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Time to move beyond salt ?

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Salt studies: the latest score

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Salt hypothesis' story

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Salt war

Do bone drugs work?

Diabetes vs. drugs, 3:0?

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The MMR vaccine war: Wakefield vs. ?

Wakefield proceedings: an exception?

Who's afraid of a littl' 1998 study?

January 2010

Antibiotic children

Physical activity benefits late-life health

Healthier life for New Year's resolution


December 2009

Autism epidemic worsening: CDC report

Rosuvastatin indication broadened

High-protein diet effects


November 2009

Folic acid cancer risk

Folic acid studies: message in a bottle?

Sweet, short life on a sugary diet


October 2009

Smoking health hazards: no dose-response

C. difficile warning

Asthma risk and waist size in women


September 2009

Antioxidants' melanoma risk: 4-fold or none?

Murky waters of vitamin D status

Is vitamin D deficiency hurting you?


August 2009

Pill-crushing children

New gut test for children and adults

Unhealthy habits - whistling past the graveyard?


July 2009

Asthma solution - between two opposites that don't attract

Light wave therapy - how does it actually work?

Hodgkin's lymphoma in children: better alternatives


June 2009

Hodgkin's, kids, and the abuse of power

Efficacy and safety of the conventional treatment for Hodgkin's:
behind the hype

Long-term mortality and morbidity after conventional treatments for pediatric Hodgkin's


May 2009

Late health effects of the toxicity of the conventional treatment for Hodgkin's

Daniel's true 5-year chances with the conventional treatment for Hodgkin's

Daniel Hauser Hodgkin's case: child protection or medical oppression?

April 2009

Protection from EMF: you're on your own

EMF pollution battle: same old...

EMF health threat and the politics of status quo

March 2009

Electromagnetic danger? No such thing, in our view...

EMF safety standards: are they safe?

Power-frequency field exposure

February 2009

Electricity and health

Electromagnetic spectrum: health connection

Is power pollution making you sick?

January 2009

Pneumococcal vaccine for adults useless?

DHA in brain development study - why not boys?

HRT shrinks brains


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December 2009

 High-protein diet effects

If you are living in the U.S. - or most any Western country - your protein intake is likely to be between elevated and high. Health wise, any dietary excess is undesirable, and proteins are no exception. But what are, exactly, high-protein diet effects on health? How serious is the downside, and isn't there something good coming from it, at least in part compensating for its negative effects?

High-protein diet changes metabolism in a number of ways and, according to a recent German study, rather quickly. Twenty four healthy young men have been put on regular (1.2g/kg/day) and high-protein diet (2.4g/kg/day) for seven days. The 7th day, the high-protein group already had altered renal function (13% higher glomerular filtration rate and 22% higher fractional filtration), as well as

significantly higher levels of blood urea nitrogen, serum uric acid, glucagon, natriuresis, urinary albumin, and urea excretion

(Frank et al, Effect of short-term high-protein compared with normal-protein diets on renal hemodynamics and associated variables in healthy young men, December 2009).

What does this mean?

Frankly, none of it is good. Elevated blood urea nitrogen means that there is more nitrogen-containing urea in the blood, indicating that kidneys could be filtering the blood less efficiently.

Elevated serum uric acid increases the risk of kidney stones and gout, and has been positively linked with insulin resistance (i.e. lowered cellular sensitivity to insulin).

Glucagon is a pancreas hormone acting opposite to insulin, i.e. rising blood glucose levels by stimulating the liver to burn its short-term energy stock, glycogen, into glucose. Elevated glucagon level indicates that the body is running short of glucose; after glycogen storages are used up, it will have to switch to burning more fats (primarily) and proteins, resulting in elevated level of ketone bodies (acetone, acetoacetate and beta-hydroxybutyrate).

This metabolic mode - so called ketosis - is considered sub-optimal and potentially unhealthy, putting more stress on the liver, and likely contributing to cardiovascular disease (if you can smell acetone in your breath, it means that your dominant metabolic mode is ketosis, producing excess acetone that is being released from blood through the lungs).

Elevated natriuresis means that more sodium is lost through urine. Since sodium pulls water out with it, the result is lower blood volume, i.e. thicker, more viscous blood - one of major factors contributing to development of cardiovascular disease.

You don't want elevated albumin (water-soluble tissue protein) neither. Normally, its molecules are too large to pass through the kidney's glomerular membrane; having more of it in the blood indicates that the integrity of this membrane is compromised.

Finally, elevated urea excretion means simply that you are loosing fluids at a higher rate; that increases the risk of dehydration, as well as the loss of minerals, which are less efficiently reabsorbed by the kidneys at a higher urine output rate.

All this is hardly news. An assessment of somewhat spotty evidence (Metges and Barth, Metabolic Consequences of a High Dietary-Protein Intake in Adulthood: Assessment of the Available Evidence, 2000) lists similar findings  with respect to the effects of high-protein diet from a number of studies:

increased insulin secretion @ 1.6 times the recommended protein intake (RPI)of 0.75g/kg/day (Remer et al, 1996)

increased renal acid excretion @ 1.7RPI (Remer and Manz, 1994)

elevated oxalate/glycolite excretion @ 2.4RPI (Holmes et al, 1993)

increased calcium excretion @ 2.4RPI (Trilok and Draper, 1989)

decreased insulin sensitivity and increased hepatic (liver) glucose excretion @ 2.5RPI

increased bone resorption (breakdown) and glomular filtration rate @ 2.8RPI (Kerstetter et al, 1999)

suppressed plasma glutamine @ 2.9RPI (Matthews and Campbell, 1992)

increased risk of microalbuminuria (elevated blood albumin) with as little as 0.1g/kg higher protein intake over the population average (Hoogeween et al, 1998)

38% higher risk of diabetes with 0.5g/kg increase in protein intake (Wolever et al, 1997)

1.9 times higher risk ratio of renal cell cancer in the group with highest protein intake (4th quartile, Chow et al,1994)

13.5 times higher risk of prostate cancer in the highest intake group (3rd tertile, Vlajinac et al, 1997)

High-protein intake produces mild acidosis (Frassetto et al, 1998), which tends to decrease protein synthesis, while increasing protein breakdown, possibly resulting in negative nitrogen balance (i.e. loss of body protein). This is, at least in part, caused by lower glutamine levels, which also may be compromising the immune function (Newsholme and Calder 1997, Hack et al. 1997, Yaqoob and Calder 1997).

Studies frequently link high-protein diets with obesity; such findings are complementary to indications that amino acids are more significant energy source (the most important source of gluconeogenesis, Jungas et al. 1992, Reeds et al. 1998) than what is assumed at present. Hence, higher level of amino acids would elevate cellular glucose level, stimulating synthesis of body fat. 

And what about the benefits of high-protein intake, like increase in body lean tissue, and muscle strength? Well, study results do not support that perception. Shifting to high-protein diet for 1 month did not affect neither strength nor muscle mass in daily weight training (Lemon et al, 1992), nor did it affect muscle tissue response to resistance training in elderly men and women (Welle and Thornton, 1998).

However, one notorious negative effect of high-protein diets - increase in the rate of urinary calcium loss - may not be as significant as it was thought to be, at least for relatively large segment of population. Some recent studies indicate that the increase in calcium excretion due to high-protein intake could be nearly offset - or rather caused - by the increase in rate of calcium absorption (Kerstetter et al 2003, Heaney and Layman 2008). According to Kerstetter, it is still difficult to tell whether or not - and to what extent - some of the additional calcium loss is depleting the bones.

A study on postmenopausal woman, in which only those with a particular form of vitamin D receptor's gene (Fok I) polymorphism had increased urinary marker for bone resorption, as a response to high-protein intake, indicates that the subject of protein intake related calcium loss is more - possibly much more - complex than the level of intake alone (Harrington et al, 2003). Not surprisingly,

individual genotype and biochemistry

are likely to be significant factor in the final outcome.

So, at best, you wouldn't need to worry that high-protein diet is endangering your calcium status. The rest of negative effects - not so lucky. This, however, doesn't mean that you should abruptly cut down your protein intake. Studies also indicate that body's protein needs are lowered by training and/or higher caloric intake, while increased by habitual higher protein intake (Millward et al, 1994). The latter is rather well established, and consistent with the general body response to the intake level, i.e. increased absorption/utilization rate at lower intake level, and lowered absorption/utilization at higher intake levels.

In other words, a quick reduction in longer-term high-protein intake

could leave your body in short supply of proteins,

even if your intake level is formally still adequate. That could inflict serious stress to body functions. Any significant change in habitual intake level should be commenced gradually - and proteins are no exception.