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Nathan Goodyear

Muscle Hypertrophy 2011 - 0 views

www.unm.edu/...hypertrophy2011UNM.html

resistance training weight lifting muscle exercise weight training

shared by Nathan Goodyear on 20 Mar 15 - No Cached
  • mechanical tension, muscle damage and metabolic stress are the three primary factors that promote hypertrophy from exercise
  • The mechanical tension is directly related to intensity of the exercise, which is the key to stimulating muscle growth
  • Muscle damage, that leads to muscle soreness, from exercise training initiates an inflammatory response, which activates satellite cells growth processes
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  • metabolic stress that is a result of the byproducts of anaerobic metabolism (i.e., hydrogen ions, lactate, inorganic phosphates) is now also believed to promote hormonal factors leading to muscle hypertrophy
  • The upper extremities tend to show more growth earlier then the lower body
  • Maximal growth occurs with loads between 80-95% of 1 repetition maximum
  • weightlifters and powerlifters show more favorable hypertrophy of type II (fast twitch) muscle fibers
  • body builders appear to have comparable hypertrophy in both the type I (slow twitch) and type II muscle fibers
  • Multi-joint exercises have been shown to produce larger increases of anabolic hormones than single-joint exercises
  • Nathan Goodyear on 20 Mar 15
     
    Review of the physiology of muscle building.  The authors review the evidence behind the types of muscle building exercises and the physiology responsible for muscle hypertrophy.  The authors point to Schoenfeld's description of mechanical tension, muscle damage, and metabolic stress to build muscle.
Nathan Goodyear

Curcumin Attenuation of Lipopolysaccharide Induced Cardiac Hypertrophy in Rodents - 0 views

www.hindawi.com/...539305

curcumin LPS lipopolysaccharides epigenetics inflammation heart disease heart health

shared by Nathan Goodyear on 04 Oct 17 - No Cached
  • Nathan Goodyear on 04 Oct 17
     
    This is just to cool. Curcumin found to inhibit LPS mediated cardiac hypertrophy. The how is fascinating. No only does LPS induce inflammatory cytokine production, but he inflammation induces disease--cardiac hypertrophy. LPS induces epigenetic changes that lead to the hypertrophy. Curcumin blocked the histone acetylation induced by LPS.
Nathan Goodyear

Relationship Between Benign Prostatic Hyperplasia/... [J Sex Med. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24612680

Testosterone men male hormone hormones BPH benign prostatic hypertrophy LUTS lower urinary tract symptoms

shared by Nathan Goodyear on 18 Mar 14 - No Cached
  • Nathan Goodyear on 18 Mar 14
     
    European study finds no correlation with Total Testosterone levels and lower urinary tract symptoms and benign prostatic hypertrophy.
Nathan Goodyear

Blood Pressure and Left Ventricular Hypertrophy During American-Style Football Particip... - 0 views

circ.ahajournals.org/...524.full

football lineman football players cardiovascular disease CVD sports hypertension sports medicine heart disease heart health blood pressure

shared by Nathan Goodyear on 17 Nov 15 - No Cached
  • Nathan Goodyear on 17 Nov 15
     
    football lineman found to have increased heart dysfunction (increased left ventricular hypertrophy and increased left ventricular mass) and hypertension, compared to all other positions, throughout one season.
Nathan Goodyear

The effect of treatment with coenzyme Q10 on the mitochondrial function and superoxide ... - 0 views

www.ncbi.nlm.nih.gov/...3031317

CoQ10 heart heart health mitochondria

shared by Nathan Goodyear on 16 Jun 17 - No Cached
  • Nathan Goodyear on 16 Jun 17
     
    IM CoQ10 useful in animal model with cardiac hypertrophy and aortic stenosis.
Nathan Goodyear

Total testosterone levels, metabolic parameters, cardiac remodeling and exercise capaci... - 0 views

informahealthcare.com/...07853890.2012.711951

low T low testosterone Low T testosterone Diabetes DM exercise men male

shared by Nathan Goodyear on 23 Apr 13 - No Cached
  • Nathan Goodyear on 23 Apr 13
     
    Low Total testosterone associated with poor exercise capacity, increased obesity, poor glucose control including diabetes, increased cardiac hypertrophy in those with CAD.  Simply put, low T in men is associated with metabolic dysregulation.
Nathan Goodyear

PPARs, Obesity, and Inflammation - 0 views

www.ncbi.nlm.nih.gov/...PMC1783744

obesity inflammation PPARs perioxisome proliferator-activated receptor

shared by Nathan Goodyear on 16 Jan 12 - No Cached
  • increase of 61% within 10 years
  • Many of the inflammatory markers found in plasma of obese individuals appear to originate from adipose tissue
  • obesity is a state of chronic low-grade inflammation that is initiated by morphological changes in the adipose tissue.
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  • secretion of MCP-1, resistin, and other proinflammatory cytokines is increased by obesity, the adipose secretion of the anti-inflammatory protein adiponectin is decreased
  • the peroxisome proliferators- activated receptor (PPAR) family are involved in the regulation of inflammation and energy homestasis
  • natural agonists, including unsaturated fatty acids and eicosanoids
  • PPARα also regulates inflammatory processes, mainly by inhibiting inflammatory gene expression
  • upregulation of COX-2 is seen in alcoholic steatohepatitis and nonalcoholic steatohepatitis and has been directly linked to the progression of steatosis to steatohepatitis, the inhibitory effect of PPARα on COX-2 may reduce steatohepatitis
  • PPARα agonists have a clear anorexic effect resulting in decreased food intake, evidence is accumulating that PPARα may also directly influence adipose tissue function, including its inflammatory status.
  • PPARα may govern adipose tissue inflammation in three different ways: (1) by decreasing adipocyte hypertrophy, which is known to be connected with a higher inflammatory status of the tissue [3, 11, 59], (2) by direct regulation of inflammatory gene expression via locally expressed PPARα, or (3) by systemic events likely originating from liver
  • PPARγ is considered the master regulator of adipogenesis
  • Unsaturated fatty acids and several eicosanoids serve as endogenous agonists of PPARγ
  • PPARγ2, which is adipose-tissue specific
  • two different molecular mechanisms have been proposed by which anti-inflammatory actions of PPARγ are effectuated: (1) via interference with proinflammatory transcription factors including STAT, NF-κB, and AP-1
  • and (2) by preventing removal of corepressor complexes from gene promoter regions resulting in suppression of inflammatory gene transcription
  • diet-induced obesity is associated with increased inflammatory gene expression in adipose tissue via adipocyte hypertrophy and macrophage infiltration
  • PPARγ is able to reverse macrophage infiltration, and subsequently reduces inflammatory gene expression
  • Inflammatory adipokines mainly originate from macrophages which are part of the stromal vascular fraction of adipose tissue [18, 19], and accordingly, the downregulation of inflammatory adipokines in WAT by PPARγ probably occurs via effects on macrophages
  • By interfering with NF-κB signaling pathways, PPARγ is known to decrease inflammation in activated macrophages
  • Recent data suggest that activation of PPARγ in fatty liver may protect against inflammation
  • PPARs may influence the inflammatory response either by direct transcriptional downregulation of proinflammatory genes
  • anti-inflammatory properties of PPARs in human obesity
  • Nathan Goodyear on 16 Jan 12
     
    PPARs play pivotal in obesity.  PPARs appear to reduce the inflammatory cascade associated with obesity.  Downregulation of PPARs are associated with increased inflammation.  Natural PPARs include unsaturated fats and eicosanoids.
Nathan Goodyear

https://g-se.com/uploads/biblioteca/full2013.pdf - 0 views

g-se.com/...full2013.pdf

resistance training weight lifting muscle exercise

shared by Nathan Goodyear on 20 Mar 15 - No Cached
  • Nathan Goodyear on 20 Mar 15
     
    Nice review of recent understanding of how resistance training promotes muscle hypertrophy adaptation.
Nathan Goodyear

http://www.ucam.edu/sites/default/files/Oct_13/mechanisms_of_muscle_hypertrophy.pdf - 0 views

www.ucam.edu/...isms_of_muscle_hypertrophy.pdf

resistance training weight lifting weight training muscle exercise

shared by Nathan Goodyear on 20 Mar 15 - No Cached
  • Nathan Goodyear on 20 Mar 15
     
    Awesome review by Schoenfeld on the physiology of muscle hypertrophy.
Nathan Goodyear

Changes in muscle mass with mechanical load: possible cellular mechanismsThis... - 0 views

www.nrcresearchpress.com/...H09-010

resistance training weight training weight lifting mTOR muscle exercise

shared by Nathan Goodyear on 20 Mar 15 - No Cached
  • Nathan Goodyear on 20 Mar 15
     
    mTOR signaling pathway involved with building muscle (hypertrophy)
Nathan Goodyear

Testosterone physiology in resistance exercise an... [Sports Med. 2010] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21058750

resistance exercise physiology testosterone men male hormone hormones

shared by Nathan Goodyear on 29 Jul 14 - No Cached
  • testosterone stimulates protein synthesis
  • promotion of muscle hypertrophy by testosterone
  • intracellular androgen receptor (AR)
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  • In general, testosterone concentration is elevated directly following heavy resistance exercise in men
  • Findings on the testosterone response in women are equivocal with both increases and no changes observed in response to a bout of heavy resistance exercise
  • Age also significantly affects circulating testosterone concentrations.
  • Aging beyond 35-40 years is associated with a 1-3% decline per year in circulating testosterone concentration in men
  • aging results in a reduced acute testosterone response to resistance exercise in men.
  • In women, circulating testosterone concentration also gradually declines until menopause, after which a drastic reduction is found.
  • acute increases in testosterone can be induced by resistance exercise
  • testosterone is an important modulator of muscle mass in both men and women
  • Nathan Goodyear on 29 Jul 14
     
    Resistance training to increase endogenous Testosterone production: more specific, the exercise must be high rep or as the authors call it--high volume.  To do this, the weight needs to be light.
Nathan Goodyear

Crescent pyramid and drop-set systems do not promote greater strength gains, muscle hyp... - 0 views

www.ncbi.nlm.nih.gov/...28130627

exercise resistance training training weight lifting muscle

shared by Nathan Goodyear on 30 Nov 17 - No Cached
  • Nathan Goodyear on 30 Nov 17
     
    no training benefit with pyramid and drop-set workouts compared to traditional resistance training.  The key is repeitition, proper technique and just doing it.
Nathan Goodyear

American College of Cardiology Foundation | Journal of the American College of Cardiolo... - 0 views

content.onlinejacc.org/article.aspx

mitochondria oxidative stress heart failure heart

shared by Nathan Goodyear on 19 Mar 13 - No Cached
  • Although currently no drugs that specifically target mitochondrial biogenesis in HF are available, acceleration of this process through adenosine monophosphate–activated kinase (AMPK), endothelial nitric oxide synthase (eNOS), and other pathways may represent a promising therapeutic approach
  • Mitochondrial biogenesis can be enhanced therapeutically with the use of adenosine monophosphate kinase (AMPK) agonists, stimulants of nitric oxide/cyclic guanosine monophosphate (NO/cGMP) pathway (including phosphodiesteraes type 5 inhibitors), or resveratrol
  • metformin, a commonly used antidiabetic drug that activates AMPK signaling
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  • Recent evidence suggests that the eNOS/NO/cGMP pathway is an important activator of mitochondrial biogenesis
  • BH4 (tetrahydrobiopterin) supplementation can prevent eNOS uncoupling and was found to reduce left ventricular hypertrophy
  • folic acid is known to replenish reduced BH4 and has been shown to protect the heart through increased eNOS activity
  • Both folate deficiency and inhibition of BH4 synthesis were associated with reduced mitochondrial number and function
  • Resveratrol, a polyphenol compound responsible for the cardioprotective properties of red wine, was recently identified as a potent stimulator of mitochondrial biogenesis
  • epidemiological studies reveal a reduced risk of cardiovascular disease in premenopausal, but not post-menopausal, women compared with men
  • post-menopausal women
    • Nathan Goodyear
      Nathan Goodyear on 19 Mar 13
       
      I would hypothesis that a change in the predominance of ER expression is one of ER beta to ER alpha: creating a more pro-inflammatory signal.
  • The majority of ROS in the heart appear to come from uncoupling of mitochondrial electron transport chain at the level of complexes I and III
  • Because the majority of ROS in HF comes from mitochondria, these organelles are the primary target of oxidative damage.
  • cardioprotective therapies such as angiotensin-converting enzyme inhibitors and ATII receptor blockers were shown to possess antioxidant properties, although it is not known whether they target mitochondrial ROS directly or indirectly
  • Nathan Goodyear on 19 Mar 13
     
    great review of mitochondrial biogenesis, oxidative stress and heart failure.  
Nathan Goodyear

The Ketogenic Diet and Sport: A Possible Marriage? : Exercise and Sport Sciences Reviews - 0 views

journals.lww.com/..._and_Sport___A_Possible.8.aspx

nutrition diet ketogenic ketogenic diet sports athletes exercise sports medicine

shared by Nathan Goodyear on 16 Nov 16 - No Cached
  • It is important to note that, although the blood level of glucose drops, it still remains at a physiological level (23), which is maintained through gluconeogenesis involving glucogenic amino acids and also glycerol released from triglycerides
  • “physiological ketosis” where KB levels may rise to 7 to 8 mmol L-1 (but without any pH change). In “pathological diabetic ketoacidosis,” on the other hand, ketonemia can exceed 20 mmol L-1 and also cause lowering of blood pH
  • in the initial phase of KD, about 16% of glucose comes from glycerol (released from triglyceride hydrolysis) and the bulk (60–65 g) from proteins via gluconeogenesis (proteins may be of either dietary or endogenous origin
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  • the protein supply consumed during a KD “preserves,” as demonstrated, lean body mass
  • The importance of glycerol as a glucose source increases progressively during ketosis; in fact, glycerol passes from supplying 16% of total glucose to an average of 60% after many days (>7 d) of complete fasting (from 38% in lean individual to 79% in the obese).
  • The possible reasons for the effectiveness of KD for weight loss may be listed as follows, in order of evidence, strongest first: Figure 3Image Tools 1. Appetite reduction: protein satiety, effects on appetite-related hormones such as ghrelin, and possibly a sort of direct appetite-blocking effect of KB 2. Reduced lipogenesis and increased fat oxidation 3. A reduction in respiratory quotient may indicate a greater metabolic efficiency in fat oxidation 4. A thermic effect of proteins and increased energy usage by gluconeogenesis
  • all data regarding biochemical and molecular mechanisms suggest that it is very difficult to increase muscle mass during a KD; use of which really should be limited to the few days immediately before competition in bodybuilding.
  • a long-term KD can interfere with some muscle hypertrophy mechanisms and this could be counterproductive if the aim of the athlete is to gain muscle mass
  • Nathan Goodyear on 16 Nov 16
     
    Great read on the ketogenic  and its application to sports/training...
Nathan Goodyear

Inflammation and insulin resistance 10.1016/j.febslet.2007.11.057 : FEBS Letters | Scie... - 0 views

www.sciencedirect.com/...S0014579307012082

inflammation insulin resistance IR PPAR TNF-alpha IL-6 IL-10 IL-1Beta JNK GLT-4 Resistin adiponectin Gherlin NF-kapppB iNOS lkkb obesity TLR-4

shared by Nathan Goodyear on 10 Jan 12 - No Cached
  • A subsequent study by Yuan et al. showed that Tnf treatment of 3T3L1 adipocytes induces insulin resistance and that this could be prevented by pretreatment of cells with aspirin
  • Activation of the Tnf receptor results in stimulation of NFκB signaling via Ikkb
  • Insulin is a pleiotropic hormone
  • ...25 more annotations...
  • the percentage of macrophages in a given adipose tissue depot is positively correlated with adiposity and adipocyte size
  • Il-10 is an anti-inflammatory cytokine produced by macrophages and lymphocytes
  • Il-10 exerts its anti-inflammatory activity by inhibiting Tnf-induced NFκB activation by reducing IKK activity [38]
  • adipose tissue macrophages are responsible for nearly all adipose tissue Tnf expression and a significant portion of Nos2 and Il6 expression
  • One theory holds that the expansion of adipose tissue leads to adipocyte hypertrophy and hyperplasia and that large adipocytes outstrip the local oxygen supply leading to cell autonomous hypoxia with activation of cellular stress pathways
  • The use of the anti-inflammatory compounds, salicylate and its derivative aspirin, for treating symptoms of T2DM dates back over 100 years
  • elevated levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin (IL-8) have all been reported in various diabetic and insulin resistant states
  • overnutrition and obesity are often accompanied by elevations in tissue and circulating FFA concentrations, and saturated FFAs can directly activate pro-inflammatory responses
  • Adipokines such as resistin, leptin and adiponectin, which are secreted by adipocytes, can also affect inflammation and insulin sensitivity
  • In skeletal muscle insulin promotes glucose uptake by stimulating translocation of the GLUT4 glucose transporter
  • macrophages are also capable of undergoing a phenotypic switch from an M1 state, which was defined as the “classically activated” pro-inflammatory macrophage, to the M2 state or the “alternatively activated” non-inflammatory cell
  • saturated fatty acids are the most potent inducers of this inflammatory response
  • Several inducers of insulin resistance, including FFAs, pro-inflammatory cytokines and oxidative stress, activate the expression of Nos2, the gene that encodes iNOS (reviewed in [33]
  • Adipose tissue insulin signaling results in decreased hormone sensitive lipase activity and this anti-lipolytic effect inhibits free fatty acid (FFA) efflux out of adipocytes.
  • In the liver, insulin inhibits the expression of key gluconeogenic enzymes and, therefore, insulin resistance in liver leads to elevated hepatic glucose production
  • elevated JNK activity in liver, adipose tissue and skeletal muscle of obese insulin resistant mice, and knockout of Jnk1 (Jnk1−/−) leads to amelioration of insulin resistance in high fat diet
  • Adipose tissue from obese mice contains proportionately more M1 macrophages, whereas, lean adipose tissue contains more M2 macrophages, and increased M1 content positively correlates with inflammation, macrophage infiltration and insulin resistance
  • C-reactive protein (CRP)
  • these studies highlight the possibility that increased iNOS activity plays a direct role in the pathogenesis of insulin resistance
  • the important role of Ikkb in the development of obesity and inflammation-induced insulin resistance.
  • It is probable that local concentrations of inflammatory mediators, such as FFAs, Tnf or other cytokines/adipokines contribute to this polarity switch
  • Tnf and other cytokines/chemokines are symptomatic of inflammation, and while they propagate and/or maintain the inflammatory state, they are not the initial cause(s) of inflammation
  • Tlr4, in particular, is stimulated by lipopolysaccharide (LPS), an endotoxin released by gram-negative bacteria
  • Tlr4 belongs to the family of Toll-like receptors that function as pattern recognition receptors that guard against microorganismal infections as part of the innate immune system.
  • Tlr4 stimulation results in the activation of both Ikkb/NFκB and JNK/AP-1 signaling, culminating in the expression and secretion of pro-inflammatory cytokines/chemokines, including, Il1b, IL-6, Tnf, Mcp1, etc. (reviewed in [57
  • Nathan Goodyear on 10 Jan 12
     
    Great review of all the known components in the inflammation, insulin resistance link
Nathan Goodyear

CpG hypermethylation of the promoter region inactivates the estrogen receptor... - 0 views

onlinelibrary.wiley.com/...full

prostate cancer ER beta ER-beta estrogen methylation BPH benign prostatic hypertrophy

shared by Nathan Goodyear on 21 Jan 14 - No Cached
  • Nathan Goodyear on 21 Jan 14
     
    ER beta expression that is lost in prostate carcinogenesis occurs via methylation at the ER beta gene promoter sites 19CpG.  What is really interesting is that ER beta expression was present in all of the samples with BPH, but was absent in 83% of the prostate cancer samples.
Nathan Goodyear

Benign prostatic hyperplasia: a new meta... [J Endocrinol Invest. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24458832

BPH benign prostatic hypertrophy Toll-like receptors TLRs hormone hormones low Testosterone T estrogen estradiol aromatase prostate metabolism

shared by Nathan Goodyear on 20 Feb 14 - No Cached
  • Nathan Goodyear on 20 Feb 14
     
    The authors of this paper describe BPH as a metabolic disease: involving inflammation with increased expression of TLRs, hormone imbalance and altered metabolism
Nathan Goodyear

Asian Journal of Andrology - Efficacy and safety of Chinese herbal medicine for benign ... - 0 views

www.nature.com/...aja2012173a.html

chinese herbal medicine BPH benign prostatic hypertrophy

shared by Nathan Goodyear on 26 Aug 13 - No Cached
  • Nathan Goodyear on 26 Aug 13
     
    Study doesn't find alot of "good" evidence to support Chinese herbal medicine in BPH.  However, the author states: "Before the introduction of conventional medication and surgery to China, the Chinese had solely relied on CHM to treat BPH for more than three thousand years".  That is 3,000 years of observational data that is being tossed out the window.
Nathan Goodyear

Prevalence of low testosterone and its relationsh... [Aging Male. 2013] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24134648

low Testosterone low T BPH BMI low Testosterone benign prostatic hypertrophy

shared by Nathan Goodyear on 30 Oct 13 - No Cached
  • Nathan Goodyear on 30 Oct 13
     
    This study found an association between increasing BMI and low T in men with BPH.
Nathan Goodyear

PLOS ONE: Probiotic Microbes Sustain Youthful Serum Testosterone Levels and Testicular ... - 0 views

journals.plos.org/...article

hormone hormones low T low Testosterone hypogonadism Testosterone probiotic L reuters probiotics Lactobacillus lactobacillus reuteri male aging

shared by Nathan Goodyear on 29 Apr 15 - No Cached
  • Studies in both humans and rodents, however, suggest that low testosterone is due to age-related lesions in testes rather than irregular luteinizing hormone metabolism
  • Various dietary factors and diet-induced obesity have been shown to increase the risk for late onset male hypogonadism and low testosterone production in both humans and mice
  • Testosterone deficiency and metabolic diseases such as obesity appear to inter-digitate in complex cause-and-effect relationships
  • ...28 more annotations...
  • dietary supplementation of aged mice with the probiotic bacterium Lactobacillus reuteri makes them appear to be younger than their matched untreated sibling mice
  • These results indicate that gut microbiota induce modulation of local gastrointestinal immunity resulting in systemic effects on the immune system which activate metabolic pathways that restore tissue homeostasis and overall health
  • all these studies we consistently observed that young and aged mice consuming purified L. reuteri organisms had particularly large testes and a dominant male behavior.
  • The testes of probiotic-fed aged mice were rescued from both seminiferous tubule atrophy and interstitial Leydig cell area reduction typical of the normal aging process. Preservation of testicular architecture despite advanced age or high-fat diet coincided with remarkably high levels of circulating testosterone. The beneficial effects of probiotic consumption were recapitulated by the depletion of the pro-inflammatory cytokine Il-17.
  • feeding of L. reuteri consistently increased the gonadal weights, consumption of a non-pathogenic strain of Escherichia coli (E. coli) K12 organisms did not affect testicular weight
  • mice with dietary L. reuteri supplements were rescued from diet-induced obesity and had normal body weight and lean physique
  • Despite the comparable numbers of ST profiles, we determined that testes from L. reuteri-treated mice had increased ST cross-sectioned profiles
  • the probiotic organism induced prominent Leydig cell accumulations in the interstitial tissue between the ST's
  • The probiotic-associated increase of interstitial Leydig cell areas was sustained with advancing age at 7 (CD vs CD+LR, P = 0.0025; CD+E.coli vs CD+LR, P = 0.0251) and 12 months
  • mice eating L. reuteri had profoundly increased levels of circulating testosterone regardless of the type of diet they consumed
  • blocking pro-inflammatory Il-17 signaling entirely recapitulates the beneficial effects of probiotics
  • previous studies we found that dietary probiotics counteract obesity [19] and age-related integumentary pathology [18] at least in part by down-regulating systemic pro-inflammatory IL-17A-dependent signaling
  • Testes histomorphometry and serum androgen concentration data were both suggestive of a probiotic-associated up-regulation of spermatogenesis in mice
  • Lactobacillus reuteri we discovered that aging male animals had larger testes compared to their age-matched controls
  • xamined testes of probiotic microbe-fed mice and found that they had less testicular atrophy coinciding with higher levels of circulating testosterone compared to their age-matched controls
  • Similar testicular health benefits were produced using systemic depletion of the pro-inflammatory cytokine Il-17 alone, implicating a chronic inflammatory pathway in hypogonadism
  • One specific aspect of this paradigm is reciprocal activities of pro-inflammatory Th-17 and anti-inflammatory Treg cells
  • Feeding of L. reuteri organisms was previously shown to up-regulate IL-10 levels and reduce levels of IL-17 [19] serving to lower systemic inflammation
  • insufficient levels of IL-10 may increase the risk for autoimmunity, obesity, and other inflammatory disease syndromes
  • Westernized diets are also low in vitamin D, a nutrient that when present normally works together with IL-10 to protect against inflammatory disorders
  • Physiological feedback loops apparently exist between microbes, host hormones, and immunity
  • The hormone testosterone has been shown to act directly through androgen receptors on CD4+ cells to increase IL-10 expression
  • studies in both humans and rodents suggest that hypogonadism is due to age-related lesions in testes rather than irregular LH metabolism
  • We postulate that probiotic gut microbes function symbiotically with their mammalian hosts to impart immune homeostasis to maintain systemic and testicular health [34]–[35] despite suboptimal dietary conditions.
  • Dietary factors and diet-induced obesity were previously shown to increase risk for age-associated male hypogonadism, reduced spermatogenesis, and low testosterone production in both humans and mice [2]–[4], [8]–[11], [14]–[17], phenotypic features that in this study were inhibited by oral probiotic therapy absent milk sugars, extra protein, or vitamin D supplied in yogurt.
  • Similar beneficial effects of probiotic microbes on testosterone levels and sperm indices were reported in male mice that had been simultaneously supplemented with selenium
  • L. reuteri-associated prevention of age- and diet-related testicular atrophy correlates with increased numbers and size of Leydig cells
  • the initial changes of testicular atrophy begin to occur in mice from the age of 6 moths onwards [7] and indicates that the trophic effect of L. reuteri on Leydig cells is a key event which precedes and prevents age-related changes in the testes of mice. This effect is reminiscent of earlier studies describing Leydig cell hyperplasia and/or hypertrophy in the mouse and the rat testis that were achievable by the administration of gonadotropins, including human chorionic gonadotropin, FSH and LH
  • Nathan Goodyear on 29 Apr 15
     
    Fascinating study on how the addition of Lactobacillus reuteri increased Testicular size, prevented testicular atrophy, increased serum Testosterone production and protected against diet-induced/obesity-induced hypogonadism.  This was a mouse model
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