The document discusses the myth that a high-fat diet leads to high cardiac mortality, noting that the original study supporting this claim selectively used data from only 6 countries. Several large prospective studies are summarized that find no association between saturated fat consumption and heart attack risk, and some find lower cardiac mortality rates associated with higher fat intake. The "truth" discussed is that cholesterol and high fat diets are not actually causes of cardiac problems, but this view is not widely publicized due to pharmaceutical industry influence.
Guidelines in Obesity management
By Dr. Usama Ragab Youssif
Obesity-related counseling should be offered to those with BMI ≥25 kg/m2
A 3% to 5% weight loss can result in meaningful reductions in triglycerides, blood glucose, hemoglobin A1c, and the risk of developing type 2 diabetes
Set an initial weight loss goal of 5% to 10% of current body weight over 6 mo
After 6 mo, focus on weight maintenance before attempting further weight loss
Participating in a weight loss program long-term can help improve weight maintenance
Guidelines in Obesity management
By Dr. Usama Ragab Youssif
Obesity-related counseling should be offered to those with BMI ≥25 kg/m2
A 3% to 5% weight loss can result in meaningful reductions in triglycerides, blood glucose, hemoglobin A1c, and the risk of developing type 2 diabetes
Set an initial weight loss goal of 5% to 10% of current body weight over 6 mo
After 6 mo, focus on weight maintenance before attempting further weight loss
Participating in a weight loss program long-term can help improve weight maintenance
Atorvastatin: Statins in CVD management. Is just lipid lowering enough Dr Vivek Baliga
When it comes to management of cardiovascular diseases, are achieving lipid lowering targets sufficient. Here Dr Vivek Baliga, Consultant Internal medicine discusses the additional benefits of statins in CVD in India.
PRESENTED BY: AYESHA KABEER
FROM: UNIVERSITY OF GUJRAT SIALKOT SUBCAMPUS
Obesity and Cardiovascular Diseases
1. Causes of Overweight and Obesity
2. Accessing Obesity
-Body Mass Index
3. Cardiovascular Diseases caused by Obesity
Prevalence of obesity.Body composition & body shape (body fat distribution ) and CVD risk .Mechanisms linking obesity with cardiovascular disease.Fat-but-Fit Paradigm and CVD,The Relationship of Metabolic Risk Factors and Cardiorespiratory Fitness. Metabolically Healthy but Obese ( MHO ) Phenotype and CVD.Obesity Paradox in Patients With CVD
Plant-based Eating: Enhancing Health Benefits, Minimizing Nutritional RisksRobin Allen
Learning Objectives
At the end of the session, the participants will be able to:
1. Know there is no single definition of a plant-based diet.
2. Discuss health aspects of vegetarian and vegan diets and quality of evidence supporting health claims.
3. Assess nutritional adequacy/status of vegetarians and/or vegans throughout the life cycle and provide strategies for meeting dietary recommendations for vitamin B12, DHA calcium, and zinc.
Overweight And Obesity : Proven Health Risks, We All Should KnowSanjiv Haribhakti
Overweight and obesity are defined as abnormal or excessive fat accumulation in the body that presents a risk to health. Obesity will have a negative effect on health, leading to reduced life expectancy and/or increased health problems. According to WHO, Obesity is one of the most serious public health problems of the 21st century. For more info visit :- http://gisurgery.info/player_presentation.php?id=133
Atorvastatin: Statins in CVD management. Is just lipid lowering enough Dr Vivek Baliga
When it comes to management of cardiovascular diseases, are achieving lipid lowering targets sufficient. Here Dr Vivek Baliga, Consultant Internal medicine discusses the additional benefits of statins in CVD in India.
PRESENTED BY: AYESHA KABEER
FROM: UNIVERSITY OF GUJRAT SIALKOT SUBCAMPUS
Obesity and Cardiovascular Diseases
1. Causes of Overweight and Obesity
2. Accessing Obesity
-Body Mass Index
3. Cardiovascular Diseases caused by Obesity
Prevalence of obesity.Body composition & body shape (body fat distribution ) and CVD risk .Mechanisms linking obesity with cardiovascular disease.Fat-but-Fit Paradigm and CVD,The Relationship of Metabolic Risk Factors and Cardiorespiratory Fitness. Metabolically Healthy but Obese ( MHO ) Phenotype and CVD.Obesity Paradox in Patients With CVD
Plant-based Eating: Enhancing Health Benefits, Minimizing Nutritional RisksRobin Allen
Learning Objectives
At the end of the session, the participants will be able to:
1. Know there is no single definition of a plant-based diet.
2. Discuss health aspects of vegetarian and vegan diets and quality of evidence supporting health claims.
3. Assess nutritional adequacy/status of vegetarians and/or vegans throughout the life cycle and provide strategies for meeting dietary recommendations for vitamin B12, DHA calcium, and zinc.
Overweight And Obesity : Proven Health Risks, We All Should KnowSanjiv Haribhakti
Overweight and obesity are defined as abnormal or excessive fat accumulation in the body that presents a risk to health. Obesity will have a negative effect on health, leading to reduced life expectancy and/or increased health problems. According to WHO, Obesity is one of the most serious public health problems of the 21st century. For more info visit :- http://gisurgery.info/player_presentation.php?id=133
The health hazards associated with obesity. Mortality morbidity
Complications related to obesity
type 2 diabetes.
high blood pressure.
heart disease and strokes.
certain types of cancer.
sleep apnea.
osteoarthritis.
fatty liver disease.
What Cancer Patients Need to Know about Cardio-Oncologybkling
Dr. Anita Arnold, cardio-oncologist at Lee Health, discusses about what cardio-oncology is, how cancer treatment can impact patients' heart health, and what cancer patients can do to help protect themselves from heart conditions arising from treatment. You'll come away from this webinar with a better understanding of how to take care of your heart during cancer treatment and why cardio-oncology is important.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
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.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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.
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.
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
1. Cholesterol and
Cardiac Mortality
Myth & Truth
Fayza Rayes
MBBCh. Msc. MRCGP
Consultant Family Physician
Joint Program of Family & Community Medicine, Jeddah
www.fayzarayes.com
3. The Original Evidence Ancel Keys cheated.
He selected data from 6
countries to create the
linear relationship.
Data were actually
available from total of
22 countries!
This is the graph of heart deaths Keys (1953). Journal of mount
Sinai Hospital New York
plotted against fat intake
4. Consumption of fat and cardiac mortality
We can make it a
straight line, it
shows very clear
positive
correlation:
5. Consumption of fat and cardiac mortality
Choosing a few
other countries
might have
given a
negative
correlation:
6. Consumption of fat and cardiac mortality
Choosing a few
other countries
the negative
correlation
become more
clear
(consumption of
>40% of
calories from fat
associated with
lower cardiac
mortality):
7. Consumption of fat and cardiac mortality
So let's look at
the whole
database from
which Keys
carefully selected
his six countries
8. Consumption of fat and cardiac mortality
Cmpare to the original
line swept in by Keys.
Things get worse if
you add in the Masai,
the Inuit, the Rendile,
the Tokelau and a few
others, shown as red
dots:
9. Cholesterol and Cardiac Mortality
Other Studies
Do people who eat more saturated fat have more heart attacks?
The following are high-impact prospective studies, showing no
association between saturated fat consumption and heart attack risk.
10. Cholesterol and cardiac mortality
Between nation
studies this figure,
credited to Dr.
Kendrick, shows
the rates of death
from CHD plotted
against the percent
of a given
population who are
frankly
hypercholesterola-
-emic. He
extracted the data
from MONICA
study
11. Negative
Correlation
WHO-MONICA Study- Multinational MONItoring of Trends and
determination in CArdiovascular Disease; a 10 year study, 7
million people,14 European countries plus the Australian
Aborigines (Aborigines are the leftmost country-lowest
cholesterol & highest death rate).
12. BMJ. 1996 Jul 13;313(7049):84-90.
Dietary fat and risk of coronary heart disease in
men: cohort follow up study in the USA
Ascherio A, Rimm EB, Giovannucci EL, Spiegelman D, Stampfer
M, Willett WC.
Source: Harvard School of Public Health, Boston, MA 02115, USA.
OBJECTIVE: To examine the association between fat intake and the
incidence of coronary heart disease in men of middle age and older.
DESIGN: Cohort questionnaire study of men followed up for six years
from 1986.
SETTING: The health professionals follow up study in the United States.
SUBJECTS: 43 757 health professionals aged 40 to 75 years free of
diagnosed cardiovascular disease or diabetes in 1986.
MAIN OUTCOME MEASURE: Incidence of acute myocardial infarction or
coronary death.
13. RESULTS: During follow up 734 coronary events were
documented, including 505 non-fatal myocardial infarctions and 229
deaths. After age and several coronary risk factors were controlled for
significant positive associations were observed between intake of
saturated fat and risk of coronary disease. For men in the top versus
the lowest fifth of saturated fat intake (median = 14.8% v 5.7% of
energy) the multivariate relative risk for myocardial infarction was 1.22
(95% confidence interval 0.96 to 1.56) and for fatal coronary heart
disease was 2.21 (1.38 to 3.54). After adjustment for intake of fibre
the risks were 0.96 (0.73 to 1.27) and 1.72 (1.01 to 2.90), respectively.
Positive associations between intake of cholesterol and risk of
coronary heart disease were similarly attenuated after adjustment for
fibre intake. Intake of linolenic acid was inversely associated with risk
of myocardial infarction; this association became significant only after
adjustment for non-dietary risk factors and was strengthened after
adjustment for total fat intake (relative risk 0.41 for a 1% increase in
energy, P for trend < 0.01).
14. CONCLUSIONS: These data do not support
the strong association between
intake of saturated fat and risk of
coronary heart disease suggested by
international comparisons. They are compatible,
however, with the hypotheses that saturated fat
and cholesterol intakes affect the risk of coronary
heart disease as predicted by their effects on
blood cholesterol concentration. They also
support a specific preventive effect of linolenic
acid intake.
15. J Intern Med. 2005 Aug;258(2):153-65.
Dietary fat intake and early mortality patterns--data from
The Malmö Diet and Cancer Study.
Leosdottir M, Nilsson PM, Nilsson JA, Månsson H, Berglund G.
Source : Department of Medicine, Lund University, University Hospital (UMAS),
Malmö, Sweden. margret.leosdottir@med.lu.se
OBJECTIVES: Most current dietary guidelines encourage limiting relative fat
intake to <30% of total daily energy, with saturated and trans fatty acids
contributing no more than 10%. We examined whether total fat intake,
saturated fat, monounsaturated, or polyunsaturated fat intake are
independent risk factors for prospective all-cause, cardiovascular and cancer
mortality.
DESIGN: Population-based, prospective cohort study.
SETTING AND SUBJECTS: The Malmö Diet and Cancer Study was set in the
city of Malmö, southern Sweden. A total of 28,098 middle-aged individuals
participated in the study 1991-1996.
MAIN OUTCOME MEASURES: Subjects were categorized by quartiles of
relative fat intake, with the first quartile used as a reference point in
estimating multivariate relative risks (RR; 95% CI, Cox's regression model).
Adjustments were made for confounding by age and various lifestyle factors.
16. RESULTS: Women in the fourth quartile of total fat intake had a
significantly higher RR of cancer mortality (RR 1.46; CI 1.04-2.04). A
significant downwards trend was observed for cardiovascular
mortality amongst men from the first to the fourth quartile (P=0.028).
No deteriorating effects of high saturated fat intake were observed for
either sex for any cause of death. Beneficial effects of a relatively high
intake of unsaturated fats were not uniform.
CONCLUSIONS: With the exception of cancer mortality for women,
individuals receiving more than 30% of their total daily energy from fat
and more than 10% from saturated fat, did not have increased
Current dietary guidelines
mortality.
concerning fat intake are thus generally
not supported by our observational
results.
17. The Truth
People consume high fat diet and people
with high serum cholesterol have
low cardiac mortality
18. But Why ??!!
Why cholesterol has received plenty of this
negative media over the last decade?
Several studies have shown that cholesterol is
not the cause behind problems of the heart.
The reason is crystal clear: The pharmaceutical
companies who manufacture cholesterol-
lowering drugs have protected their billions of
dollars by twisting the information.
19. The Bitter Truth
$ billion
Year
During the past decade Pfizer's Lipitor generated
$115 billion in cumulative global revenue
20. For More Information
Go to: http://fayzarayes.com
Or go to YouTube
http://www.youtu.be/cmwNpUJUjPg
Big Fat Fiasco pt. 1-5
Editor's Notes
The research and career of the physiologist, Dr. Ancel Keys had a profound effect on society's attitude to food and exercise. His work spanning from the 1930’s through the 1970’s, introduced many of the assumptions which we now take for granted about the relationship between diet, energy expenditure, metabolic rates and health. In 1937, Keys moved to the Universityof Minnesotawhere he organized the laboratory of physiological hygiene where he led the way in studying the effects of ageing and the body’s responses to heat, cold or starvation. He determined the relationships between height and weight, diet and blood fats, blood fats and the incidence of heart attacks. His study on the human body’s’ response to extreme conditions prompted the army to ask him to develop rations for army paratroopers. What resulted was the famous “K-rations” of World War II, the combat rations that sustained soldiers throughout the war. Dr. Keys died in 2004 at the age of 100. He is survived by his wife, Margaret Keys, a daughter, Carrie D’Andrea, and a son, Dr. Henry Keys; eight grandchildren; and six great-grandchildren
Slightly less convincing is when the choice of different countries from the same data bases suggests that dietary fat has nothing to do with heart disease and that heart disease is very rare anyway:
he link between cholesterol and saturated fat with cardiovascular disease has been a myth for over 50 years.Stephan Guyenet (Whole Health Source blog) nicely addresses the cholesterol-CVD myth, and lists the many unsupportive studies here. I also recommend the work of Drs. Malcom Kendrick and Uffe Ravnskov for more info on why elevated cholesterol is not the death sentence CW paints it to be. I believe that most (if not all) of the studies that correlated cholesterol with CVD, ignored significant confounding variables such as wheat and sugar consumption, or lumped saturated fat in with trans/hydrogenated fats.The Monica study (which assessed 21 countries over 10 years) found no meaningful correlation at all. The tiny correlation that does exist would point towards heart disease rates going down as cholesterol levels go up. People with high cholesterol actually tend to live longer.For more Paleo Diet hacks: http://paleohacks.com/questions/16596/paleo-diet-and-cholesterol-levels#ixzz2J6Vh5ROW Follow us: @PaleoHacks on Twitter | PaleoHacks on FacebookA Sampling of Unsupportive StudiesHere are references to ten high-impact prospective studies, spanning half a century, showing no association between saturated fat consumption and heart attack risk. Ignore the squirming about saturated-to-polyunsaturated ratios, Keys/Hegsted scores, etc. What we're concerned with is the straightforward question: do people who eat more saturated fat have more heart attacks? Many of these papers allow free access to the full text, so have a look for yourselves if you want:A Longitudinal Study of Coronary Heart Disease. Circulation. 1963.Diet and Heart: a Postscript. British Medical Journal. 1977. Saturated fat was unrelated to heart attack risk, but fiber was protective.Dietary Intake and the Risk of Coronary Heart Disease in Japanese Men Living in Hawaii. American Journal of Clinical Nutrition. 1978.Relationship of Dietary Intake to Subsequent Coronary Heart Disease Incidence: the Puerto Rico Heart Health Program. American Journal of Clinical Nutrition. 1980.Diet, Serum Cholesterol, and Death From Coronary Heart Disease: The Western Electric Study. New England Journal of Medicine. 1981.Diet and 20-year Mortality in Two Rural Population Groups of Middle-Aged Men in Italy. American Journal of Clinical Nutrition. 1989. Men who died of CHD ate significantly less saturated fat than men who didn't.Diet and Incident Ischaemic Heart Disease: the Caerphilly Study. British Journal of Nutrition. 1993.They measured animal fat intake rather than saturated fat in this study.Dietary Fat and Risk of Coronary Heart Disease in Men: Cohort Follow-up Study in the United States. British Medical Journal. 1996. This is the massive Physicians Health Study. Don't let the abstract fool you! Scroll down to table 2 and see for yourself that the association between saturated fat intake and heart attack risk disappears after adjustment for several factors including family history of heart attack, smoking and fiber intake. That's because, as in most modern studies, people who eat steak are also more likely to smoke, avoid vegetables, eat fast food, etc.Dietary Fat Intake and the Risk of Coronary Heart Disease in Women. New England Journal of Medicine. 1997. From the massive Nurse's Health study. This one fooled me for a long time because the abstract is misleading. It claims that saturated fat was associated with heart attack risk. However, the association disappeared without a trace when they adjusted for monounsaturated and polyunsaturated fat intake. Have a look at table 3. Dietary Fat Intake and Early Mortality Patterns-- Data from the Malmo Diet and Cancer Study. Journal of Internal Medicine. 2005.I just listed 10 prospective studies published in top peer-reviewed journals that found no association between saturated fat and heart disease risk. This is less than half of the prospective studies that have come to the same conclusion, representing by far the majority of studies to date. If saturated fat is anywhere near as harmful as we're told, why are its effects essentially undetectable in the best studies we can muster?