Higher vitamin D levels lower mortality
Vitamin D may lower dementia risk
Exercise, obesity, and atrial fibrillation risk
Vitamin E lowers hip fracture risk
Niacin and lipoproteins
A new study examined the relationship between vitamin D levels in serum and overall mortality, cardiovascular disease, respiratory disease, cancers, and fractures. This was a 13-year, prospective, population study of 14,641 men and women aged 42-82 years in the Norfolk region of the United Kingdom. The study started in 1997 and continued until 2012. The participants were categorized into 5 groups (quintiles) of vitamin D levels as 25-hydroxy vitamin D3 (25(OH)D). The groups were less than 12 ng/ml (nanograms per milliliter), 12 to 20, 20 to 28, 28 to 36, and 36 or higher.
They found that higher vitamin D levels were associated with a significant trend to lower overall mortality from all causes compared to the lowest quintile. The second lowest had a 16 percent lower mortality risk, while the highest quintile had a mortality reduction of 34 percent. After adjusting for a number of variables, they calculated that for each 8 ng/ml increase in 25(OH)D overall mortality declined by 8 percent, for heart disease the decline was 4 percent, respiratory diseases 11 percent, and for fractures11 percent. They found no relationship for cancers. (Khaw KT, et al., Serum 25-hydroxyvitamin D, mortality, and incident cardiovascular disease, respiratory disease, cancers, and fractures: a 13-y prospective population study. Am J Clin Nutr. 2014 Nov;100(5):1361-70.)
They found that the greatest reduction in mortality was in participants with vitamin D levels above 36 ng/ml. They found no evidence that high levels were in any way related to an increase in mortality, although less than 1 percent of their subjects had levels above 48 ng/ml. Deficiency levels of vitamin D are considered to be less than 30 ng/ml, according to the Vitamin D Council and optimal levels range from 30 to 100 ng/ml, depending on the source of the advice. Toxic levels are over 150 ng/ml.
I have always used 40 to 80 ng/ml as the ideal range, so 36 ng/ml seems to be a low target. The Vitamin D Council recommends 40-80 as a sufficient range. It is valuable to have blood testing done to find out your vitamin D, level and then taking enough as a supplement to raise it to the ideal range of at least 50 ng/ml. It is difficult to get adequate vitamin D from diet and sunlight alone, especially as you age or if you live in northern latitudes. Always take the natural vitamin D3, rather than the synthetic vitamin D2.
Be careful in evaluating vitamin D levels in studies compared to your blood test results to be sure the units you are using are the same as in the research. Serum nanograms per milliliter (ng/ml) are different from nanomoles/Liter (nmol/L). As an example, 10 ng/ml is equal to 25 nmol/L. Many of the studies report in nmol/L. Also, be sure you are getting the 25(OH)D3 test, not the 1,25(OH)2D test.
Another new study on vitamin D shows that it may lower the risk of dementia and Alzheimer’s disease. In this study of 1658 elderly, ambulatory patients who were free of dementia, cardiovascular disease, and stroke at the start, the participants were followed for an average of 5.6 years. During that time, 171 participants developed all-cause dementia, of which 102 cases were Alzheimer’s disease. (Littlejohns TJ, et al., Vitamin D and the risk of dementia and Alzheimer’s disease. Neurology 2014 Sep 2;83(10):920-8.)
In the group considered to be severely deficient, with vitamin D levels below 10 ng/ml, the risk of dementia from all causes was 2.25 times higher than in those with levels above 20 ng/ml. Those with levels from 10 to 20 ng/ml had a 53 percent higher risk than those with levels above 20 ng/ml. For Alzheimer’s dementia, the risk of the illness was 2.22 times higher for those in the deficient range (less than 10 ng/ml). For those in the 10 to 20 ng/ml range the risk was 69 percent higher than for those above 20ng/ml.
It is clear from these and many other studies that vitamin D plays a role far beyond bone health. My recommendations are as stated in the last article: keep levels in the range recommended by the Vitamin D Council. They recommend supplements of 5000 IU per day to achieve this, but this is quite variable, and your needs might be higher or lower.
Atrial fibrillation (AF, or Afib) is the most common cardiac arrhythmia. The left atrium, the heart chamber adjacent to the left ventricle, normally initiates the heartbeat through some if its specialized electrical fibers. From various causes, it quivers instead of beating, leaving the ventricle to “pick up the slack” and initiate its own beat. This beat is irregular and often very fast, and the entire heart function is not as efficient as it normally is because of a lack of complete coordination of the contraction. Symptoms can be palpitations, fatigue, and shortness of breath, or there may be none at all. AF may come and go for various lengths of time (minutes to days), which is called paroxysmal AF. It may also become permanent, or it may be persistent, if it can be reversed with an electrical shock or medication.
During AF, blood can accumulate in the non-beating atrial chamber leading to clots. These can sometimes dislodge, sending clots to the brain (a stroke) or abdominal organs. For this reason, people in persistent AF (longer than a week and with other risk factors) usually are prescribed an anti-clotting drug (Coumadin, also called warfarin). It is true that this is the active ingredient in some rat poisons, but in the right dose it does reduce risk of clot-related stroke in AF patients (while slightly increasing the risk of bleeding, bruising, or a stroke from bleeding). Newer drugs also inhibit clotting, but they are much more expensive and they do not have the many years of usage that Coumadin does. Also, Coumadin works by inhibiting the action of vitamin K in blood clotting, and taking vitamin K is an antidote to excessive bleeding. The newer drugs do not have antidotes.
Obesity is an independent risk factor for the development of AF. In the Women’s Health Initiative, 93,676 post-menopausal women were followed for an average of 11.5 years. They were analyzed using hospitalization records and diagnostic codes from Medicare claims for the interaction between obesity and physical activity and the association of this interaction with the incidence of AF. Some subjects were excluded because they already had AF, did not have complete data, or were underweight. Of the remaining 81,317 women, the average age was 63.4 years, and they included 7.8 percent African Americans, and 3.6 percent Hispanics. Of this entire group, 9792 developed AF.
An increased level of body mass index (BMI) and a decreased level of physical activity were independently associated with an increased risk of AF. Among the obese subjects, higher levels of physical activity reduced the AF risk associated with their weight. (Azarbal F, et al., Obesity, physical activity, and their interaction in incident atrial fibrillation in postmenopausal women. J Am Heart Assoc. 2014 Aug 20;3(4).) A half hour brisk walk per day or some bicycling is enough to see benefits. Each level of increase of physical activity conferred greater protection against AF in the obese participants, although those who were less overweight also received some benefit. Of some concern, prior to this and other studies, was that exercise might initiate AF, but this shows the opposite.
It is no secret that exercise is one of the most valuable lifestyle changes for prevention of chronic diseases. Walking, bicycling, running, dancing, gardening, and housework can all count toward the weekly total activity. The greater the amount of exercise that you do the greater the benefit, but you do not have to be a marathoner or serious athlete to protect yourself. Exercise helps reduce other risk factors, such as inflammation, insulin resistance, high blood pressure, blood lipid disorders, and endothelial dysfunction. These benefits are independent of weight loss, but they are often associated with it.
Vitamin E from diet and supplements has been shown to have many benefits for easing symptoms or prevention of chronic diseases, including heart related mortality, intermittent claudication (pain in the legs when walking due to hardening of the arteries), rheumatoid arthritis, Parkinson’s disease, and Alzheimer’s disease. A new study shows that it can also lower the risk of hip fractures. Researchers evaluated 21,774 men and women aged 65-79 years. They followed them for up to 11 years. They took baseline serum vitamin E levels (alpha-tocopherol) in 1168 participants who later suffered hip fractures and compared them to the levels of 1434 random subjects who did not.
In this Norwegian study, the serum vitamin E levels ranged from 22.6 to 38.3 micromoles per liter (μmol/L), and the level showed an inverse relationship to fracture risk. Those subjects in the lowest quartile of serum vitamin E had a 51 percent higher risk of hip fracture compared to those in the highest quartile. (Holvik K, et al., Low serum concentrations of alpha-tocopherol are associated with increased risk of hip fracture. A NOREPOS study. Osteoporos Int. 2014 Nov;25(11):2545-54.) Vitamin E is a potent antioxidant that protects cell membranes and blood lipids from free-radical damage. Oxidative stress may contribute to osteoporosis and fractures, which is one reason that vitamin E may help.
It is almost impossible have the highest serum levels of vitamin E without taking supplements. The best food sources include sunflower seeds, almonds, hazelnuts, peanut butter, spinach, and broccoli. The alpha-tocopherol used in this study is only one form of the vitamin, and the others, beta, gamma, and delta, may be just as important, or even more so for the full range of its benefits. I recommend 400 to 800 IU per day of a mixed tocopherol that is high in gamma-tocopherol. A few years ago, a study that suggested vitamin E was associated with increased mortality was inaccurately analyzed and poorly reported, and cannot be relied upon.
For neurological diseases, I suggest higher doses. Some studies have used 3200 IU per day (along with 3000 mg of vitamin C) for the treatment of Parkinson’s disease and found that the supplements delayed the need for medication by 2.5 years. For Alzheimer’s disease, researchers gave 2000 IU of vitamin E or medication (selegiline) or both and looked at outcomes of death, institutionalization, loss of functions, or severe dementia. They found that the vitamin E by itself did better than either selegiline alone or in combination with vitamin E, delaying the outcomes by almost two years.
Lipoprotein (a), pronounced “lipoprotein little a” (or written as Lp(a)), is a serum lipid that is an independent risk factor for cardiovascular disease. The level in the blood is mostly determined by genetics, but it can be influenced by estrogens, niacin (vitamin B3), and some more complicated and expensive or experimental treatments. Lp(a) is not affected by lifestyle or statin drugs (but lifestyle choices of diet and exercise do influence cardiovascular risk). (Bos S, et al., Latest developments in the treatment of lipoprotein (a). Curr Opin Lipidol. 2014 Oct 14. [Epub ahead of print])
Studies since 1955 have shown that niacin lowers serum cholesterol and raises HDL-cholesterol levels, thus modifying the risk of cardiovascular disease.
Back in 1986, the Coronary Drug Project reported that niacin lowered heart attack rates better than drugs in a study of 8341 men lasting for 6 years. At 15 years of follow-up, 9 years after the study ended, it was shown that the niacin group had an 11 percent lower mortality than the placebo group. (Canner PL, et al., Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin. J Am Coll Cardiol. 1986 Dec;8(6):1245-55.)
In a recent review of niacin treatment in diabetics, it was shown to raise HDL by 27 percent, lower LDL by 25 percent, and lower triglycerides by 39 percent. (Ding Y, et al., Effect of niacin on lipids and glucose in patients with type 2 diabetes: A meta-analysis of randomized, controlled clinical trials. Clin Nutr 2014 Sep 28. pii: S0261-5614(14)00247-7. doi: 10.1016/j.clnu.2014.09.019. [Epub ahead of print].)
Another recent study showed that niacin therapy led to a significant reduction in dense LDL and IDL (intermediate density lipoprotein) and that this was associated with a significant reduction in heart attacks. (Zambon A, et al., Effects of niacin combination therapy with statin or bile acid resin on lipoproteins and cardiovascular disease. Am J Cardiol. 2014 May 1;113(9):1494-8.)
Niacin commonly causes a flush of the skin for about 20 to 40 minutes as a result of a sudden histamine release. This is not harmful, but it may be uncomfortable. Timed release niacin usually causes less of a flush, and regular use of niacin leads to tolerance, so the flushing happens less frequently or not at all. The “non-flush” form of niacin (inositol hexaniacinate) was thought to be effective for lipid lowering without the flush, but this turned out not to work well in humans (although it does have most of the other vitamin benefits of niacin).
I take 500 mg of timed-release niacin twice per day just for preventive medicine, and I often recommend this or higher amounts for its mental health benefits. The usual amount recommended for lipid effects is 2000 to 3000 mg per day. You can start with a lower dose and build it up over time, but you may still experience the flush until you are taking it regularly.