Vitamin D deficiency was associated with several cardiovascular-related diseases, including hypertension, coronary artery disease, cardiomyopathy, and diabetes

From the American Journal of Cardiology on 3 Feb 2012.Vitamin D and CVD - AJC Feb 2012.pdf

Vitamin D Deficiency and Supplementation and Relation to Cardiovascular Health

It is very interesting in that, whilst it was an observational study, it looked not only at serum Vitamin D levels, but also at the relationship of D3 supplementation to CVD. It suggests a strong association between supplementation and reduced CVD, particularly among those who were deficient at the baseline.

See abstract and discussion below:

"Recent evidence supports an association between vitamin D deficiency and hypertension, peripheral vascular disease, diabetes mellitus, metabolic syndrome, coronary artery disease, and heart failure. The effect of vitamin D supplementation, however, has not been well studied. We examined the associations between vitamin D deficiency, vitamin D supplementation, and patient outcomes in a large cohort. Serum vitamin D measurements for 5 years and 8 months from a large academic institution were matched to patient demographic, physiologic, and disease variables. The vitamin D levels were analyzed as a continuous variable and as normal (≥30 ng/ml) or deficient (<30 ng/ml). Descriptive statistics, univariate analysis, multivariate analysis, survival analysis, and Cox proportional hazard modeling were performed. Of 10,899 patients, the mean age was 58 ± 15 years, 71% were women (n = 7,758), and the average body mass index was 30 ± 8 kg/m². The mean serum vitamin D level was 24.1 ± 13.6 ng/ml. Of the 10,899 patients, 3,294 (29.7%) were in the normal vitamin D range and 7,665 (70.3%) were deficient. Vitamin D deficiency was associated with several cardiovascular-related diseases, including hypertension, coronary artery disease, cardiomyopathy, and diabetes (all p <0.05). Vitamin D deficiency was a strong independent predictor of all-cause death (odds ratios 2.64, 95% confidence interval 1.901 to 3.662, p <0.0001) after adjusting for multiple clinical variables. Vitamin D supplementation conferred substantial survival benefit (odds ratio for death 0.39, 95% confidence interval 0.277 to 0.534, p <0.0001). In conclusion, vitamin D deficiency was associated with a significant risk of cardiovascular disease and reduced survival. Vitamin D supplementation was significantly associated with better survival, specifically in patients with documented deficiency."

Discussion

Vitamin D has important physiologic functions beyond bone and calcium metabolism. Because vitamin D receptors are involved in the expression of nearly 3,000 human genes, a deficiency could potentially affect numerous disease processes.  Cardiovascular, oncologic, and immunologic disorders have been associated with vitamin D deficiency. Our study showed an association between vitamin D deficiency and many cardiovascular disease states, including hypertension, coronary artery disease, cardiomyopathy, and cardiovascular risk factors, such as hypertension, diabetes mellitus, and hyperlipidemia.

Numerous studies and meta-analyses have suggested that vitamin D deficiency has a negative association with survival; however, the effect of vitamin D supplementation on overall mortality has not been studied. Our findings are consistent with these previous studies, suggesting poorer patient outcomes for patients with vitamin D deficiency. In addition, our data further extend these findings by demonstrating better survival with vitamin D supplementation. The benefits of vitamin D supplementation on survival were significant for those patients with a documented deficiency. This benefit was independent of the concomitant use of other cardioprotective drugs such as aspirin or statins.

These findings could have clinical implications for the usual recommended daily allowance for vitamin D. The regular intake of the recommended 400 IU/day might be adequate to avoid deficiency in many people, and supplementation of _1,000 IU/day might be required to achieve optimal levels.

When included in survival and hazard models with several disease states, vitamin D deficiency is a strong independent predictor of all-cause death. Several studies have reported on the association between obesity and low vitamin D levels, which we also observed in our study cohort. Because the prevalence of obesity is increasing in the United States, as well as in many other developed and emerging nations, vitamin D deficiency could be increasingly common in the future. In addition, our study showed an association between vitamin D deficiency and unfavorable serum lipid values.

Because vitamin D deficiency is widespread, strategies directed at population-based supplementation programs could prove beneficial. To date, however, prospective studies evaluating vitamin D supplementation are few and have not consistently shown benefit. It is possible that the lack of benefit in these studies resulted from suboptimal levels of vitamin D supplementation or other unknown factors. Many previous studies of vitamin D supplementation have used doses of 400 to 800 IU, which might not be adequate to ensure optimal serum levels, with more appropriate daily supplement doses suggested as 1,000 to 2,000 IU. Nevertheless, the growing body of observational data demonstrating relatively high rates of low vitamin D serum levels warrant additional welldesigned studies to investigate the relation between vitamin D and cardiovascular health.

Additional investigation with long-term prospective studies of various vitamin D dosage levels in both healthy and diseased populations are indicated to firmly establish the role of vitamin D supplementation on overall outcomes and mortality. Our study suggests a significant association of vitamin D supplement use and improved survival in deficient subjects, supporting the potential benefit of this intervention. Recent guidelines for the evaluation and treatment of vitamin D deficiency have been published that can help the clinician with patient treatment.

 This was a retrospective, observational study with a selected population, introducing possible selection bias. The study population was derived from patients who had had their vitamin D levels measured at a hospital laboratory and who were patients in a cardiovascular practice and included in its electronic medical records. Extrapolation to other populations might not be appropriate. Also, isolated vitamin D measurement might not reflect long-term levels. We made an arbitrary decision to use the lowest vitamin D measurement for analysis because this value was thought to most likely represent the subjects’ baseline nonsupplemented level. We were unable to accurately associate the timing of vitamin D measurement and supplement initiation. The dose and duration of vitamin D supplementation were not analyzed, and patient compliance was not measured. Inclusion of vitamin D in multivitamin supplements was not considered.

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See Am J Cardiol 2012;109:359–363

Letter to your doctor about taking statins.

If your doctor is pushing you to take a statin drug to lower your LDL Cholesterol you might consider printing out this letter and presenting it to him to point out some of the concerns about this treatment and that you would be open to his response to those concerns.
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Patient’s Details:

Dear Doctor   ____________________ 

I wish to raise the following concerns with you regarding your advice that I should lower my cholesterol with the use of statins or other medications.

Large scale studies have shown that cholesterol levels follow a normal distribution having a range of values from around 2.7 mmol/l (105 mg/dL) to 8.8 mmol/l (343 mg/dL). This same normal distribution is seen in people who do have heart disease and people who do not have heart disease [1].

I am concerned about the definition of ‘high’ cholesterol, since most adults naturally have a cholesterol level that is above the suggested target.  Furthermore, records show that cholesterol levels in industrialised countries are decreasing, not increasing [2]. What is being suggested as ‘high’ is in fact just normal in many cases. 

I am also concerned by the fact that most people who have a heart attack have an average cholesterol level, not a high cholesterol level: this has been found during studies completed on people in the UK, Australia, New Zealand and America [3]  [4]  [5].

Studies have also raised questions about so called ‘bad’ cholesterol. A study published in the American Heart Journal looked at cholesterol levels for people who have been admitted to hospital in America with coronary artery disease (CAD). The study included 136,905 people.The average LDL level for this group of people was 2.7 mmol/l (105 mg/dL) [6].Which was actually lower than the average level for the general population: the average for the general population was 3.2 mmol/l (125 mg/dL) [7].

If people with CAD have lower LDL levels than the general population, then where is the evidence that higher LDL levels cause heart disease?

The conclusion of a BBC Radio 4 program in the UK was that 99% of people who take statins for primary prevention do not benefit from them. This was admitted by the UK governments chief advisor on heart disease (Professor Boyle) [8].

Any benefit associated with statins is routinely shown as a relative percentage reduction and this is misleading for patients. To illustrate this point we could look at the Lipid Lowering Arm of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT-LLA) [9].

Within the group of people who were given the statin, 1.9% of them had a heart attack or died of heart disease, versus 3% of people in the placebo group. The statin reduced the risk by just 1.1%. Unfortunately the authors of the report described the results as a 36% relative risk reduction.

There is evidence that high cholesterol in elderly people is associated with a longer life. This was the conclusion of a study completed by a team of researchers at Yale University School of Medicine [10]. Researchers in the Netherlands also found that in the case of the elderly, life expectancy increases when cholesterol levels are higher. Those with higher cholesterol levels appeared to be better protected from cancer and infection [11].

I am also concerned that adverse effects from statins have been under-reported. The procedures used during clinical trials, such as the run-in period, may mean that the trial participants are not representative of the general population.

‘Stopped Our Statins’ is a forum for people who have experienced significant adverse effects from the use of statins. The most commonly reported adverse effects on this forum include:

Gout, Numbness / Tingling of the Hands/Feet, Muscle ~ Weakness, Cramps, Spasm, Stiffness, Insomnia, Loss of Libido, Impotence, Heart Palpitations, Heart Arrhythmias, Depression, Short Term Memory Loss, Long Term Memory Loss, Transient Global Amnesia, Neck and Shoulder Pain, Fatigue, Migraine, Headaches, Chest Pain, Digestive Disorders, Trouble Walking (Shuffling), Trouble Walking (Balance), Hand Tremors, Speech - Trouble finding the right word, Slurred Speech, Dizziness, Sciatica Pain.

Although this data is not part of a clinical trial it does provide testament to the wide range of adverse effects experienced in the real world with real people.  

Before I make the decision whether or not to lower my cholesterol through medication, I would be very grateful if you could provide a response to the points raised above.

Thank you very much for your consideration.

Yours sincerely,

 References:

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[1] Smith, J 2009 $29 Billion Reasons to Lie about Cholesterol: Making Profit by Turning Healthy   People into Patients Troubador Publishing, Leicester

[2] Blood Cholesterol Chapter 10 of the British Heart Foundation Coronary Heart Disease Statistics. July 2007

[3] Durrington, P Dyslipidaemia Lancet 2003; 362:717-731

[4] Tonkin, AM et al. Effects of Pravastatin in 3260 Patients with Unstable Angina: Results from the LIPID Study Lancet 2000; 355:1871-1875

[5] Rubins, HB et al. Distribution of Lipids in 8,500 Men with Coronary Artery Disease American Journal of Cardiology 1995; 75:1202-1205

[6] Sachdeva, A et al Lipid Levels in Patients Hospitalized with Coronary Artery Disease: An analysis of 136,905 Hospitalizations in Get with the Guidelines American Heart Journal 2009; 157:111-117

[7] Carroll, MD et al Trends in Serum Lipids and Lipoproteins of Adults, 1960-2002 Journal of the American Medical Association 2005; 294:1773-1781

[8] BBC Radio 4 Program “The Investigator” April 3, 2008 20:00hrs GMT

[9] Sever, PS et al. Prevention of Coronary and Stroke Events with Atorvastatin in Hypertensive Patients who have Average or Lower-Than-Average Cholesterol Concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial—Lipid Lowering Arm (ASCOT-LLA): A Multicentre Randomised Controlled Trial Lancet 2003; 361:1149-1158

[10] Krumholz, H et al. “Lack of Association Between Cholesterol and Coronary Heart Disease Mortality and Morbidity and All-Cause Mortality in Persons Older Than 70 Years” Journal of the American Medical Association 1994; 272:1335-1340

[11] Weverling-Rijnsburger, AW et al. “Total Cholesterol and Risk of Mortality in the Oldest Old” Lancet 1997; 350:1119-1123

Coronary-Artery Calcium (CAC) imaging

CAC screening improves CAD risk factors without increasing downstream costs: EISNER

March 24, 2011 |                                 Michael O'Riordan

Los Angeles, CA - New data from the Early Identification of Subclinical Atherosclerosis by Noninvasive Imaging Research (EISNER) study show that noninvasive imaging may actually lead to clinically meaningful improvements in coronary artery disease (CAD) risk factors in healthy individuals. Compared with individuals who did not undergo coronary-artery calcium (CAC) imaging, screening of subclinical atherosclerosis with CAC screening led to an improvement in systolic blood pressure, LDL-cholesterol levels, and a reduction in waist circumference as well as a trend toward greater weight loss among overweight individuals.

The improvements occurred without a significant increase in downstream medical costs, suggesting that CAC screening can play a "gatekeeper" role in determining a need for further noninvasive testing, say investigators.

"We wanted to find out how much impact the scan had on the way that patients take care of themselves, the way they think about changing their lifestyle and doing something about preventing heart disease," senior investigator Dr Daniel Berman (Cedars Sinai Medical Center, Los Angeles, CA) told heartwire. "There have been other studies suggesting an impact on how patients behave after seeing their scan, that as the amount of calcium on the scan went up, patients began to do more about changing their behavior. We noticed the same thing: patients who had a lot of calcium were more likely to do all the things that would prevent heart disease than patients who had less amounts of calcium. Also, the calcium-scoring group did more to change their lifestyle than the patients who did not undergo coronary scanning."

Published online March 23, 2011 in the Journal of the American College of Cardiology with first author Dr Alan Rozanski (St Luke's Roosevelt Hospital, New York), the study included 2137 healthy volunteers randomized to undergo CAC scanning or no coronary-calcium screening. Individuals in the trial were middle-aged and had CAD risk factors but did not have a history of cardiovascular disease.

Change in blood pressure and LDL cholesterol

Of the seven measured risk factors, investigators observed improvements in systolic blood pressure, LDL cholesterol, and a reduction in waist circumference among those who underwent CAC screening.  There was no difference in serum glucose levels, exercise levels, or smoking status between the two treatment arms at four years. CAD risk, as assessed by the Framingham Risk Score (FRS), increased in the no-scan volunteers but remained stable among those who received the CAC scan.

Individuals with higher amounts of calcium were patients who made the larger amount of change.

"Individuals with higher amounts of calcium were patients who made the larger amount of change," said Berman.

The incurred medical costs did not significantly differ between the two treatment arms, with procedure and medication costs totaling $3649 among those who did not undergo CAC screening and $4063 among those who did. The total incurred costs did differ by the amount of coronary calcium observed on the scan, however, with patients having a CAC score >400 significantly more likely to incur more procedural and medication costs than those with less coronary calcium. 

"Overall, in the scanned group vs the no-scan group, the downstream testing costs were similar," Berman told heartwire. "Interestingly, when you look at patients without any coronary calcium, their downstream testing costs were low. Patients who had a lot of calcium, it would be more common for them to go on to additional testing."

Change in clinical risk factors and all incurred medical costs

Parameter	No CAC scan	CAC scan	p
Systolic blood pressure (mm Hg)
Baseline	130	131	0.03
Change from baseline	-5	-7	0.02
LDL cholesterol (mg/dL)
Baseline	130	133	0.15
Change from baseline	-11	-17	0.04
Waist circumference (in)
Baseline	41.0	41.3	0.19
Change from baseline	1	0	0.01
All costs ($)	3649	4063	0.09

Incurred costs according to CAC score

Medical costs	CAC score 0	CAC score 1-99	CAC score 100-399	CAC score >400	p (trend)
All costs ($)	2623	4394	4900	9309	<0.001

Overall, there was no significant difference in the number of performed procedures among patients who underwent CAC screening. There was a trend toward more lipid-lowering medications being prescribed among those randomized to CAC screening and a significant difference in the number of new blood-pressure-lowering medications prescribed.

In a comparison between volunteers with no observable calcification on the CAC scan with those who did not undergo CAC screening, those with a CAC score of zero were significantly less likely to undergo any stress testing at four years as well as less likely to undergo cardiac catheterization and coronary revascularization. The low-CAC-score patients also incurred significantly less medical costs ($2623 among those with a CAC score of zero vs $3649 for those who did not undergo screening; p<0.001).

The results of the EISNER analysis contrast with the results of a meta-analysis published online March 14, 2011 in the Archives of Internal Medicine. As reported by heartwire, Dr Daniel G Hackam (University of Western Ontario, London) and colleagues assessed seven relevant studies and found no significant changes in the use of drug therapies, exercise, dietary therapy, smoking cessation, or diagnostic coronary catheterization or revascularization based on the results of carotid ultrasound, CAC scans, or other noninvasive imaging techniques.

To heartwire, Berman said that the EISNER data provide support for the recent American College of Cardiology Foundation (ACCF)/American Heart Association (AHA) class IIa recommendation for the use of computed tomography (CT) to measure coronary calcium. According to the ACCF/AHA, the use of CAC "is reasonable for cardiovascular risk assessment in asymptomatic adults at intermediate risk (10% to 20% 10-year risk)."

Berman has research grants from Siemens and GE/Amersham and has both research grants from and is on the speaker's bureau of Astelles and Lantheus.

« Previous heartwire article
Sensitive troponin assay associated with improved MI outcomes
Mar 24, 2011 11:45 EDTNext heartwire article »
Risk for MI doubles after TIA
Mar 25, 2011 12:00 EDT

Sources

1. Rozanski A, Gransar H, Shaw LJ, et al. Impact of coronary artery calcium scanning on coronary risk factors and downstream testing. J Am Coll Cardiol 2011; DOI:10.1016/j.jacc.2011.01.019. Available at: http://content.onlinejacc.org.
2. Hackam DG, Shojania KG, Spence JD, et al. Influence of noninvasive cardiovascular imaging in primary prevention: Systematic review and meta-analysis of randomized trials. Arch Intern Med 2011; DOI:10.1001/archinternmed.2011.69. Available at: http://archinte.ama-assn.org.

The harm of low-fat high-carbohydrate diets in cholesterol uptake in the brain.

JustMEinT has a good article on cholesterol, while mostly not referring to it in relation to heart disease, it non-the-less deals with the importance of cholesterol in our bodies and especially the brain. Following is an exerpt.

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Much research is also being uncovered now on the advantages of high HDL cholesterol levels, besides the study we mentioned above in direct relation to Alzheimer’s. A study appearing in the American Journal of Cardiology earlier this month (February 2011) showed that the higher men’s HDL cholesterol levels, the longer they lived and the more likely it was that they would reach the age of 85.4 A diet with adequate amounts of saturated fat is essential to keeping HDL high cholesterol levels. Those with deficiencies and suffering from neurological disorders need to consider a diet that is high in saturated fat, in stark contrast to the mainstream dietary advice for low-fat diets that might be causing many of these late-in-life diseases.
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I find it terribly sad, and at times seriously frustrating that Doctors are still pushing the Fat is Bad philosophy - theory - rubbish! As I have said before on this blog, Ancel Keys has much to answer for.
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Read the full article here
 
Other links in the article.
Health Impact News Daily
Coconut Oil
Dr. Mary Newport