Can you make a cake without sodium? Yes. First off, you DON'T need to add salt to make the cake rise. Many people think that yeast breads and quick breads/cakes won't rise if there's no salt. This is not true. The yeast in bread feeds off of sugar, not salt; salt just speeds it up a little. You can leave salt out of homemade bread willy-nilly. To me, it still tastes fine, but if you are going to be serving bread to people who aren't used to low-sodium cooking, you can do the following: Add a pinch (a spot about the size of the head of a nail) of regular salt to the bread, which is so much less than the recipes call for that the mgs of sodium will still be well under five mg per slice, and 2 pinches of potassium salt (such as NuSalt). You don't want to add more potassium salt for two reasons: (1) it tastes off to people who aren't used to it, and (2) normal people don't need that much potassium and it could even be problematic for them. So don't just substitute a teaspoon of NuSalt for a teaspoon of regular salt. You can also throw in a pinch of powdered ginger, along with your pinches of salt; the bread will not taste like ginger specifically, but it will taste a little less bland.
Back to cakes. Cakes don't use yeast; they use baking powder or baking soda to rise. Baking soda is sodium bicarbonate; baking powder is a mixture of baking soda, cream of tartar, and corn starch - still mostly baking soda, though. However, this is true mainly only in North America. In Europe, it is a lot more common to use baking powder made with calcium rather than with sodium. Calcium has many of the same properties as sodium - the three elements potassium, sodium, and calcium, are near each other on the table of chemical elements and all do similar things. This is why you'll see substitutes for salt involving potassium, and substitutes for baking powder involving potassium OR sodium. As I mentioned above, the substitutes involving potassium have to be used carefully, so that normal people don't get too much potassium; calcium doesn't cause that kind of concern. Most Americans don't get ENOUGH calcium in our diets, and may even benefit from the substitution of calcium-based baking powder instead of sodium-based.
The calcium baking powder most easily available in the USA is Rumford; it uses calcium phosphate instead of sodium bicarbonate. In my opinion, it's also an excellent baking powder; you are not going to lose anything in your baking by switching over to it. It does as good or better a job in cakes as regular baking powder. If your local supermarket doesn't carry Rumford, you can
order it here. (Incidentally, according to their web site, Rumford also makes a cornbread mix that uses the calcium baking powder and is completely wheat-free as well.)
Another brand of sodium-free baking powder is Featherweight; it's available from Healthy Heart Market, whose link is to the right of this post. It is made of a mixture of monocalcium phosphate, potato starch, potassium bicarbonate. The potato starch gives it a very slightly different texture from corn starch, and in my opinion it does not rise as well as Rumford; you need to use a little bit more of it. If a recipe calls for a teaspoon of baking powder, try using between one-and-a-quarter teaspoons and one-and-a-half.
And now for something completely different:
A few recent articles about heart failure; I've provided links, but in case you aren't a MedScape member, I've copied the abstracts as well, so you can get the gist of the articles.
The Role of Candesartan in the Treatment of Chronic Heart Failurehttp://www.medscape.com/viewarticle/502413?src=mp
Hugh F. Mcintyre
From British Journal of Cardiology
AbstractThe renin-angiotensin system (RAS) plays a fundamental role in cardiovascular pathophysiology. In particular, angiotensin II (AII) has been identified as a culprit in endothelial and vascular damage, elevated blood pressure, and cardiac failure. Pharmacological inhibition of this system is available through two mechanisms; the reduction of AII formation by inhibition of angiotensin-converting enzyme (ACE), and by direct blockade of the type 1 angiotensin II receptor by angiotensin II receptor blockers (ARBs).
Angiotensin-converting enzyme (ACE) inhibitors have a proven role in the management of elevated blood pressure and diabetes and may confer specific vascular benefit. In patients with chronic heart failure (CHF) secondary to left ventricular systolic dysfunction (LVSD), there is extensive evidence that, when compared to placebo, ACE inhibitors reduce morbidity and mortality. Randomised placebo controlled trials have also shown ACE inhibitors reduce all-cause mortality and major cardiovascular events after myocardial infarction.
Given the unequivocal benefit of ACE inhibitors, initial studies with ARBs in patients with LV dysfunction (in CHF and following myocardial infarction) have focused on two areas: the role of ARBs when compared with ACE inhibitors, and when combined with ACE inhibitors.
Only recently, with the results of the CHARM study, have the role of ARBs when compared to placebo in a population with CHF been clarified. This study also addressed the benefit of ARBs in patients with heart failure and preserved LV systolic function.
BNP Levels May Help Guide Carvedilol Therapy for Heart Failurehttp://www.medscape.com/viewarticle/503627?src=mp
BY Megan Rauscher
NEW YORK (Reuters Health) Apr 20 - Carvedilol therapy is associated with a sustained decline in brain natriuretic peptide (BNP) levels in patients with congestive heart failure (CHF), research shows. This suggests, according to the investigators, that "serial BNP levels can provide some guidance" regarding the odds of carvedilol-driven improvement left ventricular function.
"Beta-blocker therapy improves symptoms, left ventricular ejection fraction, and survival in patients with CHF, but chronic effects on neurohormones have not been extensively investigated," Dr. Robert P. Frantz, from the Mayo Clinic in Rochester, Minnesota and colleagues explain in the March issue of the American Heart Journal.
They examined the relationship between clinical and echocardiographic parameters and serial neurohormones in 55 patients with CHF, most of whom had nonischemic dilated cardiomyopathy, treated with carvedilol over the course of 1 year. Forty-six patients completed 12 months of follow-up.
"We found that carvedilol therapy is usually associated with a decline in plasma BNP peptide levels," Dr. Frantz told Reuters Health. "The extent of change in BNP levels correlates with extent of change in left ventricular ejection fraction."
Specifically, at 12 months, left ventricular ejection fraction improved from 26% at baseline to 39%, and NYHA class improved from 2.3 to 1.8. BNP levels fell from 453 to 208 pg/mL at 6 months. Compared with baseline, levels remained significantly lower (233 pg/mL) at 12 months (p = 0.01).
"The relationship between changes in BNP levels and ejection fraction suggests that serial measurements of BNP may be a useful guide in monitoring patients with CHF who are being treated with carvedilol, but the relationship is not sufficiently strong to obviate the role for measurement of ejection fraction," Dr. Frantz said.
"If elevated BNP levels do not decline in a patient who is being treated chronically with carvedilol, it suggests that this patient may not have had improvement in ejection fraction and should be evaluated carefully," he added.
Am Heart J 2005;149:541-547.
FDA Approvals: Hyzaar, Panzem, Decapinolhttp://www.medscape.com/viewarticle/503708?src=mp
Yael Waknine
April 21, 2005 — The U.S. Food and Drug Administration (FDA) has approved a new indication for losartan potassium plus hydrochlorothiazide tablets, allowing their use to reduce the risk of stroke in patients with hypertension and left ventricular hypertrophy; an orphan drug indication for 2-methoxyestradiol capsules, allowing their use for the treatment of ovarian cancer; and an oral rinse with a barrier mechanism of action for the reduction of gingivitis in patients aged 12 years and older.
Losartan Plus Hydrochlorothiazide (Hyzaar) for Stroke Risk Reduction in Hypertensive Patients With LVHOn April 5, the FDA approved a new indication for losartan potassium plus hydrochlorothiazide (HCTZ) tablets (Hyzaar, made by Merck & Co.), allowing its use to reduce the risk of stroke in patients with hypertension (HTN) and left ventricular hypertrophy (LVH). There is evidence, however, that this benefit does not apply to black patients.
The indication was approved in March 2003 for losartan tablets (Cozaar, made by Merck & Co.), the angiotensin II receptor blocker component of the combination product.
Approval of the indication was based on the results of the landmark Losartan Intervention for Endpoint Reduction (LIFE) study in 9,193 patients, showing that a losartan-based regimen reduced the risk of fatal and nonfatal stroke by 25% in patients with HTN and LVH compared with atenolol-based therapy for a median follow-up period of 4.8 years (total number of strokes, 232 vs 309; P = .001).
Both regimens achieved similar reductions in blood pressure and no significant differences were observed between groups with respect to risk of myocardial infarction or cardiovascular death.
The extension of this indication to the losartan-HCTZ combination tablet was based on the frequency of HCTZ coadministration with the study drug to achieve target blood pressure in both groups of the LIFE trial (losartan, 73.9%; atenolol, 72.4%). In addition, the company demonstrated that the losartan and HCTZ tablets used in the trial were bioequivalent with the combination drug.
The FDA notes that in the LIFE trial black patients with HTN and LVH receiving losartan had a higher risk of stroke compared with those receiving atenolol. This finding has not been confirmed thus far because of the difficulty of interpreting subset differences in large clinical trials. However, trial data do not support use of losartan for the reduction of cardiovascular risk in hypertensive black patients with LVH.
Losartan potassium plus HCTZ fixed-dose combination tablets were previously approved for the treatment of HTN. Their use for initial therapy is only warranted in patients with severe HTN in whom the necessity of achieving prompt control of blood pressure outweighs the associated risks
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