 2 others bring our lunch to work from home, the rest on a daily basis eat out at Taco bell, Burger King, Pizza Hut, MsDonalds, etc. Now imagine doing this again for dinner??

How much more can your body take of this diet before you become a DIABETIC?? I see it day in and day out before my eyes people eating themselves into Type II Diabetes.

Interesting: when Jenny points out that a theory applied doesn't actually work, the response isn't, "hm, perhaps the theory isn't right..." it's, "Well, then you have to be doing it wrong."  So, if I go on a rigorously-applied low-carb diet (no grains of any kind, no vegetable starches, limited fruits, no juices, fats being animal and EVOO only, and I STILL don't lose even a single pound despite cycling 20+ miles per day, Dr. Davis will unblushingly inform me that it's my fault, it's not that there's something wrong with the theory.  This is the case, by the way -- been doing this as a test since January. FWIW, my blood sugar, which before January, was typically 80 or so in the morning is now 120+, as often as not.  I'm not impressed with the results of this "health" approach, which hasn't changed even one of my health issues for the better, and appears to have worsened several rather significantly.

Meg:  Not a single pound?   Then something is very unusual.  Many of us know Jenny and her work and are familiar with her POVs. But not a single pound and claims of worse health leaves many of us speechless, What in the world would one expect to hear on an internet forum?  


Annom-  I have used R  acid large doses twice a day. I cannot say that it worked by itself. I stopped when money got tight and didn't start again. It was a part of many things I was doing at a time when I was having my best results away from using any meds. I am thinking of going back to it and a few other things.

As for exercise, only heavy lifting, strength training had any effect on my BS numbers on the short term. Walks and aerobics increased the numbers.  Type II is different for all of us. My best numbers are when I wake up and at night. go figure.

To Anonymous, who said:

"Revelo: No, my comments are not stupid. I have yet to see a Type 2 diabetic within their normal weight range, AND eating healthy. I am surrounded by fat relatives/co-workers who live on highly processed boxed packaged foods, morning, day, and night at home and work place."

Well, then you have yet to meet me.  And my father-in-law.  Your tone is very judgmental and your comments uninformed.  About 1/4 of type II diabetics are not overweight.  I have always eaten healthfully - people are always commenting on it, and now they say, "Diabetes - you?"

On the other hand, most obese people do not have diabetes, even though they may have other health problems.  Diabetes can be triggered by a poor diet and overweight, which lead to insulin resistance, but you have to have other, usually genetic, risk factors to develop diabetes.

Anonymous, I once gave a talk to a local diabetes group. What really impressed me was that there were very few obese people in the audience. One man with a "beer belly," but most were post middle age women, not skinny, but not fat. Some were thin.

I find it sad when people blame the victims. I think it's a form of self-protection. "Well, I don't do those things, so I'll never get disease X."

I know a lot of people with diabetes who eat healthy diets, but I live in a rural area where most of us have vegetable gardens and some raise animals for meat as I used to.

When you work in an urban area where everyone else in the office goes to fast food places for meals (I once noticed there was nothing but fast food available in the Harvard Medical School area and I wondered if they were trying to drum up business), it's difficult to be different, especially if you're the only one. Lots of peer pressure. People hate "holier than thou" eaters.

I recently heard a talk on obesity by Jeffrey Friedman, who discovered leptin. He said many people think obesity is caused by gluttony and sloth, adding that "this view is mostly espoused by thin people." He thinks genetics has a very large role.

Anonymous, have some compassion and have the courage to use your real name.

Megeara, I have had a similar experience, although I did lose weight on low-carb.  It may be that this diet simply isn't compatible with your particular genetic profile and how you handle lipids and carbs.  Try some other approaches, keep checking your blood sugar, and see what works best for you.

By the way, I find that supplemental fish oil and also vitamin C drive my blood sugar up.  (Both of these personal experience were backed up by research, I discovered.)  Check out if any supplements you are taking might be driving your numbers up.

Megaera--just a thought--are you doing anything close to zero-carb? For some reason, in people over 50 a zero-carb diet can cause elevated blood sugar.

I tried a zero-carb diet a couple of years ago, thinking it would help me lose weight and stave off diabetes. Instead, I gained weight and my fasting blood sugars went above 100 mg/dl for the first time in my life. I surveyed a bunch of people at my blog and found that those over 50 had similar experiences. (Google: Stargazey Observations on Protein Intake, if you want to read about it.)

I tend to agree with what Stargazey is getting at here and Dr. Davis has since rephrased:  VLC is not a cure for diabetes.  VLC is clearly one way of managing one of the major symptoms implicated in health risks associated with diabetes (e.g. hyperglycemia -> glycation).  

However, eating VLC does not cure diabetes, which at its core is pancreatic beta cell dysfunction.  Indeed it seems it can exacerbate the dysfunction as illustrated by the anecdotal evidence (don't like it but we have no real studies on this that I am aware of) that long term low carbers become more and more sensitive to any carb in the diet = worsening glycemic control.  

A normal person can handle quite the glucose excursion and mounts an appropriate insulin response to handle it.  A diabetic cannot handle this, and neither can VLC'ers or the advice to carb up with 150g/day for several days in advance of an OGTT would not be circulating around the web.

Can diabetes be cured?  Well, apparently yes.  I'm not suggesting gastric bypass surgery, but the remission rate - as in cessation of meds and "passing" an OGTT - is remarkable in morbidly obese diabetics undergoing the procedure.  In the 80-85% range in a matter of days/weeks prior to significant weight loss.  

This tells me that our beta cells are remarkably more resilient than we give them credit for - we're talking some of the most deranged metabolisms snapping back to "normal" relatively quickly.

In the short run, especially in IR obese and with weight loss, low carb generally seems to be a more successful approach.  But long term, more moderate approaches with higher carb and lower fat intake seem to be better, especially once compliance is taken to account.  

(In Westman, after randomized assignments of 97 participants, 10 of those who drew the LCKD diet didn't show up to do the study, while only 3 of the LGID did.  So they started with 38 and 46 respectively.  Of these 5 KD's dropped out for refusal/dissatisfa41%ction with the diet while only 2 dropped out of GI diet.  17 total dropped from each group.  So from assignment to completion,  27/48 = 56% of screened recruits effectively dropped the LCKD while only 20/49 = 41% dropped out of LGID.  This can definitely impact results.  And the post-6 month rebound is common in longer term studies.)

The results in the 2 year Shai study for example:  http://carbsanity.blogspot.com/2010/09/shai-and-diabetes.html

Nuttal's group has achieved some excellent results absent weight loss with their LoBAG diets - high protein (30%) with 20,30 or 40% carb splitting the 70% baby with fat.  http://carbsanity.blogspot.com/2010/09/lobag-diets-for-treatment-of-type-ii.html

I think Dr. Davis is an example of what Dr. Dansinger (who treats diabetics with a relatively low carb but less extreme version than others) refers to as a "carb cripple".

I use the antioxidant R-lipoic acid as a supplement.
Daily:  3x 200mg R-Lipoic Acid
1x 1000 mg Evening Primrose Oil
1x 1000 mcg Biotin
As suggested by Richard Bernstein in his book, “Dr. Bernstein's Diabetes Solution: The Complete Guide to Achieving Normal Blood Sugars.” The Evening Primrose Oil provides gamma-linolenic acid (GLA) that is believed to increase the effectiveness of the lipoic acid effect. The biotin replaces the body’s supply consumed in the lipoic reaction.
The R-isomer is believed to be better utilized than the S-isomer.
In Germany, R-lipoic acid is used to relieve diabetic peripheral neuropathy, however, the supplement is given intravenously.

I can not say that it has improved my blood sugar control but I continue to use it more as a “universal antioxidant”, and because of Bernstein’s endorsement. R Bernstein, a type 1 diabetic, is an endocrinologist and one of the original proponents for the use of at-home meters for measuring blood sugar levels in diabetics. He is one of the very early supporters of low carbs for blood sugar control in diabetics. He is in his 70s.

I am a type 2 diabetic on metformin and low-carbs, maintaining HbA1cs at the low-end of 5%.

For supplements this is the most expensive one I take. I go back and forth between the Doctors Best and Life Extension products, whatever is cheaper on Amazon at the time.

Perhaps Jenny/Blood Sugar 101 can add a few more comments …

Very interesting to me here, thanks everyone. Beta cells, in human adults, have their individual life span; they are not replaced from stem cells.

A few at a time, of the already differentiated, Beta cells duplicate themselves. New ones form and in the absence of hyper-glycemia (high blood sugar) can become larger than their progenitors.

This might explain how Doc gets latency, CarbSane suggest a "snapping" back, and why standard carbohydrate intake does not always induce diabetes. Each Beta cell has more than one mitochondria in order to sustain it's insulin role.

Another commentator mentions that as some Type II diabetics age they (diabetics) do better off the low carbohydrate diet. Maybe the very slow time which Beta cells self-duplicate in has reached a good formation (in those individuals) and best to  "use it, or lose it".

A low carb period gives fresh Beta cells enough of a break from high blood sugar then they can become large. Then that co-hort of Beta cells can follow the "normal" response; which is to get larger in response to  insulin demand from blood sugar (ex: when middle age Type II diabetic does "better" off of a strict low carb diet).

What stops Beta cell self-duplication in Type I diabetes is the auto-immune T cell "attack". The immune system stymies regeneration.

In Type II diabetes the inability to prevent toxic exposure side effects can be what impedes Beta cell self-duplication. Distorted  down-stream signal pathways can affect the transcription of a "fledgeling" Beta cell's replication of it's actin cyto-skeleton .

Might-o'chondri-AL, if you don't mind my asking, where do you get all your information? Are you a graduate student, perhaps?

Hi Stargzy,
I'm "semi-retired" 60 year old who hopes to avoid degeneration as I age. I've been investigating how to live well for over 40 years. Doc's blog appeals to me because he has clinical cases to draw on and good input from his readers.

When I first began looking into things maintaining health the science was much different. I am just trying to organize my thoughts on contemporary research to preserve my mental capacity.

In the Westman study, it bears noting that the gender and racial make-up of the "completers" - which is all that counts for comparisons - varies considerably between the diet study groups:
LKCD:  67% female, 67% white, 24% African-American
LGID:  79% female, 45% white, 52% African-American

On the "carbohydrates cause diabetes" front, I remain unconvinced.  When one looks at populations who are most susceptible to developing the disease, what does they tell us?  The traditional Pima ate an 80% carb diet and had low diabesity.  Expose to SAD - rates soar.  Japanese in Japan eating traditional diet with lots of rice = low diabesity rates.  Expose to SAD = rates soar.  The SAD is lower in carb by % (generally comes in at 40-45% carb for "usual" diet in studies) than the traditional diets.  So how can we say that carbs cause diabetes?

I tried to post this before, but it got lost.  

A question for Dr. Davis:  When you got diabetic blood sugars on a "healthy, whole grain" diet, were you supplementing with niacin and fish oil, which you recommend on your site?  I'm curious, because both are associated with impaired glucose tolerance in type II diabetics, and I have seen the effects of fish oil on my own glucose control.  There's a theory I've read that, while niacin has cardiovascular benefits, which is why you recommend it, food fortification with niacin may be in part responsible for increased rates of diabetes.  

Is it possible that niacin is beneficial with low-carb, but deleterious with high-carb?

Sorry for that comment above.

Afghans (people of Afghanistan) eat a wheat based diet. In fact, wheat bread is almost the entire diet of many of them (and they suffer from iodine deficiency and other problems as a result). But they have little obesity, little diabetes, no problems with insulin-resistance:

http://maisonneuve.org/pressroom/article/2010/nov/15/the-diseases-affluence/

Things are more complicated than simply "carbs = bad".

Hi Helen,
Niacin induces vaso-dilation ("flush") from the action of prostaglandins on capillaries Prostaglandins are made from the lipids stashed in our membranes.

This is how fish oil DHA/EPA (n-3) and poly-unsaturated vegetable oil (n-6) are involved; these can form Arachidonic Acid (AA)for making prostaglandins. Aspirin (salicylic acid) works as an anti-inflammatory because it blocks the AA pathway engendering prostaglandins.

1876 salicylate was known to decrease diabetic's glucose in their urine. A modern study showed injected salicylate restored acute (ie: 1st) insulin response to glucose in
10 out of 12 Type II diabetics who were administered prostaglandin.

For the 2nd insulin phase, with a few gr. glucose challenge, 12 out of 12 Type II diabetics had a 4x increase in their 2nd insulin response (ie: with a
salicylate booster before glucose administered and having those prostaglandins they got to start the test.)Prostaglandins,
in Type II diabetics, interfere with insulin response; in the controls the prostaglandins did not blunt the 1st nor the 2nd insulin "pulse" put out.

Women (some) "flush" from effect of prostaglandins at lower concentrations (ie: less niacin)than men (some). This is believed to be related to estrogen levels; suggesting that
post-menopausal women should review their original pre-menopausal niacin dose.

Doc specificly stated no one should take more than 1,500 mg. niacin without medical supervision (ex: liver enzymes
that monitor inflammation
tests). Diabetics who see their blood sugar worsen and/or liver
tests worsen while taking niacin, might be able to find their individual dose that does not induce levels of prostaglandins interfering with insulin phases 1 and/or 2.
Aspirin, as a salicylate, could be an additional way to block AA (thus prostaglandins)and foster timely insulin secretion for glucose clearance.

Another latest study showed that carbs and fats do not mix well and results into high blood sugar. YOu need to read the full studyy, to see the whole picture. healthy subjects were given hig fat meal (only fat) in the morning and their glucose and insulin remained at the fasting level for the next 5 hours. Then they were given coffee or nothing and then did glucose challenge. Sugar shut sky high (10 mmol/l ~180sh). Coffein further increases glucose.

This study again demonstrates that fat even after many outs of eating got negative effect on glucose. If if you eat low carb diet thats ok, but like most peole eat 30-40% energy from fat that leads to disaster.
'An Oral Lipid Challenge and Acute Intake of Caffeinated Coffee Additively Decrease Glucose Tolerance in Healthy Men ' http://jn.nutrition.org/content/early/2011/02/23/jn.110.132761.abstract

THis give some explanation why low fat diet work on some ppl.
Also emaging what wouldve happen if this study was done with diabetics.

Hi L/C/Andy,
Is it more likely that caffeine's classic effect on the adrenals, causing the liver to naturally put glycogen (sugar storage molecule)into circulation, is the reason blood glucose "surged" after coffee? I admit to not having read the study, so this is speculation.