Alterations in the HPA and hypothalamic-pituitary-gonadal axes with a resultant decrease in testosterone:cortisol ratios have been implicated in OTS. Proinflammatory cytokines are potent activators of the HPA system, which cause release of corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol. These cytokines suppress testosterone through central inhibition
1More
Get rid of the Stretch Marks | Best Stretch Marks Removal Laser Treatment - Pixigenus -... - 1 views
-
Stretch marks are formed deep within the dermis layer and happen due to rapid stretching, this causes damage to the skin's connecting tissues. To get rid of these stretch marks we are introducing to you our latest laser treatment i.e. PIXIGENUS. It is a unique technology to eliminate stretchmarks from various parts of the body. Watch the full video to know more. Stretch marks are caused because of rapid stretching of the skin that results into scars and discoloration of the skin. There are many reasons which can lead to stretch marks such as rapid weight reduction, quick weight gain, excessive exercise, steroids, pregnancy, hormonal changes, puberty etc. Millions of women have stretch marks, but this fact does little to lessen the embarrassment that most women feel at the appearance of these unattractive striations on their skin. Stretch marks, also known as striae, are a form of scarring on the skin with an off-color hue. Over time they may reduce, but will not disappear completely. Tearing of the dermis results into stretch marks.
6More
shared by Nathan Goodyear on 29 Jan 16
- No Cached
Overtraining Syndrome - 0 views
www.ncbi.nlm.nih.gov/...PMC3435910
overtraining syndrome OTS exercise athletes cortisol adrenals Testosterone Testosterone:Cortisol hormones
![](/images/link.gif)
-
Some have suggested that a decreased testosterone:cortisol ratio can be diagnostic of NFO and/or OTS. However, the ratio represents the physiologic strain of training rather than the athlete’s maladaption to that stress
- ...2 more annotations...
-
A prospective study found a clinically significant increase in overnight urinary cortisol:cortisone ratio during a high training load period in triathletes, who subsequently underperformed and reported fatigue
-
It is proposed that cytokines may inhibit 11β-HSD2 activity and result in relative increases in cortisol and, hence, catabolism
1More
shared by Nathan Goodyear on 16 Aug 16
- No Cached
https://www.generationucan.com/pdf/technical-breakthrough-sports-innovation.pdf - 0 views
www.generationucan.com/...kthrough-sports-innovation.pdf
sports medicine sports nutrition exercise recovery ucan
![](/images/link.gif)
1More
shared by Nathan Goodyear on 27 Sep 16
- No Cached
Increased physical activity has a greater effect than reduced energy intake on lifestyl... - 0 views
www.ncbi.nlm.nih.gov/...PMC4706091
exercise men hormones low T low Testosterone Testosterone lifestyle intervention male hormones
![](/images/link.gif)
91More
shared by Nathan Goodyear on 09 Jul 17
- No Cached
Press-pulse: a novel therapeutic strategy for the metabolic management of cancer | Nutr... - 0 views
nutritionandmetabolism.biomedcentral.com/...s12986-017-0178-2
ketogenic diet ketogenic press-pulse hyperbaric oxygen therapy HBOTnutrition diet cancer HBOT IVC IV vitamin C DCA dichloracetic acid cancer therapy cancer treatment alternative cancer treatment
![](/images/link.gif)
mamdouh_hfz liked it
-
A “press” disturbance was considered a chronic environmental stress on all organisms in an ecological community
-
“pulse” disturbances were considered acute events that disrupted biological communities to produce high mortality
- ...84 more annotations...
-
Data from the American Cancer Society show that the rate of increase in cancer deaths/year (3.4%) was two-fold greater than the rate of increase in new cases/year (1.7%) from 2013 to 2017
-
glucose is first split into two molecules of pyruvate through the Embden–Meyerhof–Parnas glycolytic pathway in the cytosol
-
Aerobic fermentation, on the other hand, involves the production of lactic acid under normoxic conditions
-
persistent lactic acid production in the presence of adequate oxygen is indicative of abnormal respiration
-
The Crabtree effect is an artifact of the in vitro environment and involves the glucose-induced suppression of respiration with a corresponding elevation of lactic acid production even under hyperoxic (pO2 = 120–160 mmHg) conditions associated with cell culture
-
the Warburg theory of insufficient aerobic respiration remains as the most credible explanation for the origin of tumor cells [2, 37, 51, 52, 53, 54, 55, 56, 57].
-
The main points of Warburg’s theory are; 1) insufficient respiration is the predisposing initiator of tumorigenesis and ultimately cancer, 2) energy through glycolysis gradually compensates for insufficient energy through respiration, 3) cancer cells continue to produce lactic acid in the presence of oxygen, and 4) respiratory insufficiency eventually becomes irreversible
-
Efraim Racker coined the term “Warburg effect”, which refers to the aerobic glycolysis that occurs in cancer cells
-
Warburg clearly demonstrated that aerobic fermentation (aerobic glycolysis) is an effect, and not the cause, of insufficient respiration
-
all tumor cells that have been examined to date contain abnormalities in the content or composition of cardiolipin
-
The evidence supporting Warburg’s original theory comes from a broad range of cancers and is now overwhelming
-
respiratory insufficiency, arising from any number mitochondrial defects, can contribute to the fermentation metabolism seen in tumor cells.
-
data from the nuclear and mitochondrial transfer experiments suggest that oncogene changes are effects, rather than causes, of tumorigenesis
-
Normal mitochondria can suppress tumorigenesis, whereas abnormal mitochondria can enhance tumorigenesis
-
Glutamine is anapleurotic and can be rapidly metabolized to glutamate and then to α-ketoglutarate for entry into the TCA cycle
-
Amino acid fermentation can generate energy through TCA cycle substrate level phosphorylation under hypoxic conditions
-
Although Warburg’s hypothesis on the origin of cancer has created confusion and controversy [37, 38, 39, 40], his hypothesis has never been disproved
-
Warburg referred to the phenomenon of enhanced glycolysis in cancer cells as “aerobic fermentation” to highlight the abnormal production of lactic acid in the presence of oxygen
-
Emerging evidence indicates that macrophages, or their fusion hybridization with neoplastic stem cells, are the origin of metastatic cancer cells
-
Radiation therapy can enhance fusion hybridization that could increase risk for invasive and metastatic tumor cells
-
Kamphorst et al. in showing that pancreatic ductal adenocarcinoma cells could obtain glutamine under nutrient poor conditions through lysosomal digestion of extracellular proteins
-
It will therefore become necessary to also target lysosomal digestion, under reduced glucose and glutamine conditions, to effectively manage those invasive and metastatic cancers that express cannibalism and phagocytosis.
-
Previous studies in yeast and mammalian cells show that disruption of aerobic respiration can cause mutations (loss of heterozygosity, chromosome instability, and epigenetic modifications etc.) in the nuclear genome
-
The somatic mutations and genomic instability seen in tumor cells thus arise from a protracted reliance on fermentation energy metabolism and a disruption of redox balance through excess oxidative stress.
-
According to the mitochondrial metabolic theory of cancer, the large genomic heterogeneity seen in tumor cells arises as a consequence, rather than as a cause, of mitochondrial dysfunction
-
A therapeutic strategy targeting the metabolic abnormality common to most tumor cells should therefore be more effective in managing cancer than would a strategy targeting genetic mutations that vary widely between tumors of the same histological grade and even within the same tumor
-
Tumor cells are more fit than normal cells to survive in the hypoxic niche of the tumor microenvironment
-
Hypoxic adaptation of tumor cells allows for them to avoid apoptosis due to their metabolic reprograming following a gradual loss of respiratory function
-
The high rates of tumor cell glycolysis and glutaminolysis will also make them resistant to apoptosis, ROS, and chemotherapy drugs
-
Despite having high levels of ROS, glutamate-derived from glutamine contributes to glutathione production that can protect tumor cells from ROS
-
It is clear that adaptability to environmental stress is greater in normal cells than in tumor cells, as normal cells can transition from the metabolism of glucose to the metabolism of ketone bodies when glucose becomes limiting
-
Mitochondrial respiratory chain defects will prevent tumor cells from using ketone bodies for energy
-
glycolysis-dependent tumor cells are less adaptable to metabolic stress than are the normal cells. This vulnerability can be exploited for targeting tumor cell energy metabolism
-
In contrast to dietary energy reduction, radiation and toxic drugs can damage the microenvironment and transform normal cells into tumor cells while also creating tumor cells that become highly resistant to drugs and radiation
-
Drug-resistant tumor cells arise in large part from the damage to respiration in bystander pre-cancerous cells
-
Because energy generated through substrate level phosphorylation is greater in tumor cells than in normal cells, tumor cells are more dependent than normal cells on the availability of fermentable fuels (glucose and glutamine)
-
Although some tumor cells might appear to oxidize ketone bodies by the presence of ketolytic enzymes [181], it is not clear if ketone bodies and fats can provide sufficient energy for cell viability in the absence of glucose and glutamine
-
A calorie restricted ketogenic diet or dietary energy reduction creates chronic metabolic stress in the body
-
The KD can more effectively reduce glucose and elevate blood ketone bodies than can CR alone making the KD potentially more therapeutic against tumors than CR
-
Campbell showed that tumor growth in rats is greater under high protein (>20%) than under low protein content (<10%) in the diet
-
Calorie restriction, fasting, and restricted KDs are anti-angiogenic, anti-inflammatory, and pro-apoptotic and thus can target and eliminate tumor cells through multiple mechanisms
-
Ketogenic diets can also spare muscle protein, enhance immunity, and delay cancer cachexia, which is a major problem in managing metastatic cancer
-
The GKI can therefore serve as a biomarker to assess the therapeutic efficacy of various diets in a broad range of cancers.
-
It is important to remember that insulin drives glycolysis through stimulation of the pyruvate dehydrogenase complex
-
The water-soluble ketone bodies (D-β-hydroxybutyrate and acetoacetate) are produced largely in the liver from adipocyte-derived fatty acids and ketogenic dietary fat. Ketone bodies bypass glycolysis and directly enter the mitochondria for metabolism to acetyl-CoA
-
Due to mitochondrial defects, tumor cells cannot exploit the therapeutic benefits of burning ketone bodies as normal cells would
-
Therapeutic ketosis with racemic ketone esters can also make it feasible to safely sustain hypoglycemia for inducing metabolic stress on cancer cells
-
ketone bodies can inhibit histone deacetylases (HDAC) [229]. HDAC inhibitors play a role in targeting the cancer epigenome
-
Therapeutic ketosis reduces circulating inflammatory markers, and ketones directly inhibit the NLRP3 inflammasome, an important pro-inflammatory pathway linked to carcinogenesis and an important target for cancer treatment response
-
Chronic psychological stress is known to promote tumorigenesis through elevations of blood glucose, glucocorticoids, catecholamines, and insulin-like growth factor (IGF-1)
-
In addition to calorie-restricted ketogenic diets, psychological stress management involving exercise, yoga, music etc. also act as press disturbances that can help reduce fatigue, depression, and anxiety in cancer patients and in animal models
-
This physiological state also enhances the efficacy of chemotherapy and radiation therapy, while reducing the side effects
-
lower dosages of chemotherapeutic drugs can be used when administered together with calorie restriction or restricted ketogenic diets (KD-R)
-
Besides 2-DG, a range of other glycolysis inhibitors might also produce similar therapeutic effects when combined with the KD-R including 3-bromopyruvate, oxaloacetate, and lonidamine
-
It is important to recognize, however, that the radiotherapy used in glioma patients can damage the respiration of normal cells and increase availability of glutamine in the microenvironment, which can increase risk of tumor recurrence especially when used together with the steroid drug dexamethasone
-
Poff and colleagues demonstrated that hyperbaric oxygen therapy (HBOT) enhanced the ability of the KD to reduce tumor growth and metastasis
-
The effects of the KD and HBOT can be enhanced with administration of exogenous ketones, which further suppressed tumor growth and metastasis
-
Besides HBOT, intravenous vitamin C and dichloroacetate (DCA) can also be used with the KD to selectively increase oxidative stress in tumor cells
-
Recent evidence also shows that ketone supplementation may enhance or preserve overall physical and mental health
-
Some tumors use glucose as a prime fuel for growth, whereas other tumors use glutamine as a prime fuel [102, 186, 262, 263, 264]. Glutamine-dependent tumors are generally less detectable than glucose-dependent under FDG-PET imaging, but could be detected under glutamine-based PET imaging
-
Many of the current treatments used for cancer management are based on the view that cancer is a genetic disease
-
Emerging evidence indicates that cancer is a mitochondrial metabolic disease that depends on availability of fermentable fuels for tumor cell growth and survival
-
Glucose and glutamine are the most abundant fermentable fuels present in the circulation and in the tumor microenvironment
-
Low-carbohydrate, high fat-ketogenic diets coupled with glycolysis inhibitors will reduce metabolic flux through the glycolytic and pentose phosphate pathways needed for synthesis of ATP, lipids, glutathione, and nucleotides
10More
shared by Nathan Goodyear on 17 Nov 16
- No Cached
PLOS ONE: The Ketogenic Diet and Hyperbaric Oxygen Therapy Prolong Survival in Mice wit... - 0 views
journals.plos.org/...article
ketogenic ketogenic diet ketones ketone bodies cancer nutrition diet hyperbaric oxygen hyperbaric therapy hyperbaric
![](/images/link.gif)
-
This finding strongly supports the efficacy of the KD and HBO2T as therapies to inhibit tumor progression and prolong survival in animals with metastatic cancer.
-
We found that the KD fed ad libitum significantly increased mean survival time in mice with metastatic cancer
-
Ketogenic diets are also known to have an appetite suppressing effect which may contribute to body weight loss
- ...5 more annotations...
-
KD with HBO2T. Combining these therapies nearly doubled survival time in mice with metastatic cancer,
-
low carbohydrate or ketogenic diets promote weight loss in overweight individuals, they are also known to spare muscle wasting during conditions of energy restriction and starvation
-
dietary-induced therapeutic ketosis in a cancer patient would prevent muscle wasting similarly as it does with athletes undergoing intense exercise
-
when given as an adjuvant treatment to advanced cancer patients, the KD improves quality of life and enhances the efficacy of chemotherapy treatment in the clinic
-
mouse study finds that ketogenic diet plus hyperbaric O2 treatment prolongs survival.
-
Hey Dear Check Out Our Online Shopping store in all Over Pakistan.As Seen as On Tv Products Like as Health Beauty,Fitness,Homeware,Kitchenware,And Other Electronic Products in Pakistan Check Out Now| www.openTeleshop.Com
1More
Crescent pyramid and drop-set systems do not promote greater strength gains, muscle hyp... - 0 views
1More
The development, retention and decay rates of strength and power in elite rugby union, ... - 0 views
1More
shared by Nathan Goodyear on 14 Sep 17
- No Cached
Making the Right Fish Choices: Fatty Acid Contents of 33 Different Fish Species. Plus: ... - 0 views
suppversity.blogspot.com/...t-fish-choices-fatty-acid.html
omega 3 omega-3 omega-6 fish nutrition diet
![](/images/link.gif)
8More
Effects of short-term high-fat overfeeding on genome-wide DNA methylation in the skelet... - 0 views
-
The induction of DNA methylation changes after 5 days of HFO supports the growing awareness of DNA methylation as a dynamic signal that is possibly relevant to short-term day-to-day metabolic adaptations, including acute exercise
- ...4 more annotations...
-
Diverging DNA methylation levels between elderly, but not young, genetically identical twins indicate that environmental exposures throughout life may permanently influence DNA methylation, suggesting some preservation of de novo DNA methylation in adults
-
our finding of a slow reversibility rate indicates the demethylation process may be somewhat impeded compared with the induction of methylation changes by diet, which could have implications for the preservation or build-up of CpG methylation over time
-
A slow reversibility of DNA methylation induced by carcinogenic agents has likewise been observed due to ingestion of high-fat diets in rodents
31More
Ibuprofen alters human testicular physiology to produce a state of compensated hypogona... - 0 views
-
We found an 18% decrease (P = 0.056) in the ibuprofen group compared with the placebo group after 14 d (Fig. 1A) and a 23% decrease (P = 0.02) after 44 d (Fig. 1C). Taken together, these in vivo data suggest that ibuprofen induced a state of compensated hypogonadism during the trial, which occurred as early as 14 d and was maintained until the end of the trial at 44 d
- ...27 more annotations...
-
We first investigated testosterone production after 24 and 48 h of ibuprofen exposure to assess its effects on Leydig cell steroidogenesis. Inhibition of testosterone levels was significant and dose-dependent (β = −0.405, P = 0.01 at 24 h and β = −0.664, P < 0.0001 at 48 h) (Fig. 2A) and was augmented over time
-
The AMH data show that the hypogonadism affected not only Leydig cells but also Sertoli cells and also occurred as early as 14 d of administration
-
Sertoli cell activity showed that AMH levels decreased significantly with ibuprofen administration, by 9% (P = 0.02) after 14 d (Fig. 1B) and by 7% (P = 0.05) after 44 d compared with the placebo group
-
Examination of the effect of ibuprofen exposure on both the ∆4 and ∆5 steroid pathways (Fig. 2B) showed that it generally inhibited all steroids from pregnenolone down to testosterone and 17β-estradiol; the production of each steroid measured decreased at doses of 10−5–10−4 M. Under control conditions, production of androstenediol and dehydroepiandrosterone (DHEA) was below the limit of detection except in one experiment with DHEA
-
Measuring the mRNA expression of genes involved in steroidogenesis in vitro showed that ibuprofen had a profound inhibitory effect on the expression of these genes (Fig. 3 B–D), consistent with that seen above in our ex vivo organ model. Taken together, these data examining effects on the endocrine cells confirm that ibuprofen-induced changes in the transcriptional machinery were the likely reason for the inhibition of steroidogenesis.
-
Suppression of gene expression concerned the initial conversion of cholesterol to the final testosterone synthesis. Hence, expression of genes involved in cholesterol transport to the Leydig cell mitochondria was impaired
-
A previous study reported androsterone levels decreased by 63% among men receiving 400 mg of ibuprofen every 6 h for 4 wk
-
We next examined the gene expression involved in testicular steroidogenesis ex vivo and found that levels of expression of every gene that we studied except CYP19A1 decreased after exposure for 48 h compared with controls
-
the changes in gene expression indicate that the transcriptional machinery behind the endocrine action of Leydig cells was most likely impaired by ibuprofen exposure.
-
Together, these data show that ibuprofen also directly impairs Sertoli cell function ex vivo by inhibiting transcription
-
ibuprofen use in men led to (i) elevation of LH; (ii) a decreased testosterone/LH ratio and, to a lesser degree, a decreased inhibin B/FSH ratio; and (iii) a reduction in the levels of the Sertoli cell hormone AMH
-
The decrease in the free testosterone/LH ratio resulted primarily from the increased LH levels, revealing that testicular responsiveness to gonadotropins likely declined during the ibuprofen exposure. Our data from the ex vivo experiments support this notion, indicating that the observed elevation in LH resulted from ibuprofen’s direct antiandrogenic action
-
AMH levels were consistently suppressed by ibuprofen both in vivo and ex vivo, indicating that this hormone is uncoupled from gonadotropins in adult men. The ibuprofen suppression of AMH further demonstrated that the analgesic targeted not only the Leydig cells but also the Sertoli cells, a feature encountered not only in the human adult testis but also in the fetal testis
-
ibuprofen displayed broad transcription-repression abilities involving steroidogenesis, peptide hormones, and prostaglandin synthesis
-
a chemical compound, through its effects on the signaling compounds, can result in changes in the testis at gene level, resulting in perturbations at higher physiological levels in the adult human
-
The analgesics acetaminophen/paracetamol and ibuprofen have previously been shown to inhibit the postexercise response in muscles by repressing transcription
-
Previous ex vivo studies on adult testis have indeed pointed to an antiandrogenicity, only on Leydig cells, of phthalates (41), aspirin, indomethacin (42), and bisphenol A (BPA) and its analogs
-
ibuprofen’s effects were not restricted to Leydig and Sertoli cells, as data showed that the expression of genes in peritubular cells was also affected
-
In the clinical setting, compromised Leydig cell function resulting in increased insensitivity to LH is defined as compensated hypogonadism (4), an entity associated with all-cause mortality
-
compensated hypogonadic men present with an increased likelihood of reproductive, cognitive, and physical symptoms
-
an inverse relationship was recently reported between endurance exercise training and male sexual libido
-
AMH concentrations are lower in seminal plasma from patients with azoospermia than from men with normal sperm levels
-
inhibin B is a key clinical marker of reproductive health (32). The function of AMH, also secreted by Sertoli cells, and its regulation through FSH remain unclear in men
-
the striking dual effect of ibuprofen observed here on both Leydig and Sertoli cells makes this NSAID the chemical compound, of all the chemical classes considered, with the broadest endocrine-disturbing properties identified so far in men.
Testosterone and cortisol in relationship to dietary nutrients and resistance exercise ... - 0 views
Interactions of Gut Microbiota, Endotoxemia, Immune Function, and Diet in Exertional He... - 0 views
Impact of COVID-19 on physical activity: A rapid review - PMC - 0 views
Physical Activity and Cancer Risk. Actual Knowledge and Possible Biological Mechanisms ... - 0 views
1More