Tuesday, November 30, 2010

Vit D panel ignores experts

The report got a stern rebuke from some well-known vitamin D researchers, who see the increases as woefully inadequate. “This was a big waste of money,” says Hollis. “I agree with their recommendations for the first year of life,” he says, citing the panel's target of 400 IU for infants, a doubling from the previous recommendation. But he was puzzled that this recommendation didn’t extend to the children’s mothers. Despite outweighing infants by ten times or more, he says, women — and men — saw their vitamin D recommended daily intake set at only 600 IU for ages 9 to 70. People over 70 should get 800 IU a day, the panel said.
The IOM [Institute of Medicine] panel consisted of 14 scientists who met eight times and reviewed the relevant literature. Hollis openly questioned the composition of the panel. “Anybody who had ever expressed an opinion [on vitamin D] was not allowed anywhere near this committee,” he says.

Thursday, November 18, 2010

March 2010 study finds proper potassium levels important to cardiovascular health (Rev A - see notes)

In the course of trying to find an inexpensive way to obtain adequate dietary potassium, I ran across 2500 mg potassium supplement per day improves heart function. Not only did it convince me that obtaining sufficient potassium is crucial, but it also provided information on a good and inexpensive form of potassium (potassium bicarbonte) to use as a supplement. I've tried potassium chloride, and I found that it's quite unpalatable unless taken with orange juice. I soon realized that the amount of orange juice required would cost an exhorbitant amount.

The following is from the aforementioned article (a summary of the medical study to which it refers):

Left Ventricular Mass And Function Predictors Of Cardiovascular Disease And Death

Left Ventricular Mass And Left Ventricular Function Are Predictors Of Cardiovascular Morbidity And Mortality

The authors of the study also noted that:

“Both [left ventricular] mass and function are important independent predictors of cardiovascular morbidity and mortality.”

Potassium Supplement Prevents Increase in Left Ventricular Mass And Impaired Left Ventricular Function

Potassium Deficiency Increases Left Ventricular Mass And Impairs Left Ventricular Function. This Is Prevented With A Potassium Supplement

“Experimental studies in dogs, mice, and human healthy volunteers showed that hypokalemia induced [left ventricular] hypertrophy and impaired [left ventricular] function.”

“Correction of hypokalemia by potassium supplementation prevented these adverse effects.”

Most populations only get 2300-2700 mg of potassium per day vs Recommended 4700 mg per day

Most populations only get 2300-2700 mg of potassium per day. US Institute of Medicine Recommends 4700 mg per day.

“[T]he adequate intake for adults recommended by the US Institute of Medicine (120 mmol/d) [4700 mg per day].”

“The current potassium intake in most populations is 60 to 70 mmol/d [2300-2700 mg per day].”

Potassium Benefits Cardiovascular System

Increasing Potassium Has Beneficial Effects On Cardiovascular System

“These results indicate that an increase in potassium intake has beneficial effects on the cardiovascular system and bone health.”

Potassium Increases Nitric Oxide

Potassium Preserves Endothelial Function by Increasing Nitric Oxide

“An increase in potassium intake has been shown to augment endothelium-dependent relaxation and preserve endothelial function through increased endothelial [ nitric oxide ] production in salt-loaded, Dahl salt-sensitive rats.”

[ A small study also found increased plasma and urinary nitric oxide in salt-sensitive people given potassium for one-week, they also note. ]

Potassium Supplement Beneficial Even In Those On Low-Salt, High-Potassium Intake

Additional Potassium Improved Endothelial Function Even in these People with a Relatively Low-Salt, High-Potassium Intake

“Our findings are of considerable interest in that the effect of potassium on endothelial function was found in individuals on a relatively low-salt and high-potassium intake.”

Potassium Supplement Protects Against Vascular Damage

Additional Potassium Protected Against Vascular Damage Induced by Salt-Loading in Salt-Sensitive Rats

“Studies in Dahl salt-sensitive rats demonstrated that potassium supplementation enhanced aortic compliance and protected against the development of vascular damage induced by salt loading, possibly through suppression of salt-induced oxidative stress.”

Blood Pressure Did Not Change

Blood Pressure Did Not Change During This One-Month Study

Interestingly, they found that office blood pressure did NOT change during the one-month study.

After one-month, blood pressure was:

142/90—Potassium Chloride
144/90—Potassium Bicarbonate

In other words, all of these benefits occurred WITHOUT a change in blood pressure.

Professor Richard Moore, MD, PhD talks about this in his book “The High Blood Pressure Solution”.

He says that people assume the problem with high blood pressure is the mechanical pressure on the blood vessels, but this is not necessarily the problem.

He notes that, in most cases, elevated blood pressure simply indicates an imbalance inside cells—too little potassium and too much sodium.

You probably already know this, but he notes that the amount of potassium + sodium inside cells is constant. So if you too much sodium and not enough potassium, it creates this imbalance inside cells.

Suggested Source of Potassium Bicarbonate

One of the best sources of potassium bicarbonate that I've found is PureBulk. Theirs is pharmaceutical grade, and although it costs a little more than food grade, I'd rather pay a little extra up front than to take chances on a lower grade, especially considering the unusual amounts I intend to use.

Considering the cardiovascular benefits that researchers have discovered by supplementing 2500 mg of potassium daily, which is far in excess of "conventional wisdom" on potassium supplementation, I'm beginning to wonder if the medical establishment has deliberately imposed potassium deficiency on mankind, knowing that few people will get enough from their diet. If so, it wouldn't be the only widespread nutritional deficiency they've tried to create.

I haven't seen any advice on how to take such large doses, but it seems to me that it would be best to split it up into a few doses spaced throughout the day, to avoid causing an electrolyte imbalance. But that's just a layman's hunch.


Rev A - Added information on source for potassium bicarbonate

Sunday, November 07, 2010

Another suppressed cardiovascular treatment?

In the course of trying to decide whether pomegranate is worth its cost, I realized that pomegranate's main benefit to the cardiovascular system is its ability to protect an important chemical compound known as nitric oxide, so that it has a better chance of doing something useful before it is destroyed by oxidation. The discovery of nitric oxide and its functions earned Louis J. Ignarro, PhD, the 1998 Nobel prize in medicine. Shortly after this discovery was announced, there was an explosion of research into nitric oxide, and approximately 7000 papers were published on the subject within a year. (Yet I had to stumble onto the subject a decade later in the course of studying the benefits of pomegranate, and I suspect that the lack of publicity on this subject is deliberate. I even found apparent disinformation about NO in a 2007 article still posted on the Life Extension Foundation website. There is no excuse for its false implications to be left hanging on a supposedly authoritative website. The relevant passage is copied below.) Searching under Dr. Ignarro's name, I found his website and his 2008 article entitled Nobel Prize Winner’s Breakthrough – Prevent Heart Attack and Stroke with Nitric Oxide, which provide guidance on boosting nitric oxide levels. I found another good introduction to the importance of nitric oxide on Dr. Mercola's site. It plugs Dr. Mercola's nitric oxide-boosting formula, but I couldn't find how much of the critical ingredient (arginine) it contains. As of this writing, Doctor's Best appears to offer the most cost-effective arginine supplement. Dr. Ignarro strongly recommends using citrulline to enhance the absorption of arginine.

NO, which has a fleeting existence on the order of seconds, is critical to cardiovascular function, and the NO which is used by the cardiovascular system is produced by an enzyme known as "endothelial nitric oxide synthase" (eNOS) in the inner layer (the endothelium) of the arteries. This enzyme converts arginine into NO. Dr. Ignarro recommends taking L-citrulline along with arginine in order to facilitate its cellular uptake.

Without intervention, NO production declines with "biological age"

Due to wear and tear on the cardiovascular system, a substance known as ADMA, which resembles arginine, is produced by the body and ends up competing with arginine for uptake by eNOS. The result is a deficiency of NO, which has several seriously detrimental effects, potentially leading to a death spiral. By supplementing arginine in sufficient quantities, it is supposedly possible to swamp out the ADMA, restore NO production, and undo the damage caused by NO deficiency. [I haven't seen any indications that suppressing ADMA is a feasible solution.]

One of my sources for this information was The Real Reason Why Health Canada Banned Arginine posted to an alternative medicine website. The basic contention of the article, which is actually a scientific paper, is that boosting arginine sufficiently will overcome a substance known as ADMA (which increases with wear and tear on the cardiovascular system, and which because of its similarity to arginine is often taken up by eNOS, thus effectively blocking a significant portion of NO production). Arginine supplementation increases the ratio of arginine to ADMA, and consequently NO production increases up to a point which I assume approximates youthful levels, or at least sufficient levels. Once sufficient NO levels are restored, the arterial health improves. There is little risk of a toxic dose of arginine, so, to answer the question implied by the title, it seems that arginine was banned in Canada to deprive Canadians of sufficient nitric oxide. I've copied the more relevant portions of the paper below and translated some of the medical terminology:

(Altern Med Rev 2005;10(1):14-23)

[Title:] L-arginine improves vascular function by overcoming the deleterious effects of ADMA, a novel cardiovascular risk factor
Alternative Medicine Review, March, 2005 by Rainer H. Boger, Eyal S. Ron

[Rainer H. Boger, MD Professor and Head, Clinical Pharmacology Unit Institute of Experimental and Clinical Pharmacology and Toxicology Center of Experimental Medicine University Hospital Hamburg-Eppendorf Martinistr. 52 D-20246 Hamburg Germany; Eyal S Ron, Ph.D.: see http://www.madash.com/.]

The endothelium [inner layer of arteries] plays a crucial role in the maintenance of vascular tone and structure. One endothelium-derived vasoactive mediator with major importance is nitric oxide (NO), which is formed from the amino acid precursor L-arginine by the enzyme endothelial nitric oxide synthase (eNOS). NO is involved in a wide variety of regulatory mechanisms of the cardiovascular system, including vascular tone (it is the major mediator of endothelium-dependent vasodilation), vascular structure (inhibition of smooth muscle cell proliferation), and cell-cell interactions in blood vessels (inhibition of platelet adhesion and aggregation; inhibition of monocyte adhesion).

Dysfunction of the endothelial L-arginine/ nitric oxide pathway is a common mechanism by which several cardiovascular risk factors mediate certain deleterious effects on the vascular wall. [Low nitric oxide allows arteries to be damaged by the following.] Among these are hypercholesterolemia, hypertension, smoking, diabetes mellitus, homocysteine, and vascular inflammation.
Circulating L-arginine concentrations have been found to be within the normal range in most clinical conditions associated with endothelial dysfunction. Few patients experience pathologically low L-arginine concentrations. However, clinical and experimental evidence suggests elevation of ADMA can cause a relative L-arginine deficiency, even in the presence of "normal" L-arginine levels (which may, in fact, be too low in these conditions). AS ADMA IS A COMPETITIVE INHIBITOR OF eNOS, ITS INHIBITORY ACTION CAN BE OVERCOME BY INCREASING THE CONCENTRATION OF THE ENZYME'S SUBSTRATE, L-ARGININE (Figure 2). The studies cited above indicate ADMA levels may be increased in conditions associated with cardiovascular diseases. Elevated ADMA concentration is one possible explanation for endothelial dysfunction and decreased NO production in these diseases. [emphasis added]
Beneficial Effects of Supplemental Sustained-release L-Arginine

From the above-mentioned studies of L-arginine, it appears an effective method of improving endothelial function would be to supplement with L-arginine. Oral L-arginine, however, is absorbed and metabolized quickly; the half-life of L-arginine in human circulating plasma is less than one hour. (66) A controlled-release formulation of L-arginine would increase the length of time in which L-arginine achieves an effective concentration.


In a preliminary study of five patients with coronary artery disease in whose myocardial perfusion [blood-flow to the heart muscle] had been maximized and stabilized on conventional cardiovascular medications, 3 g sustained-release L-arginine was given twice daily for 12 weeks. Significant improvements in heart function and myocardial perfusion were seen via PET imaging. (68)


ADMA is an endogenous and competitive inhibitor of NO synthase. [ADMA occurs naturally in the body and competes with arginine for uptake by nitric oxide synthase, the "factory" which produces nitric oxide.] Plasma levels of this inhibitor [ADMA] are elevated in patients with atherosclerosis and in those with risk factors for atherosclerosis. (34,36) In these patients, plasma ADMA levels are correlated with the severity of endothelial dysfunction and atherosclerosis. By inhibiting the production of NO, ADMA can impair blood flow, accelerate atherogenesis [the development of atherosclerosis], and interfere with angiogenesis [the growth of new capillary blood vessels].

Supplemental L-arginine improves endothelial function, myocardial perfusion [blood-flow to the heart muscle], angina, erectile dysfunction, and exercise tolerance, regardless of ADMA status. However, many patients exhibiting one of these impairments demonstrate elevated blood ADMA. Therefore, testing for plasma ADMA levels may give the physician a better idea of those patients who may respond best to prolonged L-arginine supplementation, as data are accumulating to show that patients with elevated ADMA are the most likely to benefit. The ratio of L-arginine to ADMA is considered to be the most accurate measure of eNOS substrate availability. This ratio will increase during L-arginine supplementation, regardless of initial ADMA concentration. Due to the pharmacokinetics of oral L-arginine and the positive results from preliminary studies, it appears supplementation with a sustained-release L-arginine preparation will achieve positive therapeutic results at lower dosing levels. [end of excerpts from paper by Boger & Ron]

Life Extension Foundation article implies that ADMA limits NO production

As I indicated above, I don't think it's an accident that this information has not received wider publicity. There is an enormous amount of money to be made in treating people with cardiovascular disease. I found a prime example of the apparent suppression of this information on the Life Extension Foundation's website, which I previously considered to be a trustworthy source of information on nutritional supplements. This erroneous and potentially deliberately false information is contained in the following passage from The Intimate Link Between Erectile Dysfunction and Heart Disease:

Disruption in Nitric Oxide Synthesis

The body’s source for nitric oxide production is the amino acid L-arginine, which is naturally found in many foods. The average American ingests about 3,000–5,000 mg of L-arginine per day, as it is an amino acid naturally contained in many foods. Meats of all varieties, nuts, and dairy products are rich in L-arginine, so the body is accustomed to intake levels of several thousand milligrams every day.

A deficiency of L-arginine, however, does not generally disrupt nitric oxide synthesis because L-arginine availability is not the rate-limiting step in this process. [Actually, a deficiency of arginine RELATIVE to rising ADMA levels is the culprit, so this is a half-truth.] In fact, research over the past five years has identified an endogenous (occurs in the body naturally) inhibitor called “asymmetric dimethylarginine” or ADMA, an amino acid which blocks the production of nitric oxide. By acting as an L-arginine mimic, this damaging look-alike effectively elbows out L-arginine and pushes it off to the side in the biochemical pathway leading to the synthesis of nitric oxide. ADMA is relatively elevated in patients with hypertension, high levels of cholesterol, triglycerides, homocysteine and low-density lipoprotein (LDL), and low levels of high-density lipoprotein (HDL), as well as with aging itself. This inhibitor of nitric oxide synthesis may very well be the common factor shared by all of these abnormal conditions. Increased levels of this detrimental inhibitor (ADMA) block nitric oxide production, leading to endothelial dysfunction.

[Note that the article "neglects" to mention that sufficient arginine can swamp out the ADMA and restore nitric oxide production, perhaps because doing so would make several of LEF's pricey supplements obsolete.]