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Nathan Goodyear

Testosterone replacement therapy and the risk of prostate cancer - 0 views

www.ncbi.nlm.nih.gov/...PMC4814970

Testosterone testosterone therapy saturation theory cancer prostate cancer male hormones

shared by Nathan Goodyear on 01 Oct 16 - No Cached
  • When the level of circulating androgen is below normal, some androgen receptors are inactive, and the secondary downstream effects are decreased. Once androgen receptors within the prostate are saturated, however, increasing testosterone will no longer have an effect
  • the saturation point is thought to occur at low physiologic testosterone levels
  • Only the subset of individuals with pretreatment testosterone level <250 ng dl−1 had PSA level correlating with free and total testosterone level
  • ...7 more annotations...
  • none of the men stopped testosterone supplementation due to prostate cancer recurrence, and none demonstrated cancer progression
  • PSA level did transiently rise in one patient; however, none exceeded a PSA of 1.5 ng ml−1 to raise concern for biochemical recurrence
  • after 19 months on TRT, 10 hypogonadal patients with a history of undergoing a radical retropubic prostatectomy for prostate cancer had no PSA recurrence and had statistically significant improvements in serum total testosterone and hypogonadal symptoms
  • Similarly, Kaufman and Graydon14 examined case records of seven hypogonadal men who had undergone curative RP with symptoms of hypogonadism and low serum testosterone levels treated with testosterone replacement. No biochemical or clinical evidence of cancer recurrence was noted
  • In a much larger case series, Khera et al.15 reviewed the records of 57 men who received TRT following RP. After an average of 36 months following RP, testosterone replacement was initiated and followed for an average of 13 months. Mean testosterone values rose significantly and once again, there was no increase in PSA values and, therefore, no diagnosed biochemical recurrence
  • Four of the patients in the treatment group were found to have cancer recurrence, compared with eight in the control group
  • All biochemical recurrences were seen in individuals with high-risk disease
  • Nathan Goodyear on 01 Oct 16
     
    Good review of data on Testosterone therapy and prostate cancer risk: the take home is there is no increased risk.  Also, included is a discussion of the prostate saturation theory.
Nathan Goodyear

Role of maximum standardized uptake value in fluorodeoxyglucose positron emission tomog... - 0 views

www.ncbi.nlm.nih.gov/...PMC3785187

PET scan PET_CT scan maxSUV cancer breast

shared by Nathan Goodyear on 19 Mar 18 - No Cached
  • 18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT) is an effective and popular technique for evaluating patients before and after breast cancer surgery.
  • Quantitative FDG-PET/CT imaging is becoming prevalent in cancer treatment as it measures glucose metabolism that reflects the growth potential and metabolic activity of malignant tumors
  • The FDG-PET/CT findings of primary lesions in colorectal and lung cancers correlate with metastasis and prognosis because FDG reflects tumor viability
  • ...15 more annotations...
  • The technique is valuable for predicting the prognosis of patients with recurrent breast cancer and for determining and predicting the outcomes of neoadjuvant chemotherapy
  • FDG-PET/CT is useful not only for evaluating metastasis but also for predicting the prognosis of recurrent breast cancer and measuring treatment effects
  • reports remain limited to small-scale clinical trials of about 100 patients.
  • MaxSUV, which is the most popular FDG-PET/CT value, can vary up to 30 % because of differences among PET/CT devices and among the operators who create the images
  • the degree of malignancy would increase with an increase in maxSUV when ER or HER-2 signaling is involved.
  • Factors that determine the rate of cancer progression include T-factor (tumor diameter) and N-factor (presence or absence/number of lymph node metastasis)
  • The prognostic factors applied in breast cancer can be broadly divided into those that determine staging and those that determine biological tumor characteristics
  • Prognosis was previously predicted based on T, N, and M staging, which indicates the degree of progression. However, prognosis is now predicted and treatment regimes are presently selected by also considering ER and HER-2 levels, which determine the nature of the tumor
  • maxSUV presently serves as an indicator of metabolic activity during cancer therapy. For instance, the maxSUV of primary lung and hematological cancer lesions correlates with metastasis and prognosis, whereas maxSUV also seems useful for predicting the prognosis of recurrent breast cancer and in determining and predicting the outcome of neoadjuvant chemotherapy
  • The maxSUV cut-off calculated from ROC curves for recurrence was 3.0
  • Factors that determine the nature of tumors also include ER, HER-2, Ki-67 labeling index, and nuclear grade
  • both ER status and maxSUV as independent prognostic factors
  • maxSUV has a closer correlation with prognosis
  • maxSUV, clinical T-factor and ER were significant prognostic factors
  • Our results showed that maxSUV has the potential to be a novel prognostic factor and that it can be used to determine future therapies
  • Nathan Goodyear on 19 Mar 18
     
    Retrospective, multi-facility finds maxSUV can be used in prognosis in cancer.  Others have shown benefit in recurrence risk.  MaxSUV was found to be an independent factor.
Nathan Goodyear

Testosterone Replacement Therapy in Patients with Prostate Cancer After Radical Prostat... - 0 views

www.ncbi.nlm.nih.gov/...PMC4544840

Testosterone low T low Testosterone Testosterone therapy prostate cancer PSA biochemical recurrence male hormones hormones cancer prostate

shared by Nathan Goodyear on 10 Oct 16 - No Cached
  • Nathan Goodyear on 10 Oct 16
     
    One of the largest studies to date on Testosterone therapy in men post radical prostatectomy for prostate cancer.  This study supports the use of Testosterone therapy in this men with close f/u. A higher biochemical recurrence rate was found in the control group versus the treatment group, though there were 4 with biochemical recurrences in the treatment group.
Nathan Goodyear

Full article: Local recurrence of brain metastasis reduced by intra-operative hyperther... - 0 views

www.tandfonline.com/...02656736.2018.1488004

hyperthermia metastasis recurrence brain cancer local recurrence

shared by Nathan Goodyear on 26 Apr 21 - No Cached
  • Nathan Goodyear on 26 Apr 21
     
    Hyperthermia reduces recurrence risk by 55% of metastatic brain cancer after surgery over conventional therapies.
Nathan Goodyear

Testosterone replacement for hypogonadism after treatment of early prostate cancer with... - 0 views

www.ncbi.nlm.nih.gov/...17183557

low T low Testosterone Testosterone therapy Testosterone prostate prostate cancer

shared by Nathan Goodyear on 18 Sep 16 - No Cached
  • Nathan Goodyear on 18 Sep 16
     
    Testosterone therapy post brachytherapy radiation found to have no recurrence and/or documented cancer progression in follow up out to 9 years.  Not all the men included in this study had none detectable psa levels.  PSA levels were all less than 1 ng/ml; 74.2% were none detectable, but 22% were detectable up to 0.5 ng/ml.  One of the patients had a transient rise in psa, but no recurrence or cancer progression was noted, and therapy was continued.
Nathan Goodyear

Natural Killer Cells in Pregnancy and Recurrent Pregnancy Loss: Endocrine and Immunolog... - 0 views

edrv.endojournals.org/...44.full

natural killer cells pregnancy loss recurrent immune system miscarriage NK

shared by Nathan Goodyear on 15 Apr 12 - No Cached
  • NK cells have been the cells most extensively studied, primarily because they constitute the predominant leukocyte population present in the endometrium at the time of implantation and in early pregnancy
  • parental chromosomal abnormalities, uterine anatomic anomalies, endometrial infections, endocrine etiologies (luteal phase defect, thyroid dysfunction, uncontrolled diabetes mellitus), antiphospholipid syndrome, inherited thrombophilias, and alloimmune causes
  • estrogen
  • ...28 more annotations...
  • progesterone
  • prolactin
  • In summary, in vivo animal experiments have shown an inhibitory role of estrogen on peripheral NK cell lytic activity, which is partly due to suppression of NK cell output by the bone marrow and partly due to suppression of individual NK cell cytotoxicity. However, in vitro studies so far have failed to show conclusively a direct effect of estrogen on NK cells.
  • At the progesterone concentrations believed to be present in the uterus [up to 10−5 m at the maternal-fetal interface (35)], studies consistently show inhibition of lymphocyte proliferation (33) and inhibition of NK cytolytic activity in vitro
  • The exact role of prolactin in NK cell regulation is unknown.
  • The overall effects of estrogen on NK cells are likely multifactorial, therefore, and depend on the type of cell affected as well as the kind of ER expressed by that cell.
  • It is known that progesterone can directly affect T cell differentiation in vitro, suppressing development of the Th1 pathway and enhancing differentiation along the Th2 pathway (44)
  • Th1 cells predominantly produce interferon-γ (IFN-γ), IL-2, and TNF-β and are involved in cell-mediated immunity. Th2 cells produce IL-4, IL-5, IL-6, IL-10, and IL-13 and stimulate humoral immunity
  • Furthermore, in response to progesterone, γδ T cells produce progesterone-induced blocking factor (PIBF) (54
  • A defining characteristic of NK cells is their ability to lyse target cells without prior sensitization and without restriction by HLA antigens.
  • NK cell function is mainly regulated by IL-2 and IFN-γ
  • IL-2 causes both NK cell proliferation and enhanced cytotoxicity. IFN-γ augments NK cytolytic activity, but does not cause NK proliferation. The two cytokines act synergistically to augment NK cytotoxicity (6).
  • The largest leukocyte population in the endometrium consists of NK cells named large granulated lymphocytes
  • there is a significant increase in the number of uNK cells throughout the secretory phase, which peaks in early pregnancy when uNK cells comprise about 75% of uterine leukocytes (62)
  • Second, uNK cell phenotype changes during the normal menstrual cycle and early pregnancy (68)
  • general proinflammatory effect of estrogen, causing an influx of macrophages and neutrophils, which is antagonized by progesterone through its receptor (70, 71).
  • The mechanism of such a progesterone-induced local immunosuppression is unclear.
  • progesterone plays an important role in proliferation and differentiation of uNK cells (32).
  • Through promotion of a uterine Th2 environment, progesterone could indirectly affect uNK cell function
  • The mechanism of this increase in uNK cell numbers has been addressed in both human and mouse models, and is likely the result of: 1) recruitment of peripheral NK cells to the uterus, and 2) proliferation of existing uNK cells
  • prolactin system plays an important role in implantation and the maintenance of pregnancy
  • the exact pathways of hormonal regulation of NK cells remain to be delineated.
  • The exact function of uNK cells has not yet been unequivocally determined
  • uNK cells express a different cytokine profile, compared with resting peripheral NK cells. mRNAs for granulocyte CSF, M-CSF, GM-CSF, TNF-α, IFN-γ, TGF-β, and leukemia inhibitory factor (LIF) have been found in decidual CD56+ cells
  • Their increased numbers in early pregnancy, their hormonal dependence, and their close proximity to the infiltrating trophoblast all suggest that they play an important role in the regulation of the maternal immune response to the fetal allograft and the control of trophoblast growth and invasion during human pregnancy
  • role of uNK cell-derived cytokines on trophoblast growth and differentiation (114, 115, 116, 117).
  • Th1 immunity to trophoblast is associated with RPL, whereas Th2 immunity is associated with a successful pregnancy
  • RPL is associated with Th1 immunity, for which NK cells are partly responsible.
  • Nathan Goodyear on 15 Apr 12
     
    dysregulated immune system plays role in recurrent miscarriage.  Specifically, this article discusses natural killer cells (NK).
Nathan Goodyear

Vitamin D and breast cancer recurrence in the Women's Healthy Eating and Living (WHEL) ... - 0 views

www.ajcn.org/...108.abstract

vitamin D breast cancer recurrence

shared by Nathan Goodyear on 01 Feb 12 - No Cached
  • Nathan Goodyear on 01 Feb 12
     
    Vitamin D shown to reduce breast cancer recurrence in premenopausal women.  Same association not found in postmenopausal women.
Nathan Goodyear

Excess Body Weight Associated With Increased Risk for Cancer Recurrence After Treatment... - 0 views

www.aacr.org/...aacr-in-the-news.aspx

prostate cancer obesity overweight men recurrence weight

shared by Nathan Goodyear on 16 May 12 - No Cached
  • Nathan Goodyear on 16 May 12
     
    overweight and obesity associated with higher risk of prostate cancer recurrence.  No surprise here.  Excess fat will increase inflammatory cytokines and aromatase conversion of Testosterone to Estradiol: also producing inflammation.
Nathan Goodyear

Preoperative hyperthermia combined with chemotherapy and radiotherapy for patients with... - 0 views

pubmed.ncbi.nlm.nih.gov/1293242

local recurrence cancer surgery hyperthermia

shared by Nathan Goodyear on 25 Apr 21 - No Cached
  • Nathan Goodyear on 25 Apr 21
     
    Hyperthermia + chemotherapy and radiation reduce local recurrence from surgery.
Nathan Goodyear

Stress And Fear Can Affect Cancer's Recurrence -- ScienceDaily - 0 views

www.sciencedaily.com/...080227142656.htm

cancer recurrence fear stress metastasis

shared by Nathan Goodyear on 07 Nov 20 - No Cached
  • Nathan Goodyear on 07 Nov 20
     
    Stress and fear suppress immune system increasing recurrence and metastasis.
Nathan Goodyear

Surgically induced accelerated local and distant tumor growth is significantly attenuat... - 0 views

pubmed.ncbi.nlm.nih.gov/15734421

cancer metastasis surgery

shared by Nathan Goodyear on 13 Aug 20 - No Cached
  • Nathan Goodyear on 13 Aug 20
     
    Cox II inhibition helps to slow surgical induced metastatic and local recurrence of cancer. Surgery does cause metastasis and local recurrence and cox II inhibition stops spread.
Nathan Goodyear

Luteal start vaginal micronized progesterone improves pregnancy success in women with r... - 0 views

www.fertstert.org/...abstract

progesterone infertility miscarriage pregnancy hormones women

shared by Nathan Goodyear on 18 Jan 17 - No Cached
  • Nathan Goodyear on 18 Jan 17
     
    Recurrent early pregnancy losses can be prevented not with provera, not with progestin, but with progesterone. The use of progesterone by the functional medicine movement has long been advocated and supported in the science; now the allopathic medicine will try to claim it as its own.
Nathan Goodyear

Effect of Coenzyme Q10 on Th1/Th2 Paradigm in Females with Idiopathic Recurrent Pregnan... - 0 views

www.ncbi.nlm.nih.gov/...25800618

CoQ10 pregnancy inflammation IFN-gamma

shared by Nathan Goodyear on 25 Apr 16 - No Cached
  • Nathan Goodyear on 25 Apr 16
     
    CoQ10 reduced Th1 inflammatory cytokines in those women with recurrent early pregnancy loss.  CoQ10 specifically, reduced IFN-gamma.
Nathan Goodyear

Studies on activity of... [J Huazhong Univ Sci Technolog Med Sci. 2004] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...15641696

preeclampsia NK cell immune tolerance pregnancy recurrent miscarriage miscarriages

shared by Nathan Goodyear on 19 Apr 12 - No Cached
  • Nathan Goodyear on 19 Apr 12
     
    As NK over activity has been shown to play in role in recurrent miscarriages, so it appears that loss if immune tolerance (elevated NK activity) may play a role in preeclampsia
Nathan Goodyear

Growth hormone treatment and risk of recurr... [Childs Nerv Syst. 2009] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...19142625

growth hormone growth cancer hormones

shared by Nathan Goodyear on 09 Jul 12 - No Cached
  • Nathan Goodyear on 09 Jul 12
     
    Growth hormone did not show to increase brain tumor progression or recurrence; this dispels the myth that GH causes/progresses cancer.
Nathan Goodyear

Metabolic syndrome as a prognostic factor for breast cancer recurrences - Pasanisi - 20... - 0 views

onlinelibrary.wiley.com/...full

Testosterone women metabolic syndrome metabolic syndrome breast cancer

shared by Nathan Goodyear on 12 Mar 14 - No Cached
  • Nathan Goodyear on 12 Mar 14
     
    Women with metabolic syndrome have increased recurrence of breast cancer after initial therapy.  Likewise, Increasing Testosterone was associated with increasing risk of metabolic syndrome.  This is the opposite of men.  One wonders what this massive doping of Testosterone that is underway is doing to women?  Are we merely feeding disease?
Nathan Goodyear

ScienceDirect - Homeopathy : Pharmacoeconomic comparison between homeopathic and antibi... - 0 views

www.sciencedirect.com/...S1475491604001298

homeopathy treatment antibiotic children cold flu rhinopharyngitis

shared by Nathan Goodyear on 27 Sep 11 - No Cached
  • Nathan Goodyear on 27 Sep 11
     
    head to head study of homeopathy and antibiotics shows homeopathy to be more effective in recurrent acute rhinopharyngitis in children
Nathan Goodyear

British Journal of Cancer - A pilot clinical study of [Delta]9-tetrahydrocannabinol in ... - 0 views

www.nature.com/...6603236a.html

THC cannabinoids cancer Tetrahydrocannabinol CBD

shared by Nathan Goodyear on 15 Dec 14 - No Cached
  • Nathan Goodyear on 15 Dec 14
     
    Pilot study of THC for advanced, recurrent glioblastoma multiforme.  The infused THC appeared to be safe and provide some anti proliferative activity, but all patients died within 1 year.
Nathan Goodyear

Cancer cells metabolically "fertilize" the tumor microenvironment with hydrogen peroxid... - 0 views

www.ncbi.nlm.nih.gov/...PMC3180189

cancer reverse warburg effect warburg effect NF-kapppB HIF-1alpha Cav-1 H2O2

shared by Nathan Goodyear on 12 Nov 14 - No Cached
  • reducing oxidative stress with powerful antioxidants, is an important strategy for cancer prevention, as it would suppress one of the key early initiating steps where DNA damage and tumor-stroma metabolic-coupling begins. This would prevent cancer cells from acting as metabolic “parasites
  • Oxidative stress in cancer-associated fibroblasts triggers autophagy and mitophagy, resulting in compartmentalized cellular catabolism, loss of mitochondrial function, and the onset of aerobic glycolysis, in the tumor stroma. As such, cancer-associated fibroblasts produce high-energy nutrients (such as lactate and ketones) that fuel mitochondrial biogenesis and oxidative metabolism in cancer cells. We have termed this new energy-transfer mechanism the “reverse Warburg effect.
  • Then, oxidative stress, in cancer-associated fibroblasts, triggers the activation of two main transcription factors, NFκB and HIF-1α, leading to the onset of inflammation, autophagy, mitophagy and aerobic glycolysis in the tumor microenvironment
  • ...38 more annotations...
  • oxidative stress and ROS, produced in cancer-associated fibroblasts, has a “bystander effect” on adjacent cancer cells, leading to DNA damage, genomic instability and aneuploidy, which appears to be driving tumor-stroma co-evolution
  • tumor cells produce and secrete hydrogen peroxide, thereby “fertilizing” the tumor microenvironment and driving the “reverse Warburg effect.”
  • This type of stromal metabolism then produces high-energy nutrients (lactate, ketones and glutamine), as well as recycled chemical building blocks (nucleotides, amino acids, fatty acids), to literally “feed” cancer cells
  • loss of stromal caveolin (Cav-1) is sufficient to drive mitochondrial dysfunction with increased glucose uptake in fibroblasts, mimicking the glycolytic phenotype of cancer-associated fibroblasts.
  • oxidative stress initiated in tumor cells is transferred to cancer-associated fibroblasts.
  • Then, cancer-associated fibroblasts show quantitative reductions in mitochondrial activity and compensatory increases in glucose uptake, as well as high ROS production
  • These findings may explain the prognostic value of a loss of stromal Cav-1 as a marker of a “lethal” tumor microenvironment
  • aerobic glycolysis takes place in cancer-associated fibroblasts, rather than in tumor cells, as previously suspected.
  • our results may also explain the “field effect” in cancer biology,5 as hydrogen peroxide secreted by cancer cells, and the propagation of ROS production, from cancer cells to fibroblasts, would create an increasing “mutagenic field” of ROS production, due to the resulting DNA damage
  • Interruption of this process, by addition of catalase (an enzyme that detoxifies hydrogen peroxide) to the tissue culture media, blocks ROS activity in cancer cells and leads to apoptotic cell death in cancer cells
  • In this new paradigm, cancer cells induce oxidative stress in neighboring cancer-associated fibroblasts
  • cancer-associated fibroblasts have the largest increases in glucose uptake
  • cancer cells secrete hydrogen peroxide, which induces ROS production in cancer-associated fibroblasts
  • Then, oxidative stress in cancer-associated fibroblast leads to decreases in functional mitochondrial activity, and a corresponding increase in glucose uptake, to fuel aerobic glycolysis
  • cancer cells show significant increases in mitochondrial activity, and decreases in glucose uptake
  • fibroblasts and cancer cells in co-culture become metabolically coupled, resulting in the development of a “symbiotic” or “parasitic” relationship.
  • cancer-associated fibroblasts undergo aerobic glycolysis (producing lactate), while cancer cells use oxidative mitochondrial metabolism.
  • We have previously shown that oxidative stress in cancer-associated fibroblasts drives a loss of stromal Cav-1, due to its destruction via autophagy/lysosomal degradation
  • a loss of stromal Cav-1 is sufficient to induce further oxidative stress, DNA damage and autophagy, essentially mimicking pseudo-hypoxia and driving mitochondrial dysfunction
  • loss of stromal Cav-1 is a powerful biomarker for identifying breast cancer patients with early tumor recurrence, lymph-node metastasis, drug-resistance and poor clinical outcome
  • this type of metabolism (aerobic glycolysis and autophagy in the tumor stroma) is characteristic of a lethal tumor micro-environment, as it fuels anabolic growth in cancer cells, via the production of high-energy nutrients (such as lactate, ketones and glutamine) and other chemical building blocks
  • the upstream tumor-initiating event appears to be the secretion of hydrogen peroxide
  • one such enzymatically-active protein anti-oxidant that may be of therapeutic use is catalase, as it detoxifies hydrogen peroxide to water
  • numerous studies show that “catalase therapy” in pre-clinical animal models is indeed sufficient to almost completely block tumor recurrence and metastasis
  • by eliminating oxidative stress in cancer cells and the tumor microenvironment,55 we may be able to effectively cut off the tumor's fuel supply, by blocking stromal autophagy and aerobic glycolysis
  • breast cancer patients show systemic evidence of increased oxidative stress and a decreased anti-oxidant defense, which increases with aging and tumor progression.68–70 Chemotherapy and radiation therapy then promote further oxidative stress.69 Unfortunately, “sub-lethal” doses of oxidative stress during cancer therapy may contribute to tumor recurrence and metastasis, via the activation of myofibroblasts.
  • a loss of stromal Cav-1 is associated with the increased expression of gene profiles associated with normal aging, oxidative stress, DNA damage, HIF1/hypoxia, NFκB/inflammation, glycolysis and mitochondrial dysfunction
  • cancer-associated fibroblasts show the largest increases in glucose uptake, while cancer cells show corresponding decreases in glucose uptake, under identical co-culture conditions
  • Thus, increased PET glucose avidity may actually be a surrogate marker for a loss of stromal Cav-1 in human tumors, allowing the rapid detection of a lethal tumor microenvironment.
  • it appears that astrocytes are actually the cell type responsible for the glucose avidity.
  • In the brain, astrocytes are glycolytic and undergo aerobic glycolysis. Thus, astrocytes take up and metabolically process glucose to lactate.7
  • Then, lactate is secreted via a mono-carboxylate transporter, namely MCT4. As a consequence, neurons use lactate as their preferred energy substrate
  • both astrocytes and cancer-associated fibroblasts express MCT4 (which extrudes lactate) and MCT4 is upregulated by oxidative stress in stromal fibroblasts.34
  • In accordance with the idea that cancer-associated fibroblasts take up the bulk of glucose, PET glucose avidity is also now routinely used to measure the extent of fibrosis in a number of human diseases, including interstitial pulmonary fibrosis, postsurgical scars, keloids, arthritis and a variety of collagen-vascular diseases.
  • PET glucose avidity and elevated serum inflammatory markers both correlate with poor prognosis in breast cancers.
  • PET signal over-estimates the actual anatomical size of the tumor, consistent with the idea that PET glucose avidity is really measuring fibrosis and inflammation in the tumor microenvironment.
  • human breast and lung cancer patients can be positively identified by examining their exhaled breath for the presence of hydrogen peroxide.
  • tumor cell production of hydrogen peroxide drives NFκB-activation in adjacent normal cells in culture6 and during metastasis,103 directly implicating the use of antioxidants, NFκB-inhibitors and anti-inflammatory agents, in the treatment of aggressive human cancers.
  • Nathan Goodyear on 12 Nov 14
     
    Good description of the communication between cancer cells and fibroblasts.  This theory is termed the "reverse Warburg effect".
Nathan Goodyear

Dietary Insulin Load and Cancer Recurrence and Survival in Patients With Stage III Colo... - 0 views

academic.oup.com/...5038128

insulin diet nutrition cancer colon cancer

shared by Nathan Goodyear on 26 Jun 18 - No Cached
  • Nathan Goodyear on 26 Jun 18
     
    New prospective study of 1023 patients finds that high-insulogenic diet, also know as a traditional American diet, high glycemic, high sugar diet... is associated with an increased risk of cancer recurrence and mortality compared to low insulogenic diet.  The authors concluded that this would be beneficial for after surgical resection in people with stage III colon cancer. My question, is why wait on the development of cancer: use a low-insulogenic diet to prevent the cancer all together or when diagnosed implement immediately.  Why wait? Treat early! Prevent!
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