High Protein Diet Safe for Bones! Acid Load due to Meat Protein does not Compromise Calcium Metabolism.

Reading the caption of this post, some of you may rightly ask themselves: "Why does he even mention this? Of course, meat is safe - meat is natural and eating meat is what man is made for!" So, if you already knew all that, you can stop reading now. If, however, you still belong to the misguided brotherhood of the followers of the holy food pyramid with your "healthy" grains, pasta and cereals at the bottom, you may be interested in the results from an older scientific paper I just came across while posting an answer to a forum post of someone who was concerned that his bones will become brittle if he increases his protein intake beyond the 0.8g/kg body weight barrier.

In November 2010, Cao & Nilsen (Cao. 2010) published a review which analyzed the outcome of studies that investigated the effect of the purported renal acid load resulting from a high protein intake (above the current Recommended Dietary Allowance of 0.8 g protein/kg body weight) on increased urinary calcium excretion. With reference to more recent findings they write:

Neither whole body calcium balance is, nor are bone status indicators, negatively affected by the increased acid load. Contrary to the supposed detrimental effect of protein, the majority of epidemiological studies have shown that long-term high-protein intake increases bone mineral density and reduces bone fracture incidence. The beneficial effects of protein such as increasing intestinal calcium absorption and circulating IGF-I whereas lowering serum parathyroid hormone sufficiently offset any negative effects of the acid load of protein on bone health.

By the way, I am already looking forward to the huge steaks I am going to have for lunch, today ;-)

Reactive Oxygen Specimen (ROS) Trigger Muscle Hypertrophy via IGF-1 Signaling

I have touched on the "usefulness" of oxidation, only yesterday. Now, a very recent study appears to confirm the notion that a controlled amount of inflammation is necessary in order to achieve metabolic and muscular adaptations.

Figure 1: Eesult of the quantitative analysis of myotube diameter after IGF-I and NAC treatment (Handayaningsih. 2011)

Scientists from Division of Diabetes and Endocrinology and Division of Cellular and Molecular Medicine at the Kobe University Graduate School of Medicine published a paper (Handayaningsih. 2011) describing an investigation into the role of Reactive Oxygen Specimen (ROS) in the IGF1-signaling pathway. In this study N-Acetyl-Cystein (NAC), commonly used by recreational athletes as an "ergogenic" aid, blunted myocyte response to IGF1 and thus inhibited muscle hypertophy (cf. Figure 1):

While treatment with H2O2 significantly enhanced IGF-I-induced phosphorylation of the IGF-I receptor (IGF-IR), IGF-IR phosphorylation was markedly attenuated when cells were treated with antioxidants. The downstream signaling pathway, Akt-mTOR-p70S6K was subsequently down-regulated. Furthermore, thephosphorylationof FoxO1by IGF-I decreased concomitantly with the restoration of the expression of its target genes, Atrogin-1 and muscle RING finger 1, which are related to muscle atrophy.

Before you now go and flush all your vitamins and antioxidants down the toilette, you should consider that this is an in-vitro study with a narrow and limited ROS stimulation and not a large scale exercise supplementation study showing that the 500-1.000 mg of NAC you take on a daily basis will completely forestall muscle growth. If anything, it should remind you that excessive "inflammation" could be the "root of all evil" (cf. Super Human Radio), but excessive antioxidant supplementation certainly ain't a solution.