Glutamine is a major metabolic fuel for both brain tumor cells and tumor-associated macrophages (TAMs)
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How Posture Affects your Concentration - 0 views
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Posture may be one of the most overlooked aspects of health but it affects most of our body and mental functions. If you want to be a whole new person with the perfect mental sharpness, you can always seek assistance from posture or fitness experts.
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Good place to start on the understanding, yet oversimplified. The dosage has to be individually determined based on tumor burden, body size...A one size fits all approach never works. One cannot simple treat statistics; but, instead, must treat people...which are not statistics.
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In a single sentence, my experience of India and about the surgeon has been incredible. I really can't comment the Dr. Naresh Trehan enough. I had no problem coming again. It cost him only £4,800 and that included the cost of my flight from Congo to India and back. I feel very fit and fine now than what I was feeling earlier."
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Vitamin C for Sepsis and Septic Shock - PubMed - 0 views
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Review article on vitamin C in the treatment of sepsis and septic shock. The most common dose is 1.5 gram Q6 is inadequate secondary to all the constraints on vitamin C, i.e., 1/2 life, metabolic demands, deficiency, weight, inflammation…A one size fits all approach never WORKS!
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Metabolic management of brain cancer - 0 views
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the malignant phenotype of brain tumor cells that survive radiotherapy is often greater than that of the cells from the original tumor.
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Conventional chemotherapy has faired little better than radiation therapy for the long-term management of malignant brain cancer
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most conventional radiation and brain cancer chemotherapies can enhance glioma energy metabolism and invasive properties, which would contribute to tumor recurrence and reduced patient survival [34].
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We contend that all cancer regardless of tissue or cellular origin is a disease of abnormal energy metabolism
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complex disease phenotypes can be managed through self-organizing networks that display system wide dynamics involving oxidative and non-oxidative (substrate level) phosphorylation
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As long as brain tumors are provided a physiological environment conducive for their energy needs they will survive; when this environment is restricted or abruptly changed they will either grow slower, growth arrest, or perish [8] and [19]
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New information also suggests that ketones are toxic to some human tumor cells and that ketones and ketogenic diets might restrict availability of glutamine to tumor cells [68], [69] and [70].
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The success in dealing with environmental stress and disease is therefore dependent on the integrated action of all cells in the organism
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Tumor cells survive in hypoxic environments not because they have inherited genes making them more fit or adaptable than normal cells, but because they have damaged mitochondria and have thus acquired the ability to derive energy largely through substrate level phosphorylation
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Cancer cells survive and multiply only in physiological environments that provide fuels (mostly glucose and glutamine) subserving their requirement for substrate level phosphorylation
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Integrity of the inner mitochondrial membrane is necessary for ketone body metabolism since β-hydroxybutyrate dehydrogenase, which catalyzes the first step in the metabolism of β-OHB to acetoacetate, interacts with cardiolipin and other phospholipids in the inner membrane
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the mitochondria of many gliomas and most tumors for that matter are dysfunctional
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Cardiolipin is essential for efficient oxidative energy production and mitochondrial function
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Any genetic or environmental alteration in the content or composition of cardiolipin will compromise energy production through oxidative phosphorylation
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The Crabtree effect involves the inhibition of respiration by high levels of glucose
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the Warburg effect involves elevated glycolysis from impaired oxidative phosphorylation
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the Crabtree effect can be reversible, the Warburg effect is largely irreversible because its origin is with permanently damaged mitochondria
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The continued production of lactic acid in the presence of oxygen is the metabolic hallmark of most cancers and is referred to as aerobic glycolysis or the Warburg effect
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We recently described how the retrograde signaling system could induce changes in oncogenes and tumor suppressor genes to facilitate tumor cell survival following mitochondrial damage [48].
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In addition to glycolysis, glutamine can also increase ATP production under hypoxic conditions through substrate level phosphorylation in the TCA cycle after its metabolism to α-ketoglutarate
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mitochondrial lipid abnormalities, which alter electron transport activities, can account in large part for the Warburg effect
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targeting both glucose and glutamine metabolism could be effective for managing most cancers including brain cancer
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The bulk of experimental evidence indicates that mitochondria are dysfunctional in tumors and incapable of generating sufficient ATP through oxidative phosphorylation
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Cardiolipin defects in tumor cells are also associated with reduced activities of several enzymes of the mitochondrial electron transport chain making it unlikely that tumor cells with cardiolipin abnormalities can generate adequate energy through oxidative phosphorylation
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The Crabtree effect involves the inhibition of respiration by high levels of glucose
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Warburg effect involves elevated glycolysis from impaired oxidative phosphorylation
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TCA cycle substrate level phosphorylation could therefore become another source of ATP production in tumor cells with impairments in oxidative phosphorylation
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Caloric restriction, which lowers glucose and elevates ketone bodies [63] and [64], improves mitochondrial respiratory function and glutathione redox state in normal cells
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DR naturally inhibits glycolysis and tumor growth by lowering circulating glucose levels, while at the same time, enhancing the health and vitality of normal cells and tissues through ketone body metabolism
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DR is anti-angiogenic
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DR also reduces angiogenesis in prostate and breast cancer
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We suggest that apoptosis resistance arises largely from enhanced substrate level phosphorylation of tumor cells and to the genes associated with elevated glycolysis and glutaminolysis, e.g., c-Myc, Hif-1a, etc, which inhibit apoptosis
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Modern medicine has not looked favorably on diet therapies for managing complex diseases especially when well-established procedures for acceptable clinical practice are available, regardless of how ineffective these procedures might be in managing the disease
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More than 60 years of clinical research indicates that such approaches are largely ineffective in extending survival or improving quality of life
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The process is rooted in the well-established scientific principle that tumor cells are largely dependent on substrate level phosphorylation for their survival and growth
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Glucose and glutamine drive substrate level phosphorylation
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targeting the glycolytically active tumor cells that produce pro-cachexia molecules, restricted diet therapies can potentially reduce tumor cachexia
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It is important to recognize, however, that “more is not better” with respect to the ketogenic diet
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Blood glucose ranges between 3.0 and 3.5 mM (55–65 mg/dl) and β-OHB ranges between 4 and 7 mM should be effective for tumor management
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Dr Seyfriend presents his metabolic approach to the treatment of brain cancer.
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Changes in cortisol and testostero... [J Sports Med Phys Fitness. 2000] - PubMed - NCBI - 0 views
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anabolic catabolic long endurance training competition T:C testosterone cortisol sports athlete athletics
shared by Nathan Goodyear on 19 Feb 13
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long endurance competitive events associated with catabolic hormone balances found in a low T:C ratio. This occurs primarily through an elevation in cortisol and small drop in Testosterone. The recovery phase is anabolic through a rise in T:C, primarily through a return to baseline by cortisol and an increase in Testosterone.
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Telomerase at the intersection of cancer and aging - 0 views
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telomere telomeres telomerase telomerase activator aging disease cancer
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The anti-aging role of telomerase has been demonstrated to be largely mediated by its canonical role in elongating telomeres, which prevents the accumulation of critically short telomeres and loss of tissue homeostasis
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Short telomeres, and subsequent DDR activation, could occur both in cancer and aging
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increased abundance of short telomeres correlates with higher genomic instability and decreased longevity in various organisms, including mice, zebrafish, and yeast
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mice deficient for telomerase or for telomere binding proteins are characterized by accelerated age-related defects
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In humans, short telomeres are considered good indicators of an individual’s health status and correlate with both genetic and environmental factors
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Although recent findings strongly support the idea that short telomeres drive several age-related diseases 38 we cannot exclude the possibility that in some situations short telomeres may be a consequence of the disease itself.
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the current view is that telomerase deficiency may contribute to the early steps of cancer development by fueling chromosomal instability, while subsequent activation of telomerase may be necessary to allow tumor growth and tumor progression towards more malignant states
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telomerase activation can be an early event in cancer, it is not necessary for cancer initiation
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telomerase can stimulate tumor progression by ensuring maintenance of telomeres above a critically short length, thus preventing induction of cellular senescence or apoptosis
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Almost all human cancers present activation of telomerase as a hallmark, most likely as a mechanism to allow unlimited cell proliferation of tumor cells
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recent evidence demonstrated that short telomeres alone could lead to genomic instability and cancer
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Getting rid of telomerase can also be problematic; the lack of telomerase could lead to increased chromosomal instability, which in turn could be at the basis for cancer initiation when tumor suppressor barriers are bypassed
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telomerase activation is a potential therapeutic strategy for the treatment of age-related diseases
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telomerase activation in adult or old mice by means of a gene therapy strategy was shown to be sufficient to improve metabolic fitness, neuromuscular capacity, and prevent bone loss, as well as significantly increase both median and maximum longevity, without increased cancer incidence
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These studies suggest that telomerase expression could be considered a feasible approach to reverse tissue dysfunction and extend healthy lifespan without increasing cancer incidence
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humans almost completely lose telomerase activity from somatic tissues in the adulthood
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a change of paradigm seems to be occurring in telomerase biology, with a switch from viewing telomerase as fueling cancer to reversing aging
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Telomerase expression in a background of high levels of tumor suppressors or in aged organisms seems to prevent its expected pro-cancer activity and yet it still functions as an anti-aging factor
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Telomerase activity and longer telomere length is shown to correlated inversely with many chronic diseases of aging. In contrast, telomerase activity is found to be involved in carcinogenesis. Increased carcinogenic potential of telomerase activity has not borne out in studies. In addition, increased CD8 cell activity as a result of telomerase activation will actually decrease carcinogenic potential via NK activation.
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Testosterone and glucose metabolism in men: current concepts and controversies - 0 views
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80% of E2 production in men, that will cause low T in men, comes from SQ adiposity. This leads to increase in visceral adiposity.
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Only 5% of men with type 2 diabetes have elevated LH levels (Dhindsa et al. 2004, 2011). This is consistent with recent findings that the inhibition of the gonadal axis predominantly takes place in the hypothalamus, especially with more severe obesity
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Metabolic factors, such as leptin, insulin (via deficiency or resistance) and ghrelin are believed to act at the ventromedial and arcuate nuclei of the hypothalamus to inhibit gonadotropin-releasing hormone (GNRH) secretion
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kisspeptin has emerged as one of the most potent secretagogues of GNRH release
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Consistent with the hypothesis that obesity-mediated inhibition of kisspeptin signalling contributes to the suppression of the HPT axis, infusion of a bioactive kisspeptin fragment has been recently shown to robustly increase LH pulsatility, LH levels and circulating testosterone in hypotestosteronaemic men with type 2 diabetes
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Figure 4
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Interestingly, a recent 16-week study of experimentally induced hypogonadism in healthy men with graded testosterone add-back either with or without concomitant aromatase inhibitor treatment has in fact suggested that low oestradiol (but not low testosterone) may be responsible for the hypogonadism-associated increase in total body and intra-abdominal fat mass
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This does not fit with the research on receptors, specifically estrogen receptors. These studies that the authors are referencing are looking at "circulating" levels, not tissue levels.
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A smaller study with a similar experimental design found that acute testosterone withdrawal reduced insulin sensitivity independent of body weight, whereas oestradiol withdrawal had no effects
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Obesity and dysglycaemia and associated comorbidities such as obstructive sleep apnoea (Hoyos et al. 2012b) are important contributors to the suppression of the HPT axis
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This is supported by observational studies showing that weight gain and development of diabetes accelerate the age-related decline in testosterone
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Weight loss can reactivate the hypothalamic–pituitary–testicular axis
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The hypothalamic–pituitary–testicular axis remains responsive to treatment with aromatase inhibitors or selective oestrogen receptor modulators in obese men
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Kisspeptin treatment increases LH secretion, pulse frequency and circulating testosterone levels in hypotestosteronaemic men with type 2 diabetes
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Several observational and randomised studies reviewed in Grossmann (2011) have shown that weight loss, whether by diet or surgery, leads to substantial increases in testosterone, especially in morbidly obese men
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This suggests that weight loss can lead to genuine reactivation of the gonadal axis by reversal of obesity-associated hypothalamic suppression
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There is pre-clinical and observational evidence that chronic hyperglycaemia can inhibit the HPT axis
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in those men in whom glycaemic control worsened, testosterone decreased
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successful weight loss combined with optimisation of glycaemic control may be sufficient to normalise circulating testosterone levels in the majority of such men
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weight loss, optimisation of diabetic control and assiduous care of comorbidities should remain the first-line approach.
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In part, the discrepant results may be due to the fact men in the Vigen cohort (Vigen et al. 2013) had a higher burden of comorbidities. Given that one (Basaria et al. 2010), but not all (Srinivas-Shankar et al. 2010), RCTs in men with a similarly high burden of comorbidities reported an increase in cardiovascular events in men randomised to testosterone treatment (see section on Testosterone therapy: potential risks below) (Basaria et al. 2010), testosterone should be used with caution in frail men with multiple comorbidities
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The retrospective, non-randomised and non-blinded design of these studies (Shores et al. 2012, Muraleedharan et al. 2013, Vigen et al. 2013) leaves open the possibility for residual confounding and multiple other sources of bias. These have been elegantly summarised by Wu (2012).
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Effects of testosterone therapy on body composition were metabolically favourable with modest decreases in fat mass and increases in lean body mass
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This suggests that testosterone has limited effects on glucose metabolism in relatively healthy men with only mildly reduced testosterone.
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it is conceivable that testosterone treatment may have more significant effects on glucose metabolism in uncontrolled diabetes, akin to what has generally been shown for conventional anti-diabetic medications.
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the evidence from controlled studies show that testosterone therapy consistently reduces fat mass and increases lean body mass, but inconsistently decreases insulin resistance.
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Interestingly, testosterone therapy does not consistently improve glucose metabolism despite a reduction in fat mass and an increase in lean mass
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the majority of RCTs (recently reviewed in Ng Tang Fui et al. (2013a)) showed that testosterone therapy does not reduce visceral fat
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visceral and abdominal adiposity are biologically different and thus the risks associated with the two are different.
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yet low T is associated with an increase in visceral adiposity--confusing!
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testosterone therapy decreases SHBG
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testosterone is inversely associated with total cholesterol, LDL cholesterol and triglyceride (Tg) levels, but positively associated with HDL cholesterol levels, even if adjusted for confounders
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Although observational studies show a consistent association of low testosterone with adverse lipid profiles, whether testosterone therapy exerts beneficial effects on lipid profiles is less clear
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Whereas testosterone-induced decreases in total cholesterol, LDL cholesterol and Lpa are expected to reduce cardiovascular risk, testosterone also decreases the levels of the cardio-protective HDL cholesterol. Therefore, the net effect of testosterone therapy on cardiovascular risk remains uncertain.
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data have not shown evidence that testosterone causes prostate cancer, or that it makes subclinical prostate cancer grow
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compared with otherwise healthy young men with organic androgen deficiency, there may be increased risks in older, obese men because of comorbidities and of decreased testosterone clearance
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recent evidence that fat accumulation may be oestradiol-, rather than testosterone-dependent
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Best Lower body workouts for women - Fitness Dada - 0 views
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It is a myth that lower body workouts can be performed with the health club's machines. If you really want to reshape or resize the lower body part then you need the gender appropriate and well-framed exercise program that can be done from home.
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