Posts from hackertalks.com

7 Year old monitor started to have panel issues today, no initiating event. Did the normal trouble shooting, shut every component down, disconnected, swapped cables, updated firmware, changed resolutions, etc… issue persisted.

Dr. Calogero (Carlo) Longhitano is an Associate Professor of Psychiatry at James Cook University and a psychiatrist at North Queensland Forensic MH Services. He obtained his MD in 1999 (Italy) before completing his psychiatric residency in Oxford and London (United Kingdom).

Dr Paul Mason obtained his medical degree with honours from the University of Sydney, and also holds degrees in Physiotherapy and Occupational Health. He is a Specialist Sports Medicine and Exercise Physician.

Dr Andrew McIntyre is a Gastroenterologist and Hepatologist who graduated and gained his qualifications in 1990 from Queensland University. He opened the doors to Buderim Gastroenterology in 1997. Dr. McIntyre has extensive experience in all aspects of Gastroenterology with a special interest in ERCP and associated Therapeutic Intervention.

Dr Justine Birchall graduated from the University of Melbourne Medical School in 1993. After completing her GP training in towns such as Timboon, Point Lonsdale, Drysdale, and Bannockburn, Justine returned to Melbourne. Dr Birchall has been able to maintain her interest across the breadth of general practice, enjoying caring for patients before birth and even through the final stages of life. She has a keen interest in preventative health care, particularly related to immunisation, nutrition, prevention of cardiovascular disease and cancer screening.

Diagrammatic Pieces define the pieces moves on the item itself. This removes the need to memorize the moveset to the symbol needed in many forms of chess

Dr Helena Popovic MBBS is a medical doctor and international speaker who shows people how to boost their brain at any age or stage of life. She graduated from the University of Sydney and has spent over 30 years researching the brain and teaching people how to reach their full potential. She also provides a roadmap for living longer, stronger, healthier and happier.

TLDR: Is it crazy to put a big TV on the floor for a couch battle station so that my eyes at couch height are at the top of the TV on the floor?

Ketogenic metabolic therapy (KMT) is a medical nutrition therapy to address certain health and disease conditions. It is increasingly used for many non-communicable diseases that are rooted in abnormal metabolic health. Since chronic kidney disease (CKD) is commonly caused by overnutrition leading to hyperglycemia, insulin resistance and diabetes mellitus, the carbohydrate restriction inherent in KMT may offer a therapeutic option. Numerous studies have found that various forms of KMT are safe for individuals with CKD and may lead to improvement of renal function. This is in contrast to the current standard pharmacological approach to CKD that only slows the relentless progression towards renal failure. Kidney care providers, including physicians and dietitians, are usually not aware of non-standard dietary interventions, including KMT, and often criticize KMT due to common misconceptions and uncertainty about the underlying science, including the common misconception that KMT must involve high protein or meat consumption. This review article discusses the rationales for using KMT, including plant-dominant KMT, for treatment of CKD, clarifies common misconceptions, summarizes the results of clinical studies and discusses why KMT is emerging as an effective medical nutrition therapy (MNT) to consider for patients with kidney disease. KMT, including its plant-dominant versions, can expand a practitioner’s kidney health toolbox and will likely become a first-line therapy for CKD in certain CKD-associated conditions such as obesity, metabolic syndrome and polycystic kidney disease.

Sometimes I read papers in the sauna, sometimes I just think. What do you do?

Results - We randomized 26 patients, of whom 21 (81%) completed the ketogenic diet; only one withdrawal was attributed to the ketogenic diet. While on the ketogenic diet, patients achieved sustained physiological ketosis (12-week mean beta-hydroxybutyrate level: 0.95 ± 0.34 mmol/L). Compared with usual diet, patients on the ketogenic diet increased their mean within-individual ADCS-ADL (+ 3.13 ± 5.01 points, P = 0.0067) and QOL-AD (+ 3.37 ± 6.86 points, P = 0.023) scores; the ACE-III also increased, but not significantly (+ 2.12 ± 8.70 points, P = 0.24). Changes in cardiovascular risk factors were mostly favourable, and adverse effects were mild.

Purpose of review: Although there is an extensive literature on the efficacy of the low carbohydrate diet (LCD) for weight loss and in the management of type 2 diabetes, concerns have been raised that the LCD may increase cardiovascular disease (CVD) risk by increasing the level of low-density lipoprotein cholesterol (LDL-C). We have assessed the value of LDL-C as a CVD risk factor, as well as effects of the LCD on other CVD risk factors. We have also reviewed findings that provide guidance as to whether statin therapy would be beneficial for individuals with high LDL-C on an LCD.

Most studies on ketosis have focused on short-term effects, male athletes, or weight loss. Hereby, we studied the effects of short-term ketosis suppression in healthy women on long-standing ketosis. Ten lean (BMI 20.5 ± 1.4), metabolically healthy, pre-menopausal women (age 32.3 ± 8.9) maintaining nutritional ketosis (NK) for > 1 year (3.9 years ± 2.3) underwent three 21-day phases: nutritional ketosis (NK; P1), suppressed ketosis (SuK; P2), and returned to NK (P3). Adherence to each phase was confirmed with daily capillary D-beta-hydroxybutyrate (BHB) tests (P1 = 1.9 ± 0.7; P2 = 0.1 ± 0.1; and P3 = 1.9 ± 0.6 pmol/L). Ageing biomarkers and anthropometrics were evaluated at the end of each phase. Ketosis suppression significantly increased: insulin, 1.78-fold from 33.60 (± 8.63) to 59.80 (± 14.69) pmol/L (p = 0.0002); IGF1, 1.83-fold from 149.30 (± 32.96) to 273.40 (± 85.66) µg/L (p = 0.0045); glucose, 1.17-fold from 78.6 (± 9.5) to 92.2 (± 10.6) mg/dL (p = 0.0088); respiratory quotient (RQ), 1.09-fold 0.66 (± 0.05) to 0.72 (± 0.06; p = 0.0427); and PAI-1, 13.34 (± 6.85) to 16.69 (± 6.26) ng/mL (p = 0.0428). VEGF, EGF, and monocyte chemotactic protein also significantly increased, indicating a pro-inflammatory shift. Sustained ketosis showed no adverse health effects, and may mitigate hyperinsulinemia without impairing metabolic flexibility in metabolically healthy women.

A ketogenic diet (KD) has shown promise as an adjunctive therapy for neurological and neuropsychiatric disorders, including bipolar disorder and major depressive disorder (MDD). We examined tolerance for a KD in young adults with MDD and assessed symptoms of depression and metabolic health. Students (n = 24) with a confirmed diagnosis of MDD at baseline receiving standard of care counseling and/or medication treatment were enrolled in a 10–12 week KD intervention that included partial provision of ketogenic-appropriate food items, frequent dietary counseling, and daily morning tracking of capillary R-beta-hydroxybutyrate (R-BHB). Primary outcome measures for mood symptoms included the Patient Health Questionnaire (PHQ-9) and Hamilton Rating Scale for Depression (HRSD). Additional outcomes included body composition, neurocognitive function, and blood hormonal and inflammatory markers. Sixteen students (10 women, 6 men, mean age 24 yr) completed the intervention. Nutritional ketosis (R-BHB > 0.5 mM) was achieved 73% of the time. Depressive symptoms decreased by 69% (PHQ-9) and 71% (HRSD) post-intervention (p < 0.001), with improvement occurring within 2–6 weeks. Global well-being increased nearly 3-fold (p < 0.001). Participants lost body mass (−6.2%; p = 0.002) and fat mass (−13.0%; p < 0.001). Serum leptin decreased (−52%; p = 0.009) and brain-derived neurotropic factor increased (+32%; p = 0.029). Performance improved on several cognitive tasks. In students with mild to moderate depression based on PHQ-9 and HRSD, implementation of a WFKD for 10–12 weeks is a feasible adjunctive therapy and may be associated with improvements in depression symptoms, well-being, body composition, and cognition.

I see this gets some attention on reddit every year or so, I have been doing my own survey and here is what I've found for modern cars

Alzheimer’s disease (AD) has characteristic histopathological, molecular, and biochemical abnormalities, including cell loss; abundant neurofibrillary tangles; dystrophic neurites; amyloid precursor protein, amyloid-β (APP-Aβ) deposits; increased activation of prodeath genes and signaling pathways; impaired energy metabolism; mitochondrial dysfunction; chronic oxidative stress; and DNA damage. Gaining a better understanding of AD pathogenesis will require a framework that mechanistically interlinks all these phenomena. Currently, there is a rapid growth in the literature pointing toward insulin deficiency and insulin resistance as mediators of AD-type neurodegeneration, but this surge of new information is riddled with conflicting and unresolved concepts regarding the potential contributions of type 2 diabetes mellitus (T2DM), metabolic syndrome, and obesity to AD pathogenesis. Herein, we review the evidence that (1) T2DM causes brain insulin resistance, oxidative stress, and cognitive impairment, but its aggregate effects fall far short of mimicking AD; (2) extensive disturbances in brain insulin and insulin-like growth factor (IGF) signaling mechanisms represent early and progressive abnormalities and could account for the majority of molecular, biochemical, and histopathological lesions in AD; (3) experimental brain diabetes produced by intracerebral administration of streptozotocin shares many features with AD, including cognitive impairment and disturbances in acetylcholine homeostasis; and (4) experimental brain diabetes is treatable with insulin sensitizer agents, i.e., drugs currently used to treat T2DM. We conclude that the term “type 3 diabetes” accurately reflects the fact that AD represents a form of diabetes that selectively involves the brain and has molecular and biochemical features that overlap with both type 1 diabetes mellitus and T2DM.

Aim: Mobile health (mHealth) applications have been reported to be effective in improving glycaemic control and cardiometabolic health, but mainly as part of shorter-term intervention studies. The aim of this study is to examine the effect of the ongoing Defeat Diabetes mHealth low-carbohydrate diet (LCD) intervention on clinical markers and cardiometabolic risk after 6 months of intervention.

Purpose of review - Quality or quantity of food has been at the heart of the diet debate for decades and will seemingly continue for many to come unless tightly controlled studies are conducted. To our knowledge, there has never been an overfeeding study comparing the effects of multiple diets.

(T2D → Carbs)

Ketogenic: The Science of Therapeutic Carbohydrate Restriction in Human Health presents the most up-to-date and evidence-based science and research available in the field of TCR, with the purpose of training medical and allied healthcare professionals on the effective therapeutic use of low-carbohydrate and ketogenic nutrition in clinical practice. This book explores the appropriate, safe, and effective use of TCR to improve patient outcomes in a broad range of chronic metabolic conditions and aims to promote health.

https://store.steampowered.com/app/3522600/Demon_Bluff/ single player deduction game for folks who want to scratch the Avalon/social deduction itch. You can join the playtest to get instant free access

Highly recommend. The red planet you can sleep on