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There are more than 90,000 vitamin and dietary supplement products sold in the US. They come in pills, powders, drinks, and bars. And they all anticipate some better versions of ourselves—selves with sturdier bones, slimmer waist lines, heftier muscles, happier intestines, better sex lives, and more potent noggins. They foretell of diseases dodged and aging outrun.

On the whole, we believe them. Supplements are a $30 billion industry in the US. Recent surveys suggest that 52 percent of Americans take at least one supplement—and 10 percent take four or more. But should we? Are we healthier, smarter, stronger, or in any way better off because of these daily doses?

The answer is likely no. Most supplements have little to no data to suggest that they’re effective, let alone safe. They’re often backed by tenuous studies in rodents and petri dishes or tiny batches of people. And the industry is rife with hype and wishful thinking—even the evidence for multivitamins isn’t solid. There are also outright deadly scams. What’s more, the industry operates with virtually no oversight.

The Food and Drug Administration is not authorized to review supplements for safety and efficacy before they hit the market. That means the bottles and capsules that line the aisles of grocery stores, pharmacies, and specialty shops may not contain what they say they do. They may have wildly variable amounts of supplements in each batch. They may have hidden, illicit components like amphetamines. They may even have harmful contaminants such as lead and cadmium.

And even after these potentially dangerous drugs hit the market, the FDA lacks the capacity to keep up with all the products and health claims in order to flush out bad actors. It’s hard to blame them. Doctors, too, have trouble keeping up with the 90,000 plus products.

To help out, two experts at Harvard have put together a quick guide of effective supplements recently. Preventative medicine experts JoAnn Manson and Shari Bassuk lay out which ones are actually effective and when. It’s a relatively short list. Here's what they and other experts recommend, along with a quick crash course for navigating the world of supplements.

Healthy adults don't need a multivitamin.
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If you're over 50 or on certain medications you may need more vitamin B12.
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Vitamin D supplements are recommended for breastfed babies.
Caltrate, a calcium and Vitamin D dietary supplement, may help reduce the risk of fractures in people over 65.
Women who are pregnant or trying to conceive should take folic acid.
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Omega 3 fatty acids are said to help with ADHD and autism, but there's not enough data to back that up.
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Supplements for muscle building, weight loss, and sexual performance are the most risky.
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First, the pair emphasizes: the best way to get vitamins and minerals is through food in a healthy diet. Eaten in food, micronutrients are often better absorbed into the body and present in optimal ratios. That’s in contrast to gulping a hunk of concentrated compounds in a pill.

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Time for primary review 27 days.

This review concentrates on the function, molecular determinants and pharmacology of ion channels that reside in the sarcolemma and that contribute to the distinct phases of the altered transmembrane action potentials of myocytes surviving in the infarcted heart. The discussion will be divided into two general categories. First, substrate findings will be discussed and linked to the time course of arrhythmias as they are known to occur in experimental myocardial infarction models. This section will be followed by a discussion of the ion channel changes in myocytes remote from the infarct area, that is, in areas of regional hypertrophy. Finally, what is known about the molecular determinants of ion channels of myocytes from these diseased hearts is presented.

Various arrhythmic phases occur after the onset of experimentally produced myocardial ischemia and infarction in animal hearts. Current hypotheses maintain that the mechanisms of some of these cardiac arrhythmias can be understood in terms of the alterations in cellular electrical activity in specific regions of the heart post myocardial infarction (MI) (see [1] ). For example, in hearts of large animals, acute coronary artery occlusion results in rapid ventricular arrhythmias (ventricular tachycardias and fibrillation) (acute phase). It is unlikely that chronic or persistent changes in ion channel function underlie these acute arrhythmias. Over the following 24–48 h (subacute phase of infarction) post occlusion, delayed spontaneous arrhythmias of ventricular origin (subendocardial Purkinje) occur in experimental models and may have counterparts in humans [2–4] . During the healing (days, weeks) or healed (months) infarct phase, sustained ventricular tachycardias are inducible in both animal and human hearts suggesting that the reentrant substrate is present. The site of origin of the ventricular arrhythmias in these hearts depends on the location of the surviving cells overlying the infarcted region. In one canine model, these reentrant arrhythmias have been mapped to an area described as the epicardial border zone [1] .

Numerous studies have described the specific changes in action potential (AP) configuration that occur in the canine subendocardial Purkinje fiber and the subepicardial ventricular fiber postcoronary artery occlusion. Generally, by 24–48 h after total coronary artery occlusion the APs of the subendocardial Purkinje fibers show reduced resting potentials and maximal action potential upstroke velocity (V̇ max ), as well as an increase in total time of repolarization. On the other hand, the cells of the epicardial border zone of the canine infarction model show a reduction in V̇ max , and a shortening and triangularization of the action potential by 5 days after total artery occlusion. By 14 days post occlusion further shortening of the AP occurs. Then by the time of the healed infarct (2 months), AP voltage profiles have returned to nearly normal [5] suggesting the presence of a process that might be termed ‘reverse remodeling’ ( Fig. 1 ). In addition, changes in conduction of the impulse at various times after coronary artery occlusion as well as the altered refractoriness of the tissue in the infarcted myocardium have been documented. Electrical changes at the level of the myocyte and the role they play in providing the substrate for inducible reentrant arrhythmias have been reviewed [1] .

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