Showing posts with label Sarcopenia. Show all posts
Showing posts with label Sarcopenia. Show all posts

Tuesday, November 10, 2009

'Roid Rage: Vitamin D3 -- DO IT (Part II)

Vitamin D and Athletes

Vitamin D is not just a sun-derived vitamin, but is a crucial steroid precursor that is transformed into one of the most potent hormones in the human body for strength, power, lung function and regulating gene expression in every organ system.

Athletes need Vitamin D.

Dr. Cannell has written quite extensively about the role of vitamin D in athletes.

See prior post: 'Roid Rage Vitamin D3 -- DO IT (Part I)



Don't miss Dr. T's recent post: Vitamin D Summary of Actions. SUPERB!




Vitamin D: Flu, Asthma, Bronchitis, H1N1 Protection

Swine Flu H1N1.

Worried? Don't be.

Baby wanna be a millionaire? Vitamin D3... just do it. Baby by me, 50 cents YO.


Many factors can predispose an individual to be immunocompromised and more susceptible to the flu or H1N1 or bronchitis:
--sleep deprivation
--mental stress
--excessive physical training
--fatigue
--hypothyroidism, adrenal fatigue
--VITAMIN D INSUFFICIENCY
--VITAMIN D DEFICIENCY
--poor, unbalanced gut biofilms (read Dr. Ayers Cooling Inflammation)
--gluten/wheat, lectins, omega6 and associated inflammation
--nutritional deficiencies
--et cetera


Vitamin D stores may be depleted under all the circumstances above.

For the past season, naturally, I've been a total ding dong, frequently skipping my vitamin D supplement and sunlight. Yeah missed a boatload of doses. (*haaa* Yeah, I am THE vitamin-D-fairy-godmother and I hand it out like candy... wtf I s*ck) So... Three weeks ago my asthma came back full force and within days I was in the middle of a bronchitis/coughing attack again with a fever for 2 days. Last episode was EONS ago. Couldn't shake it but after a boost of vitamin D via a modified Stoss protocol (20,000 to 50,000 IU for 3 days) that Dr. Cannell frequently discusses for prophylaxis or acute treatment of influenzae or other viral infections, my coughing and infection were completely gone. My cough was almost gone OVERNIGHT. On the other hand, Dr. Cannell talks about much higher doses. Since I was not deficient, just 'insufficient', I used a lower dose.

The bronchitis was entirely aborted, shortened to a few days not a few MONTHS or a few WEEKS like the normal course of chronic bronchial inflammation I had experienced annually in the past. I ran 13.1 miles a week later and was fine (though my power and pace s*cked). My ghetto batgrrrl picture wasn't so bad though *wink*. Vitamin D does a body better. My skin, hair, muscles, recovery, breathing and body fat are all far better now that I'm back on the program.

Prior post: Stoss protocol Vitamin D3 Nature's Antibiotic

Vitamin D deficiency and chronic lung disease. Gilbert CR, Arum SM, Smith CM. Can Respir J. 2009 May-Jun;16(3):75-80.

Vitamin D and respiratory health. Hughes DA, Norton R. Clin Exp Immunol. 2009 Oct;158(1):20-5. Review.




Vitamin D Associated with Fitness, Power, Strength and Lower Body Fat

Two research articles highlight the relationship between higher vitamin D levels and athletic performance. The first showed a positive relationship between higher VO2 max and higher blood vitamin D (p<0.05) in n=59 adolescent and young females. Incidentally, lower body fat (p<0.05) was associated with higher vitamin D levels.

The second study reviewed baseline vitamin D concentrations (which were LOW low low) in 99 female athletes age 12-14 yo and found "Jumping mechanography to measure muscle power, velocity, jump height, and Esslinger Fitness Index from a two-legged counter movement jump and force from multiple one-legged hops was performed. Body height, weight, and serum concentrations of 25(OH)D, PTH, and calcium were measured. RESULTS: Median serum 25(OH)D concentration was 21.3 nmol/liter (range 2.5-88.5 [median 8 ng/ml with range 1-35.4 ng/ml]) and PTH 3.7 pmol/liter (range 0.47-26.2). After correction for weight using a quadratic function, there was a positive relationship between 25(OH)D and jump velocity (P = 0.002), jump height (P = 0.005), POWER (P = 0.003), Esslinger Fitness Index (P = 0.003), and force (P = 0.05). There was a negative effect of PTH upon jump velocity (P = 0.04). CONCLUSION: From these data we conclude that vitamin D was significantly associated with muscle power and force in adolescent girls."


Girl Power!

Association among cardiorespiratory fitness, body fat, and bone marker measurements in healthy young females.
Mowry DA, Costello MM, Heelan KA. Mowry DA, Costello MM, Heelan KA. J Am Osteopath Assoc. 2009 Oct;109(10):534-9.

Vitamin D status and muscle function in post-menarchal adolescent girls.
Ward KA, et al. J Clin Endocrinol Metab. 2009 Feb;94(2):559-63.




Vitamin D Alters Gene Expression

Many components of our diet are in fact potent modulators of genetic expression. Vitamin D is among many. In a variety of clinical trials, vitamin D lowers CRP (inflammation), increases testosterone (I've seen it and HH reports his anecdotal experience here), thyroid hormone, and (in rats) raises estrogen. Is this helpful for athletes? There are many mechanisms by which vitamin D exerts benefits for athletes including improved breathing, lung function, oxygenation, immunity protection, muscle strength, endurance, muscle power and hormone optimization (e.g. the big 'T').

Micronutrients and amino acids, main regulators of physiological processes. Verheesen RH, Schweitzer CM. Med Hypotheses. 2009 Oct;73(4):498-502.

Human physiology is supposed to be a complex interaction of regulating processes, in which hormones, genes, their proteins and apoptosis are thought to play a dominant role. We hypothesize that regulation of physiological processes is mainly influenced by amino acids and micronutrients with hormones, proteins, apoptosis and gene modifications being their derivatives. Furthermore, we suppose that the cells power plant, the mitochondrion, is in fact an intracellular bacterium, living in absolute symbiosis. Because of its intracellular existence it depends on the host's micronutrients completely. Within the host these micronutrients regulate their own formation, degradation, uptake and excretion. Known deficiencies, such as iodine and vitamin D, affect billions of people. Many micronutrients neither have been investigated, nor have they been studied in relation to each other and solid data are not available. Optimal levels of many micronutrients and all amino acids are not known.

Amino acids, vitamins and minerals are capable of altering gene expression, inducing apoptosis and regulating chemical processes. It makes them highly attractive for creating better health, against low cost, as we have already proven in the case of rickets, cretinism and scurvy in severe deficiencies. By creating optimal living conditions and study mitochondria from a symbiotic point of view we suppose that diseases not only can be prevented, but the course of diseases can be altered as well.





Ask Your MD for A Blood Test

Tracking of blood vitamin D levels (known as [25(OH)D]) is necessary to make sure you have the optimal range, not too high and not too low. Other labs to track are calcium and magnesium (and PTH if you have plaque or chronic kidney disease). Supplementation with either over-the-counter Vitamin D3 or prescription ergocalciferol (which is inferior and should be avoided) is contraindicated if you have a condition called sarcoidosis or isolated hypercalcemia (high calcium).

With dose initiation or increases, the blood levels take about 4-6 wks to stabilize. Consider requesting a blood test to confirm the value (either self-directed ZRT at heartscanblog or the vitaminDcouncil.org).

Dr. Harris MD discusses the accuracy of the vitamin D tests available on the market. Don't be blinded by his scorching hot brilliance or body. Paleo nutrition blog: HERE and HERE.

Dr. Cannell MD advises goal serum vitamin D [25(OH)D] 60 to 80 ng/ml (or 150-200 nmol/L). Personally my breathing and hormones appear to me the most optimal at 70s ng/ml. The past year I checked the [25(OH)D] twice and it was not more than 60. Incidentally, I did not feel so 'right on' as compared to when I had levels in the 70s. Everyone perhaps owns a 'set point' and you might need to figure what that is for yourself depending on your athletic performance, pulmonary function, immunity, mood and other metrics.

Hopefully your doc will not ignore the healing power of diet and certain nutritional supplements like vitamin D. (bwt don't bring the below article in -- the suggested doses are pathetically low baby doses).





Low Vitamin D = Low Strength

Low serum Vitamin D concentrations are independently associated with SARCOPENIA decreased muscle strength:

Thursday, May 29, 2008

Sarcopenia: 'Poverty of the Flesh' (Greek)

Sarcopenia is a clinical term referring to the loss of muscle mass, strength and function. Starting in our 30s - 40's we begin to lose lean skeletal muscle mass at an average rate of 5% annually. The value of skeletal muscle mass for heart protection cannot be underestimated. Muscle mass, movement, and many dietary components maintain a low inflammatory status in our bodies via the PPAR-Delta receptor and other critical mechanisms. Decline of mass may be age-related but more and more, dysfunction is a sign of the times -- as a society we engage in less and less physical/intense activities, eat more and more excessive nutrient-poor foods, and are prodigiously sedentary for extended periods of time with 'time-saving' devices. (We lost our TV remote control recently (we don't even watch much TV) and boy we've been a bit more active...) Figure 1. Identical twins of different body size and composition due to different training regimes (endurance running vs. field, including dynamic intense and resistance training. Rennie MJ. Body maintenance and repair: how food and exercise keep the musculoskeletal system in good shape. Exp Physiol. 2005 Jul;90(4):427-36. (the G. L. Brown Prize Lecture)



Movement appears more crucial for certain insulin-resistant individuals (including myself) due to our genes. Movement does not need be structured or scripted activity. All physical movement in essence is effective. This includes housekeeping, car washing, hunting/gathering... (even s..e..x..) counts. And movement appears to defy physics. The more movement engaged... and the more intense... the less effort later. (???!) Is that like life? The more we love 'n give... the more we l-i-v-e?





Variations in PPARD determine the change in body composition during lifestyle intervention: a whole-body magnetic resonance study. Thamer C, et al. J Clin Endocrinol Metab. 2008 Apr;93(4):1497-500.



CONTEXT: We recently demonstrated that single-nucleotide polymorphisms (SNPs) in the peroxisome proliferator-activated receptor-delta gene (PPARD), i.e. rs1053049, rs6902123, and rs2267668, affect the improvement of mitochondrial function, aerobic physical fitness, and insulin sensitivity by lifestyle intervention (LI).

OBJECTIVE: The objective of the study was to determine whether the aforementioned PPARD SNPs influence the change in body composition and ectopic fat storage during LI.

DESIGN: A total of 156 subjects at an increased risk for type 2 diabetes were genotyped for rs1053049, rs6902123, and rs2267668 and participated in a LI program. Body fat depots, ectopic liver fat, and muscle volume of the leg were quantified using magnetic resonance spectroscopy and imaging.

RESULTS: With regard to body composition, carriers of the minor SNP alleles displayed reduced responses to LI, i.e. LI-induced reduction in adipose tissue mass (nonvisceral adipose tissue: rs1053049, P = 0.02; rs2267668, P = 0.04; visceral adipose tissue: rs1053049, P = 0.01) and hepatic lipids (rs1053049, P = 0.04; rs6902123, P = 0.001; independent of changes in adiposity) as well as LI-induced increase in relative muscle volume of the leg (rs1053049, P = 0.003; rs2267668, P = 0.009) were less pronounced in homo- and heterozygous carriers of the minor alleles as compared with homozygous carriers of the major alleles.

CONCLUSION: SNPs rs1053049, rs6902123, and rs2267668 in PPARD affect LI-induced changes in overall adiposity, hepatic fat storage, and relative muscle mass. Our findings provide a mechanistic explanation for the involvement of these genetic variations in the development of insulin resistance and type 2 diabetes. PMID: 18252792





All the PPAR receptors have similar ligands -- endogenous and exogenous fatty acids (short-chain, medium-chain, long-chain, MUFA, PUFA, SFA, etc) and eicosanoids (steroidal products from the prostaglandin cascade, including COX derivatives). They truly are pivotal controllers when all lifestyle and nutritional factors are optimized. Although such a wide-range of substances can bind and activate these receptors, Amino Acids (via the mTOR pathway) appear to be one the most potent stimulators of PPAR. Amino Acid sufficiency can determine and maximize all the functions of PPAR-Gamma (and Alpha and Delta) -- metabolism, maintenance and synthesis of muscle fibers, thermogenesis, burning fat, storing fat, and the overall balancing of energy. Not only can PPARs regulate diabetes/insulin resistance and heart disease, but with their optimization of function, PPARs can also reverse these conditions. PPARs ameliorate atherosclerosis. Both food and omega-3 trials and drug (alpha, gamma, delta) trials demonstrate this already.



Don't be sarcopenic... Build a wealth of heart protection in your flesh. How much meaningful movement do you have in your daily life?







Regulation of peroxisome proliferator-activated receptor-gamma activity by mammalian target of rapamycin and amino acids in adipogenesis.
Kim JE, Chen J. Diabetes. 2004 Nov;53(11):2748-56.



Adipocyte differentiation is a developmental process that is critical for metabolic homeostasis and nutrient signaling. The mammalian target of rapamycin (mTOR) mediates nutrient signaling to regulate cell growth, proliferation, and diverse cellular differentiation. It has been reported that rapamycin, the inhibitor of mTOR and an immunosuppressant, blocks adipocyte differentiation, but the mechanism underlying this phenomenon remains unknown. Here we show that mTOR plays a critical role in 3T3-L1 preadipocyte differentiation and that mTOR kinase activity is required for this process. Rapamycin specifically disrupted the positive transcriptional feedback loop between CCAAT/enhancer-binding protein-alpha and peroxisome proliferator-activated receptor-gamma (PPAR-gamma), two key transcription factors in adipogenesis, by directly targeting the transactivation activity of PPAR-gamma. In addition, we demonstrate for the first time that PPAR-gamma activity is dependent on amino acid sufficiency, revealing a molecular link between nutrient status and adipogenesis. The results of our further investigation have led us to propose a model in which the mTOR pathway and the phosphatidylinositol 3-kinase/Akt pathway act in parallel to regulate PPAR-gamma activation during adipogenesis by mediating nutrient availability and insulin signals, respectively. It is interesting that troglitazone (a thiazolidinedione drug WHICH BINDS PPAR-Gamma) reversed the inhibitory effects of rapamycin and amino acid deprivation, implicating therapeutic values of thiazolidinedione drugs to counter certain side effects of rapamycin as an immunosuppressant. PMID: 15504954



(Diagram from here; Williamson DL, et al. Exercise-induced alterations in extracellular signal-regulated kinase 1/2 and mammalian target of rapamycin (mTOR) signalling to regulatory mechanisms of mRNA translation in mouse muscle. J Physiol. 2006 June 1; 573(Pt 2): 497–510. )