Wednesday, October 21, 2015

Low Grade Metabolic Acidosis May Eat Away Your Bones and Blow Up Your Belly Via Empowering Glucocorticoids!

The way we eat and live is not just obesogenic it is also acidogenic... or is the former just a consequence of the latter? 
I've written about the nasty effects of low grade metabolic acidosis which include calcium loss and brittle bones, nitrogen / protein loss and decreased protein synthesis, impaired growth hormone and IGF-1 production and more in a 2013 SuppVersity Science Round-Up (read it).

For you, as a SuppVersity veteran who's read this and related articles, it should thus not be surprising that scientists from the German Aerospace Center in Cologne were now able to establish a new, mechanistic link between the "long-term ingestion of habitually acidifying western diets may constitute an independent risk factor for bone degradation and cardiometabolic diseases" (Buehlmeier. 2015).

As Judith Buehlmeier and her colleagues point out, we have long been aware of the ill effects of low-grade metabolic acidosis (LGMA), as induced by high dietary acid load or sodium chloride (NaCl) intake and a lack of alkaline foods and nutrients in the average Western diet. What has hitherto not been fully elucidated is the underlying mechanisms, which is not as simple as the dissolving tooth in a glass of coke would suggest.
You can learn more about bicarbonate and pH-buffers at the SuppVersity

The Hazards of Acidosis

Build Bigger Legs W/ Bicarbonate

HIIT it Hard W/ NaCHO3

Creatine + BA = Perfect Match

Bicarb Buffers Creatine

Alkalosis Boosts Muscle Activity
In their latest study, the researchers from the German Aerospace Center in Cologne and their colleagues from the Universities of Bonn and Heidelberg do now present the first convincing evidence that the previously cited catabolic / anti-anabolic effects of chronic low-grade acidosis (LGMA) are triggered by interactions of the acid–base balance with the metabolism of glucocorticoids (GC). In said, study, the researchers "aimed to investigate GC activity/metabolism under alkaline supplementation and NaCl-induced LGMA" in eight young, healthy, normal-weight men who participated in two crossover designed interventional studies.
Figure 1: Correcting a diet-induced low grade metabolic acidosis with K-bicarbonate reduces the nitrogen loss of 750mg - 1000mg per day (per 60kg BW) in post- menopausal women in a prev. study (Frassetto. 1997)
  • In Study A, two 10-day high NaCl diet (32 g/d) periods were conducted, one supplemented with 90 mmol KHCO3/day.
  • In Study B, participants received a high and a low NaCl diet (31 vs. 3 g/day), each for 14 days. During low NaCl, the diet was moderately acidified by replacement of a bicarbonate-rich mineral water (consumed during high NaCl) with a non-alkalizing drinking water. 
In repeatedly collected 24-h urine samples, potentially bioactive GCs (urinary-free cortisol / free cortisone), as well as tetrahydrocortisol (THF), 5a-THF, and tetrahydrocortisone (THE), were analyzed.
Even Low Grade Acidosis Will Increase Your Diabetes Risk | learn more!
Beware! It does not take much to mess you up! A quantitative analysis of the data from the study at hand shows that even increases of dietary acid loads in the magnitude of only 30 mEq/d, which drive the renal net acid excretion into a range that is commonly seen in people on the standard Western diet (60–70 mEq/d), suffice to affect glucocorticoid activity in ways that may ruin your bone, heart and muscle health. In that, the main offenders are grains, not meats. Grains contribute an estimated 38% to the net acid load of the avg. Westerner (Sebastian. 2002).
A brief glimpse at the glucocorticoid levels in the urine of the subjects (see Figure 2) shows that with supplementation of 90 mmol KHCO3, the marker of total adrenal GC secretion dropped (p = 0.047) and potentially bioactive-free GCs were reduced (p = 0.003).
Figure 2: aily adrenal cortisol secretion as indexed by the sum of excretion rates of the 3 major urinary glucocorticoid (GC) metabolites tetrahydrocortisol, 5a-tetrahydrocortisol, and tetrahydrocortisone (THF + aTHF + THE) as well as excretions of potentially bioactive-free GCs (UFF + UFE | Buehlmeier. 2015)
This is particularly interesting if we also take into account that in Study B, the GC secretion and potentially bioactivefree GCs did not exhibit the expected fall with NaCl-reduction as net acid excretion was raised by 30 mEq/d. In conjunction study A + B do thus underline the important role of alkalizing agents like bicarbonate or potassium - irrespective of the total intake of NaCl, of which the study at hand confirms that it is part of the problem. Its ill effects, however, appear to be mediated mainly, if not exclusively, via the acidifying effects of chloride.
Bottom line: As the authors point out, their study is the first to provide convincing evidence that the ill effects of chronic low-grade metabolic acidosis are mediated via enhanced glucocorticoid activity and secretion. In that, the pro-acidic effects of NaCl, as well as the lack of alkalizing foods and nutrients in the Western diet are the main motors of dietary induced glucocorticoid elevations.

Inactivity amplifies the ill effect of glucocorticoids on muscle loss by up to 213% (Ferrando. 1999).
These elevations are - in spite of being still in the physiological range - significant enough to compromise bone quality (Bedford. 2010; Shi. 2015), cardiometabolic health & diabetes (Prodam. 2013; Qi, 2007), and protein turnover (Frassetto. 1997 | see Figure 1; Buehlmeier. 2012), and appear to be particularly unfavorable under conditions of physical inactivity (Ferrando. 1999 | see Figure on the right). Reason enough for the authors to conclude that "[a]ccordingly, higher dietary acid loads may, in the long run, constitute an independent GC-driven musculoskeletal and cardiometabolic risk factor related with western dietary habits" (Buehlmeier. 2015) | Comment!
  • Bedford, Jennifer L., and Susan I. Barr. "The relationship between 24-h urinary cortisol and bone in healthy young women." International journal of behavioral medicine 17.3 (2010): 207-215.
  • Buehlmeier, Judith, et al. "Alkaline salts to counteract bone resorption and protein wasting induced by high salt intake: results of a randomized controlled trial." The Journal of Clinical Endocrinology & Metabolism 97.12 (2012): 4789-4797.
  • Ferrando, Arny A., et al. "Inactivity Amplifies the Catabolic Response of Skeletal Muscle to Cortisol 1." The Journal Of Clinical Endocrinology & Metabolism 84.10 (1999): 3515-3521.
  • Frassetto, L., R. Curtis Morris Jr, and A. Sebastian. "Potassium bicarbonate reduces urinary nitrogen excretion in postmenopausal women." The Journal of Clinical Endocrinology & Metabolism 82.1 (1997): 254-259.
  • Qi, Dake, and Brian Rodrigues. "Glucocorticoids produce whole body insulin resistance with changes in cardiac metabolism." American Journal of Physiology-Endocrinology and Metabolism 292.3 (2007): E654-E667.
  • Prodam, Flavia, et al. "High-end normal adrenocorticotropic hormone and cortisol levels are associated with specific cardiovascular risk factors in pediatric obesity: a cross-sectional study." BMC medicine 11.1 (2013): 44.
  • Sebastian, Anthony, et al. "Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors." The American journal of clinical nutrition 76.6 (2002): 1308-1316.
  • Shi, Lijie, et al. "Higher glucocorticoid secretion in the physiological range is associated with lower bone strength at the proximal radius in healthy children: importance of protein intake adjustment." Journal of Bone and Mineral Research 30.2 (2015): 240-248.