The pancreatic hormone insulin regulates the trafficking and metabolism of carbohydrate and fat. Since insulin influences fatty acid flux in fat tissue, and manipulating insulin can influence body fatness, this has raised the possibility that insulin plays a role in common obesity. Two competing hypotheses propose that 1) elevated insulin is a compensatory response to insulin resistance that develops with fat gain, or 2) elevated insulin outpaces insulin resistance and favors fat gain. Each hypothesis appears to be supported by a large amount of evidence. This presentation will outline a framework capable of reconciling this seemingly conflicting evidence.
Peter Attia, MD presenting at the Ancestral Health Symposium 2012 (AHS12)
The Straight Dope on Cholesterol
Abstract:
Cholesterol is one of the most misunderstood molecules in the human body. Much like fire, it can be an essential tool for life, if used properly, or a destructive force if allowed to run amok. In this presentation, Peter Attia will explain how the body creates, moves, and utilizes this vital molecule and how what you eat can tip the balance in your favor. By the end of this talk you'll know more about cholesterol than 99% of the physicians in this country.
Bio:
Peter Attia is the President and co-founder of the Nutrition Science Initiative (NuSI), a California-based 501(c)(3). Peter is also a physician and former McKinsey & Company consultant, where he was a member of both the corporate risk and healthcare practices. Peter earned his M.D. from Stanford University and holds a B.Sc. in mechanical engineering and applied mathematics from Queen's University in Kingston, Ontario, Canada, where he also taught and helped design the calculus curriculum.
Peter Attia, MD presenting at the Ancestral Health Symposium 2012 (AHS12)
The Straight Dope on Cholesterol
Abstract:
Cholesterol is one of the most misunderstood molecules in the human body. Much like fire, it can be an essential tool for life, if used properly, or a destructive force if allowed to run amok. In this presentation, Peter Attia will explain how the body creates, moves, and utilizes this vital molecule and how what you eat can tip the balance in your favor. By the end of this talk you'll know more about cholesterol than 99% of the physicians in this country.
Bio:
Peter Attia is the President and co-founder of the Nutrition Science Initiative (NuSI), a California-based 501(c)(3). Peter is also a physician and former McKinsey & Company consultant, where he was a member of both the corporate risk and healthcare practices. Peter earned his M.D. from Stanford University and holds a B.Sc. in mechanical engineering and applied mathematics from Queen's University in Kingston, Ontario, Canada, where he also taught and helped design the calculus curriculum.
Miki Ben-Dor — Interdisciplinary Reconstruction of the Paleolithic Diet (AHS13)Ancestral Health Society
Several anthropologist have stated that there were many Paleolithic diets, presumably questioning the meat/fat centric Paleo practice or the ancestral paradigm altogether. A review of recent findings relating to the reconstruction of Paleolithic diets from various scientific areas of enquiry will be presented and likely ratios of animal to plant sourced food will be discussed. It will be argued that despite the apparent variability in Paleolithic diets, valid practical dietary guidance can be gained from their study.
Miki Ben-Dor — Interdisciplinary Reconstruction of the Paleolithic Diet (AHS13)Ancestral Health Society
Several anthropologist have stated that there were many Paleolithic diets, presumably questioning the meat/fat centric Paleo practice or the ancestral paradigm altogether. A review of recent findings relating to the reconstruction of Paleolithic diets from various scientific areas of enquiry will be presented and likely ratios of animal to plant sourced food will be discussed. It will be argued that despite the apparent variability in Paleolithic diets, valid practical dietary guidance can be gained from their study.
AHS13 Hamilton Stapell — The End of Paleo: Is the Ancestral Health Movement G...Ancestral Health Society
Hamilton's talk may be viewed at http://youtu.be/ArcSIg3cYcw
Complete abstracts along with presenter bios and photos, are available on our website:
http://www.ancestralhealth.org/post/2013-ancestral-health-symposium-ahs13
Abstract:
The current Ancestral Health movement is often thought to be on the verge of going mainstream. Many within the movement believe this would lead to positive health (and financial) outcomes for both individuals and society as a whole. However, the transition from a small, highly-devoted group of adherents to a mass following will be far more difficult than commonly assumed. In addition, this presentation will gauge the current size of the Ancestral Health movement by examining empirical data. It also identifies the two types of individuals that typically go paleo. The key commonality between both groups is a very high level of motivation, which also suggests limited penetration of the Ancestral Health movement in the future.
A new theory suggests that acid reflux is caused by carbohydrate malabsorption, small intestinal bacterial overgrowth (SIBO) and microbe-induced gas pressure. The pressure drives acid reflux much like dropping a Mentos in a bottle of coke. Difficult-to-digest Carbohydrates lactose, fructose, resistant starch, fiber and sugar alcohols are most likely to cause malabsorption and symptoms of SIBO-related conditions such as GERD and IBS. A novel calculation called fermentation potential (FP) can measure the gut symptom potential of any food. The low FP approach was successfully tested in a small clinical study in the Boston area.
AHS13 Grayson Wheatley - What is Optimal Health? Complexity Science, Chaos Th...Ancestral Health Society
An ancestral lifestyle relies on alignment of nutrition, physical activity and sleep for achieving optimal health and well-being. New research in complexity science - a rapidly evolving body of work that studies dynamic networking systems - has cast doubt on the effectiveness of how we measure expected outcomes in health and medicine. Complex systems may better explain human health by focusing not on single data elements as “cause-and-effect” but on the interactions among complex biological systems. The implications of complexity science and chaos theory on leading an ancestral lifestyle and achieving optimal health will be discussed.
Journal club slides for Grizzly Bears Exhibit Augmented Insulin Sensitivity w...Dave Bridges
Journal Club Slides for the article ""Grizzly Bears Exhibit Augmented Insulin Sensitivity while Obese Prior to a Reversible Insulin Resistance during Hibernation"." available at http://dx.doi.org/10.1016/j.cmet.2014.07.008
Insulin Sensitivity VS. Insulin Resistance: in this blog Shawn explains the relationship between blood sugar levels, insulin and weight loss. Get started now!
Insulin Resistance is a hormone produced by your pancreas (a gland that sits behind your stomach) that helps to regulate your blood sugar levels. It’s primary job is to move the sugar from your bloodstream into the cells of your body so they can use it for energy, perfecto!
Fight against polycystic ovary syndrome problems (pcos pcod)furocyst01
It may cause issues with your intervals and make it hard to become pregnant. PCOS can also cause undesirable changes in how you look. When it is not treated, over the years it may result in other health issues, like diabetes and cardiovascular disease. Most women with Polycystic Ovary Syndrome Problems develop many tiny cysts in their ovaries. That’s why it’s known as PCOS. The cysts aren’t dangerous but contribute to hormone imbalances. Early identification and treatment can help control the symptoms and avoid long-term issues.
It becomes really difficult for a woman with PCOS to lose weight due to various reasons. We provide you with health tips for a better and healthy life.
I presented a hyperemesis case for a Case Study Seminar where university faculty were invited to attend and RD\'s from the community could receive CPE\'s for attending.
Similar to AHS13 Stephan Guyenet Insulin and Obesity: Reconciling Conflicting Evidence (20)
AHS13 Adele Hite - The Real Paleo Challenge: How a Fad on the Fringe Can Beco...Ancestral Health Society
Adele's AHS13 talk, The Real Paleo Challenge: How a Fad on the Fringe Can Become a Force for Change, may be viewed on our youtube channel:
http://youtu.be/l1r8yF02oc8
For complete schedule, bios, abstracts, please see our website:
http://www.ancestralhealth.org/post/ahs13-detailed-schedule
Dr. Lassek's talk may be viewed here:
http://www.youtube.com/watch?v=gJhT_ANNy4E
Abstract: One puzzle is why human males have such a strong preference for women with hourglass figures and low weights that can compromise fertility. The second is why slender young women typically have about one third of their weight in body fat, more than bears starting to hibernate, and why human infants are also very fat. Finally, why do women typically gain another twenty pounds or more during their reproductive years? The answer may lie in the roles that fat plays in providing essential fatty acids needed for the growth of a very large brain and in regulating overall fetal growth.
Over the past century, industrialized societies have seen a meteoric rise in the so-called diseases of civilization: obesity, cardiovascular disease, osteoporosis, autoimmune disease and cancer. These disorders are often associated with apparent "deficiencies" in critical nutrients such as vitamins, minerals and hormones. This talk will examine the arguments for and against supplementation, together with the evidence from interventional studies. The focus will be on the supplementation with Vitamin C, Vitamin D, and calcium. I will argue that the case for supplementation as a long-term preventive strategy has not be made, and often overlooks the compensating effects of homeostatic regulation.
AHS13 Tony Federico — Processed Foods and Processed Friends: Is Facebook a Ne...Ancestral Health Society
Human beings crave social connection in much the same way that we crave sugary, salty, and fatty foods. In this sense, smartphone enabled social media use parallels the fast food drive-through. Chronic daily use of social media can create dependency and is a threat to emotional and psychological well-being just as over consumption of energy dense foods can lead to diabetes, heart disease, and other diseases of civilization. Moderating the consumption of "processed friends" is just as important as moderating the consumption of processed foods for maintaining and improving total health and wellness.
AHS13 Tim Gerstmar - It Ain't Your Great-Grandparents World: Environmental To...Ancestral Health Society
Humanity has released approximately 100,000 new chemical compounds into the environment, mostly in the past 100 years. Compounds our bodies have never seen before and weren't designed to deal with. In this talk we will discuss some of the common environmental toxins and how they have been shown to be harmful to human health. We will also discuss: testing methods for quantifying toxicity, how the body detoxifies (the seven organs involved) and provide simple methods audience members can take to reduce their toxic burden, as well as briefly discuss more intensive, physician practices for detoxification for people who need it.
AHS13 Alyssa Rhoden — Give Them Grains? Analyzing Approaches to World Hunger Ancestral Health Society
Feeding the world is a compelling problem that is expected to worsen. A proposed solution is to increase the number of available calories by diverting more crops from animal feed to direct human consumption. I analyze this approach, taking into account the types of food that can be produced. The results indicate that current crops are rather poor at delivering nutritious food and that repurposing grains is an unlikely solution to world hunger. I will discuss alternative methods by which we can maximize production of nutritious foods and the importance of the ancestral health community’s involvement in the sustainable agriculture movement.
Depression is an insidious issue in the US and elsewhere. Lifestyle habits that are very different from our ancestral environment may be to blame, and one particularly problematic area is food choice. Depressive symptoms share much in common with the adaptive features of sickness behavior, which is functional when operating in an environment of ancestrally normal immune stressor. Modern diets likely activate the immune system (primarily the inflammatory response) and induce the cascade of adaptive responses that collective make up sickness behavior. Due to their similarities, these may then diagnosed as depression. In this talk, I discuss the links among diet, depression, and inflammation, as well as highlighting some specific dietary components that contribute to this response.
AHS13 Paul Ralston — The Effect of Diet on Chronic Spinal Pain Disorders Ancestral Health Society
Despite the high frequency of spinal related pain disorders, few patients or physicians understand or even acknowledge the role nutrition plays in pain perception. This presentation will explain the anatomy of the most common spinal structures responsible for being sources of pain. The lecture will also examine the robust role diet plays in increasing or decreasing the perception of pain.
AHS13 Shilpi Mehta — Nutrition for the Eyes, Brain and Heart: An Eye Doctor's...Ancestral Health Society
Ocular health is strongly connected to systemic body health especially in cardiovascular, neuronal, and inflammatory diseases. The eye is the window to the health of the body and inflammation elsewhere can manifest symptoms in the eye. I suggest an anti-inflammatory Paleolithic inspired diet is likely to improve and possibly prevent ocular diseases such as dry eyes, cataracts, macular degeneration, glaucoma, etc. which have inflammatory origins. I will discuss common ocular conditions that have inflammatory causes, an evolutionary perspective on eye diseases, and offer practical recommendations for food and supplements to optimize eye health, which also help the body, especially the heart and brain.
Persistent lack of progress by mainstream (non-evolutionary) medicine suggests evolutionary thinking is necessary for progress, but many examples – involving Weston Price, sleep, depression, weight control, omega-3, acne, depression, and fermented foods -- suggest it is far from sufficient. Evolutionary thinking helps solve health problems because it greatly narrows the possibilities worth study but it does not narrow the possibilities far enough (there is too much uncertainty) to by itself produce practical solutions. For example, evolutionary thinking helped me find a new theory of weight control but I had learn more to find a practical way to lose weight.
Dry Eye Disease (DED) has become a substantial economic burden to industrialized society. It is estimated to cost as much as $18K/year/patient in lost productivity for a total of $55B/year in the United States alone. Severe, untreated dry eye disease can result in significant morbidity and potential loss of vision. The role that diet plays in the inflammation and lipid abnormalities associated with dry eye disease has only recently been discovered and is still not widely accepted in the medical community.
AHS13 Colin Champ — Intermittent Fasting and Carbohydrate Restriction in Canc...Ancestral Health Society
Dietary manipulation, including intermittent fasting, carbohydrate restriction, and ketogenic diets, all ancestral in etiology, appear to increase the efficacy of radiation therapy for cancer treatment in preclinical and clinical trials. Clinical trials incorporating such dietary manipulation are necessary.
AHS13 Anastasia Boulais — Is Sun Worshipping Increasing Your Risk of Melanoma? Ancestral Health Society
Those of us familiar with the evolutionary medicine model have come to question many of the conventional public health recommendations and, along with them, the complete sun avoidance. Dr Anastasia Boulais will describe the delicate balance between the benefits and risks of sun worshipping based on current evidence. The talk will focus on particular patterns of sun exposure which may increase the risk of formation of cutaneous melanoma. Other factors, such as diet, vitamin D status and even training patterns, contributing to that risk will be discussed. Anastasia will conclude with an overview of protective lifestyle factors.
AHS13 Jeffrey Rothschild — Time-restricted Feeding, an Overview of the Curren...Ancestral Health Society
Time-restricted feeding is a method of intermittent fasting which allows ad libitum energy intake within a window of 4-12 hours, inducing a 12-20h daily fasted window. A wide variety of health benefits have been seen in animal and human trials, this presentation will review the current research and suggest practical applications.
AHS13 Russ Crandall and Paul Jaminet — The Perfectly Healthy Meal: How Ancest...Ancestral Health Society
We examine the principles of recipe and meal design in three approaches – standard Paleo, traditional cuisines, and Perfect Health Diet – to evaluate their similarities and differences. We then compare and contrast how various traditional recipes are implemented in the three approaches, and discuss the relative merits of each approach. Our goal is to answer the question: how can we synthesize the best of each approach to design the most healthful, satisfying, nourishing, delicious food possible?
ASH13 Scott Hall and Robb Wolf — Evaluation of the Impact of a Paleolithic Di...Ancestral Health Society
Traditional cardiovascular risk factors including cholesterol may not provide the best tools for predicting individuals at risk for future cardiovascular disease and current insulin resistance. Novel and emerging evaluations of lipoproteins may provide a more accurate assessment of future cardiovascular risk. In an observational study of a small group of law enforcement officers, we studied the changes in both traditional and nontraditional risk factors when instructed in a “paleo” diet over 6 months. Overall, we found an encouraging impact on both traditional and nontraditional risk factors over the course of the study. It is proposed that a “paleo” diet supplemented with exercise has a positive effect on cardiovascular risk factors and may be a treatment recommendation for individuals at risk.
The Consuming Instinct: What Juicy Burgers, Ferraris, Pornography and Gift Giving Reveal About Human Nature
Gad Saad, Ph.D.
I offer a synopsis of my work in the evolutionary consumption area. This will be achieved by discussing key tenets from my books (The Consuming Instinct and The Evolutionary Bases of Consumption) including that: (1) many consumption acts can be mapped onto four key Darwinian modules (survival, mating, kin selection, and reciprocal altruism); and (2) cultural products (e.g., song lyrics, movie plotlines) are fossils of the human mind that highlight a shared biological-based human nature.
AHS13 Jeff Leighton — The Role of Omega 3 Oils in the Treatment of Chronic In...Ancestral Health Society
Inflammation is associated with virtually all chronic, progressive diseases such as heart disease, vascular disease, asthma, IBS, autoimmune diseases, rheumatoid arthritis, osteoarthritis and even chronic neurological diseases such as Alzheimer’s disease. The signals that induce inflammation are multifactorial. High dose omega 3 has the potential to be as or more effective than pharmaceutical therapies. We will report on a series of omega 3 studies that compared dose response, dose timing, (e.g. once a day or twice a day), and food intake (with or without) in four separate cohorts.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
2. The contents of this presentation do not represent the views
of the University of Washington or Dr. Michael W. Schwartz
Man digging potatoes, undated
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Fastinginsulin(pmol/L)
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Obesity is Associated with Elevated Insulin
Folsom et al. Diabetes Care 20:935. 1997
lean overweight obese
5. How to Test a Hypothesis
A hypothesis is a model of reality
Good hypotheses make testable predictions
Testing a hypothesis means doing experiments
to see how well it predicts outcomes
In many cases, hypotheses can be tested
using existing data
13. Insulin Makes You Burn What You Eat
500 kcal of fat in
100 kcal of CHO in
-500 kcal of fat out
100 kcal of CHO out
= 0 change in body
fat content
100 kcal of fat in
500 kcal of CHO in
100 kcal of fat out
500 kcal of CHO out
= 0 change in body
fat content-
Insulin
15. Changing Adiposity Should Change Insulin
1. Does fat gain increase fasting insulin?
Sims 1968: 3-5 months of intense overfeeding; 26% weight gain.
“As in spontaneous obesity [fasting] serum insulin as well as the
ratio of insulin to glucose is increased in experimental obesity.”
Erdmann 2007: 4.5 months of moderate overfeeding; 13.6 lbs of weight gain.
Fasting insulin +118%
2. Does fat loss decrease fasting insulin?
YES
YES
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60
70
0 3 6 9 12
Fastinginsulin(pmol/L)
FatMass(kg)
Time (months)
insulin
fat massPolyzogopoulou 2003:
Bariatric surgery
Major fat loss
16. Changing Insulin Levels Should
Change Adiposity
- insulin + insulin “insulin lipohypertrophy”
NEJM Image Challenge. 2012.
Mehran et al. Cell Metab 16:723. 2012
Bluher et al. Dev Cell 3:25. 2002
17. Study Follow-up (yrs) Association
Swinburn 3.5 None
Valdez 8 Partial inverse
Hoag 4.3 Inverse
Schwartz >3 Inverse
Hodge 5 None
Boyko 5 Inverse
Sigal 16.7 Positive
Lazarus 3-3.7 Pos and neg
Zavaroni 14 Positive
Folsom 7 None
Folsom 6 Inverse
Gould 4.4 Partial inverse
Lakka 4 None
Masuo 5 None
Sandhu 4.5 None
Odeleye 9.3 Positive
Srinivasan 3 None
Byrnes 1 None
Johnson 3-6 Positive
Salbe 5 Inverse
Maffeis 14 Partial inverse
Savoye 2.5 Partial positive
Elevated Insulin Should Predict Future Fat Gain
Hivert et al. Int J Obesity 31:731. 2007.
Higher insulin predicts more fat gain:
Higher insulin predicts less fat gain:
No association:
5
8
9
20. Is Insulin Action Actually Increased in Obesity?
Ins SI Action
LowNormalHigh
Lean healthy
Ins SI Action
LowNormalHigh
Uncontrolled type 1 Diabetes
Ins SI Action
LowNormalHigh
Insulin lipohypertrophy
Ins SI Action
LowNormalHigh
Obesity
?? ??
30. Preserving Lean-type Insulin Signaling Should
Prevent Obesity
Ins SI Action
LowNormalHigh
Lean healthy
Ins SI Action
LowNormalHigh
Obese
Ins SI Action
LowNormalHigh
???
Obesity -> insulin: mice should become obese
Insulin -> obesity: mice should remain lean
31. Chow HFD
Inflammation and Insulin Resistance
Inflammation
Insulin
resistance
Elevated
insulin
Han et al. Science 339:218. 2012
32. Chow HFD
Inflammation and Insulin Resistance
Han et al. Science 339:218. 2012
mutant
Inflammation
Insulin
resistance
Elevated
insulin
33. Preserving Lean-type Insulin Signaling
Should Prevent Fat Gain
Weight and fat gain are normal despite the preservation of
lean-type insulin signaling
Elevated insulin and obesity are readily uncoupled
Han et al. Science 339:218. 2012
Bodyweight(g)
Chow
HFD
Fatmass(g)
Chow HFD
34. Preserving Lean-type Insulin Signaling
Should Prevent Fat Gain
Similar findings have been reported in:
TNFα KO mice (Uysal 1997)
Clonidine-treated dogs (Rocchini 1999)
Myeloid IR KO mice (Mauer 2010)
NLRP3 KO mice (Vandanmagsar 2011)
aP2 KO mice (Hotamisligil 1996)
Hepatic PTP1B KO mice (Delibegovic 2008)
Muscle PTP1B KO mice (Delibegovic 2007)
Adipose JNK1 KO mice (Sabio 2008)
35. Preserving Lean-type Insulin Signaling
Should Prevent Fat Gain
BMI = 45.2
Kloting et al. Am J Physiol Endo Metab. 299:E506. 2010
Insulin sensitive
Low fasting insulin
Insulin resistant
High fasting insulin
36. Preserving Lean-type Insulin Signaling
Should Prevent Fat Gain
Obesity
Elevated
insulin
Obesity
Elevated
insulinX
48. Implications
Preventing obesity reduces the risk of
metabolic disturbances that
contribute to many modern disorders
Diabetes
Cardiovascular disease
Dementia
Cancer
Suppressing insulin secretion in the obese using drugs is unlikely
to be beneficial because it may further impair metabolic control
51. Implications
In obesity, elevated insulin secretion is attempting to
compensate for reduced insulin sensitivity
Compensation is often incomplete, resulting in
insufficient insulin action
In susceptible people, compensation can
eventually fail, leading to diabetes
52. • Show graph of relationship between insulin
sensitivity and fasting insulin
• Make point that they increase in parallel
• Does that also occur in fat tissue?
• Graph of FFA vs. fat mass from Frayn paper
• Graph of FFA Ra vs fat mass
• Excel file of graphs and refs in talk folder
• RQ is inversely associated with fasting insulin
(Ravussin paper in Endo folder)
53. • Fasting insulin and insulin resistance are closely
related (Olefsky 1973 in Endo folder) with graph
• 2 of 3 conclusions of the paper:
• “Increases in fasting insulin levels and increase in
resistance to insulin mediated glucose uptake are
closely related”
• “The increases in fasting insulin levels which we
have observed appear to be compensatory
attempts to overcome the resistance to glucose
uptake”
54. Outline
• Obesity and insulin association
• Cause or effect of obesity? Two hypotheses
• Each hypothesis makes testable predictions, many have already been tested. Use this as
framework.
• Insulin biology
– Fasting and postprandial
• Data supporting fattening effect
– Diabetes and insulin therapy (T1DM photos in Frayn book)
– Man with lipoma belly
– FIRKO and Ins +/-
– But what we really want to know is insulin’s effect in common obesity
• Data supporting hypothesis that insulin resistance causes hyperinsulinemia
– Defects in a number of points in the insulin signaling pathway causes hyperinsulinemia.
– Blocking insulin resistance blocks hyperinsulinemia.
• Testing the hypothesis in common obesity
– Prospective data
– 20+% of obese have normal insulin level
– Glucose and fatty acid data for obese
– Animal models w suppressed insulin resistance (ap2, TNF, iNOS, myeloid JNK (2012 Science paper Han et
al), myeloid insulin receptor, CCR2 KO, clonidine dogs, MCP-1 KO, MHCII, liver-specific PTP1B KO)
– Animal models of hyperinsulinemia (glucose vs. fructose, LIKK mouse, LIRKO mouse, hepatic JNK
overexpression, three studies where insulin caused weight loss in rodents, also discuss those that caused wt
gain and hypoglycemia)
– This supports standing hypothesis
• Many of the complications of obesity are due to a combination of insulin deficiency and excess
(hyperglycemia, diabetes risk, hyperlipidemia, hypertension)
• Conclusions
Editor's Notes
The two most widely recognized hypotheses to explain this association are that… These two are not mutually exclusive
What is a hypothesis? It says “this is how I think XYZworks”. So that’s what we’re going to try to do here today.
Insulin plays many roles in the body, but its central role is as an energy traffic cop.
And if we look in the blood after a mixed meal, glucose and insulin increase after a mixed meal, and free fatty acids decline. FFAs are the body’s main circulating fat fuel. Why do FFAs go down in response to insulin? To understand that, we need to examine the biology of the fat cell, or adipocyte.
There’s no denying that insulin causes the adipocyte to shut down whole-body fatty acid delivery.
In sum, insulin INCREASES the activity of the pathways that put fat into fat cells, and DECREASES the activity of pathways that take it out. If obesity is about fat going into and out of fat cells, this seems like something we should care about. You can see this process in action following a meal containing carbohydrate or protein, the two macronutrients that stimulate insulin release the most.
Kitavans, Bantu, Kuna, Okinawan, mainland Japanese, Chinese, Indian, Maori, New Guinea highlander, Maya, Pima, 1920s potato farmers in Minnesota
Insulin is the main factor that coordinates between these two scenarios in response to carbohydrate and protein availability. However, if you eat excess calories of any of the macronutrients, it spares fat burning beyond your metabolic rate and net fat storage is positive. This occurs whether you are overeating carbohydrate or fat.
Sims 1968. Prisoners overfed for 3-5 months, gained 26% of body weight. Bariatric surgery was Roux en Y plus biliopancreatic diversion
Mention FIRKO, INS+/-. T1DM man after 31 years of insulin injection into the same spot. OK, so we’ve shown that insulin can influence fat mass in the context of disease and pharmacology, but what about in the context of obesity?
Well that’s strange. Maybe it’s time to go back to the drawing board and examine our assumptions.
Hyperinsulinemia should not be dissociable from obesity
It’s well established that inflammation is a key mechanism in the development of insulin resistance, and that insulin resistance leads to elevated insulin. When animals are genetically unable to activate inflammatory pathways, they often don’t develop insulin resistance with age or on fattening diets. In one recent example of this, researchers made a mouse that lacks the critical inflammatory proteins Jun kinase 1 and 2 specifically in key immune cells called macrophages. These mice are unable to mount a normal inflammatory response. When fed a fattening diet, a normal mouse develops insulin resistance and elevated insulin. When these mice are fed a fattening diet, they develop neither.
It’s well established that inflammation is a key mechanism in the development of insulin resistance, and that insulin resistance leads to elevated insulin. When animals are genetically unable to activate inflammatory pathways, they often don’t develop insulin resistance with age or on fattening diets. In one recent example of this, researchers made a mouse that lacks the critical inflammatory proteins Jun kinase 1 and 2 specifically in key immune cells called macrophages. These mice are unable to mount a normal inflammatory response. When fed a fattening diet, a normal mouse develops insulin resistance and elevated insulin. When these mice are fed a fattening diet, they develop neither.
In fact, we see that insulin levels and fat gain are readily uncoupled.
Either preventing or attenuating the development of the insulin resistance-hyperinsulinemia complex has little or no effect on body fat gain.
If we manipulate insulin action in extreme ways, we can get big effects on body fatness.. But that’s not what happens in common obesity.
If we manipulate insulin action in extreme ways, we can get big effects on body fatness.. But that’s not what happens in common obesity.
If we manipulate insulin action in extreme ways, we can get big effects on body fatness.. But that’s not what happens in common obesity.
If we manipulate insulin action in extreme ways, we can get big effects on body fatness.. But that’s not what happens in common obesity.
If we manipulate insulin action in extreme ways, we can get big effects on body fatness.. But that’s not what happens in common obesity.
If we manipulate insulin action in extreme ways, we can get big effects on body fatness.. But that’s not what happens in common obesity.
42-fold increased risk. All types of diabetes. 5-year follow-up.
The two most widely recognized hypotheses to explain this association are that… These two are not mutually exclusive
The two most widely recognized hypotheses to explain this association are that… These two are not mutually exclusive