Obesity | Leaders in Pharmaceutical Business Intelligence (LPBI) Group

Archive for the ‘Obesity’ Category

Obesity related insulin resistance is regulated by gut associated immune cells

Posted in Artificial Pancreas for Type1 Diabetes, Diabetes Mellitus, Diagnostic Immunology, Gestational diabetes, Glycobiology: Biopharmaceutical Production, Glycobiology: Biopharmaceutical Production, Pharmacodynamics and Pharmacokinetics, Gut Microbiome and Obesity, Human Immune System in Health and in Disease, Immunology, Immunotherapy, Inflammatory Pathophysiology, Nutrition Disorders, Obesity, Population Health Management, Population Health Management, Nutrition and Phytochemistry, Signaling & Cell Circuits, Synergistic Innate and Adaptive Immunotherapy, tagged Gut, IgA, immune system, Insulin resistance, Obesity on September 20, 2019| Leave a Comment »

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

Obesity is a global concern that is associated with many chronic complications such as type 2 diabetes, insulin resistance (IR), cardiovascular diseases, and cancer. Growing evidence has implicated the digestive system, including its microbiota, gut-derived incretin hormones, and gut-associated lymphoid tissue in obesity and IR. During high fat diet (HFD) feeding and obesity, a significant shift occurs in the microbial populations within the gut, known as dysbiosis, which interacts with the intestinal immune system. Similar to other metabolic organs, including visceral adipose tissue (VAT) and liver, altered immune homeostasis has also been observed in the small and large intestines during obesity.

A link between the gut microbiota and the intestinal immune system is the immune-derived molecule immunoglobulin A (IgA). IgA is a B cell antibody primarily produced in dimeric form by plasma cells residing in the gut lamina propria (LP). Given the importance of IgA on intestinal–gut microbe immunoregulation, which is directly influenced by dietary changes, scientists hypothesized that IgA may be a key player in the pathogenesis of obesity and IR. Here, in this study it was demonstrate that IgA levels are reduced during obesity and the loss of IgA in mice worsens IR and increases intestinal permeability, microbiota encroachment, and downstream inflammation in metabolic tissues, including inside the VAT.

IgA deficiency alters the obese gut microbiota and its metabolic phenotype can be recapitulated into microbiota-depleted mice upon fecal matter transplantation. In addition, the researchers also demonstrated that commonly used therapies for diabetes such as metformin and bariatric surgery can alter cellular and stool IgA levels, respectively. These findings suggested a critical function for IgA in regulating metabolic disease and support the emerging role for intestinal immunity as an important modulator of systemic glucose metabolism.

Overall, the researchers demonstrated a critical role for IgA in regulating intestinal homeostasis, metabolic inflammation, and obesity-related IR. These findings identify intestinal IgA+ immune cells as mucosal mediators of whole-body glucose regulation in diet-induced metabolic disease. This research further emphasized the importance of the intestinal adaptive immune system and its interactions with the gut microbiota and innate immune system within the larger network of organs involved in the manifestation of metabolic disease.

Future investigation is required to determine the impact of IgA deficiency during obesity in humans and the role of metabolic disease in human populations with selective IgA deficiency, especially since human IgA deficiency is associated with an altered gut microbiota that cannot be fully compensated with IgM. However, the research identified IgA as a critical immunological molecule in the intestine that impacts systemic glucose homeostasis, and treatments targeting IgA-producing immune populations and SIgA may have therapeutic potential for metabolic disease.

References:

https://www.nature.com/articles/s41467-019-11370-y?elqTrackId=dc86e0c60f574542b033227afd0fdc8e

https://www.jci.org/articles/view/88879

https://www.nature.com/articles/nm.2353

https://diabetes.diabetesjournals.org/content/57/6/1470

https://www.sciencedirect.com/science/article/pii/S1550413115001047?via%3Dihub

https://www.sciencedirect.com/science/article/pii/S1550413115002326?via%3Dihub

https://www.sciencedirect.com/science/article/pii/S1931312814004636?via%3Dihub

https://www.nature.com/articles/nature15766

https://www.sciencedirect.com/science/article/pii/S1550413116000371?via%3Dihub

https://www.nature.com/articles/nm.2001

https://www.sciencedirect.com/science/article/abs/pii/S1550413118305047?via%3Dihub

Read Full Post »

2019 Wolf Prize in Medicine to Dr. Jeffrey Friedman @RockefellerUniv for Discovery of the Satiety Protein Hormone, Leptin which Regulates the Sensation of Hunger

Posted in Interviews with Scientific Leaders, Obesity, Wolf Prize in Medicine on June 10, 2019| Leave a Comment »

2019 Wolf Prize in Medicine to Dr. Jeffrey Friedman @RockefellerUniv for Discovery of the Satiety Protein Hormone, Leptin which Regulates the Sensation of Hunger

Reporter: Aviva Lev-Ari, PhD, RN

Medicine: The satiety hormone
The prize in Medicine will be awarded to Jeffrey Friedman from Rockefeller University in New York, for discovering the hormone leptin, which regulates the sensation of hunger.
Friedman (65) grew up in New York and graduated from medical school at the early age of 22. Later on, he fell in love with research, acquired his PhD in Molecular Genetics, and received a faculty position at Rockefeller. He was interested in understanding the factors that contribute to obesity, and studied a strain of mice with a mutation in a specific gene that made the mice fatter than regular mice. Friedman wanted to understand how a change in just one gene could lead to such an extreme transition, and after eight years of research using the most advanced genetic tools of the time, he identified the gene ob, and later, its product – a protein hormone he termed leptin. He found that leptin, secreted by fat cells into the blood, affects the brain. Under fat shortage leptin levels drop – leading to an increased appetite; while high levels of leptin signal the presence of excess fat and lead to a sensation of fullness, or satiety. Therefore, in certain situations of obesity, leptin treatment may assist in reducing appetite and facilitating weight loss.
Friedman’s studies paved the way for a fuller understanding of the system that regulates hunger and satiety, which has led to the development of new drugs and treatment.

A hormone that revealed the mechanism of hunger regulation and served to develop treatments for obesity. Jeffrey Friedman | Photograph: Wolf Foundation

SOURCE

https://davidson.weizmann.ac.il/en/online/sciencenews/2019-wolf-prize

Jeffrey M. Friedman

Jeffrey M. Friedman, Marilyn M. Simpson Professor and head of Rockefeller’s Laboratory of Molecular Genetics, has been named the recipient of the 2019 Wolf Prize in Medicine. He is being recognized for his discovery of leptin, a hormone secreted by fat cells that modulates food intake and energy expenditure.
Friedman’s 1994 discovery of leptin, and of its receptor in the brain encoded by the obese gene, shed new light on the pathogenesis of obesity. He and his colleagues have since shown that leptin acts on sets of neurons in brain centers that regulate food intake and energy expenditure, and has powerful effects on reproduction, metabolism, other endocrine systems, and immune function. Defects in the leptin gene are associated with severe obesity in animals and humans.
“Jeff’s research has transformed our understanding of obesity. The fact that loss of a single hormone made by fat cells has such a profound effect on our drive to consume calories establishes a biological basis for obesity that is clearly not a simple failure of will-power,” says Rockefeller President Richard P. Lifton. “His research has opened a new field with great potential for advancing health and the understanding of the biological basis of behavior. This prestigious prize is richly deserved.”
Since 1978, the Wolf Foundation in Israel has awarded annual prizes in the arts and sciences, which are presented by the President of Israel. In addition to Friedman’s prize for Medicine, this year’s Wolf Prize recipients include an architect, a professor of agriculture and resource economics, two chemists, and a mathematician. The awardees will be honored at a Jerusalem ceremony led by the Israeli president, Reuven Rivlin, in May.
Previous Rockefeller recipients of the Wolf Prize in Medicine include Maclyn McCarty in 1990 and Jeffrey V. Ravetch in 2015. Three Rockefeller faculty have been recipients of the Wolf Prize in Physics: Mitchell Feigenbaum and Albert Libchaber in 1986 and George Uhlenbeck in 1979.

SOURCE

https://www.rockefeller.edu/news/24785-jeffrey-m-friedman-receive-2019-wolf-prize-medicine/

ALL WOLF PRIZES IN MEDICINE AWARDED

http://www.wolffund.org.il/index.php?dir=site&page=winners&name=&prize=3016&year=&field=3006

The Wolf Prize in Medicine is awarded once a year by the Wolf Foundation in Israel.^[1] It is one of the six Wolf Prizes established by the Foundation and awarded since 1978; the others are in Agriculture, Chemistry, Mathematics, Physics and Arts. The Prize has been stated to be the second most prestigious award in science, and a significant predictor of the Nobel Prize.^[2]

Table of ALL WOLF PRIZES IN MEDICINE AWARDED, 1978 – 2019

https://en.wikipedia.org/wiki/Wolf_Prize_in_Medicine

Hypertriglyceridemia: Evaluation and Treatment Guideline

Posted in Biomarkers & Medical Diagnostics, Biomedical Measurement Science, Cardiovascular Pharmacogenomics, Cardiovascular Research, Chemical Biology and its relations to Metabolic Disease, Chronic Thromboembolic Pulmonary Hypertension (CTEPH) and Pulmonary Arterial Hypertension (PAH), Clinical Diagnostics, Clinical Genomics, Diabetes Mellitus, Disease Biology, Endocrine Diseases, Epigenetics and Cardiovascular Risks, Frontiers in Cardiology and Cardiovascular Disorders, Lipid metabolism, Liver & Digestive Diseases Research, Metabolism, Myocardial Metabolism, Nutrition, Nutrition Disorders, Nutritional Supplements: Atherogenesis, lipid metabolism, Obesity, Origins of Cardiovascular Disease, Pancreatic adenocarcinoma classifier, Pancreatic cancer, Population Health Management, Population Health Management, Genetics & Pharmaceutical, tagged Cardiovascular disease, Cholesterol, diet, hypertriglyceridemia, life style, pancreatitis, triglycerides on January 22, 2019| Leave a Comment »

Hypertriglyceridemia: Evaluation and Treatment Guideline

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

Severe and very severe hypertriglyceridemia increase the risk for pancreatitis, whereas mild or moderate hypertriglyceridemia may be a risk factor for cardiovascular disease. Individuals found to have any elevation of fasting triglycerides should be evaluated for secondary causes of hyperlipidemia including endocrine conditions and medications. Patients with primary hypertriglyceridemia must be assessed for other cardiovascular risk factors, such as central obesity, hypertension, abnormalities of glucose metabolism, and liver dysfunction. The aim of this study was to develop clinical practice guidelines on hypertriglyceridemia.

The diagnosis of hypertriglyceridemia should be based on fasting levels, that mild and moderate hypertriglyceridemia (triglycerides of 150–999 mg/dl) be diagnosed to aid in the evaluation of cardiovascular risk, and that severe and very severe hypertriglyceridemia (triglycerides of >1000 mg/dl) be considered a risk for pancreatitis. The patients with hypertriglyceridemia must be evaluated for secondary causes of hyperlipidemia and that subjects with primary hypertriglyceridemia be evaluated for family history of dyslipidemia and cardiovascular disease.

The treatment goal in patients with moderate hypertriglyceridemia should be a non-high-density lipoprotein cholesterol level in agreement with National Cholesterol Education Program Adult Treatment Panel guidelines. The initial treatment should be lifestyle therapy; a combination of diet modification, physical activity and drug therapy may also be considered. In patients with severe or very severe hypertriglyceridemia, a fibrate can be used as a first-line agent for reduction of triglycerides in patients at risk for triglyceride-induced pancreatitis.

Three drug classes (fibrates, niacin, n-3 fatty acids) alone or in combination with statins may be considered as treatment options in patients with moderate to severe triglyceride levels. Statins are not be used as monotherapy for severe or very severe hypertriglyceridemia. However, statins may be useful for the treatment of moderate hypertriglyceridemia when indicated to modify cardiovascular risk.

References:

https://www.medpagetoday.com/clinical-connection/cardio-endo/77242?xid=NL_CardioEndoConnection_2019-01-21

https://www.ncbi.nlm.nih.gov/pubmed/19307519

https://www.ncbi.nlm.nih.gov/pubmed/23009776

https://www.ncbi.nlm.nih.gov/pubmed/6827992

https://www.ncbi.nlm.nih.gov/pubmed/22463676

https://www.ncbi.nlm.nih.gov/pubmed/17635890

Read Full Post »

Micronutrients, Macronutrients and Dietary Patterns: Nutrition and Fertility

Posted in Minerals in Medicine, Nutrition, Nutrition and Phytochemistry, Nutritional Supplements: Atherogenesis, lipid metabolism, Obesity, Reproductive Andrology, Embryology, Genomic Endocrinology, Preimplantation Genetic Diagnosis and Reproductive Genomics on December 11, 2018| Leave a Comment »

Micronutrients, Macronutrients and Dietary Patterns: Nutrition and Fertility

Reporter: Aviva Lev-Ari, PhD, RN

Folic acid. Folic acid is important for germ cell production and pregnancy. The recommended daily dose to prevent neural tube defects is 400-800 µg. Women who take folic acid-containing multivitamins are less likely to be anovulatory, and the time to achieve a pregnancy is reduced. Those who consume more than 800 µg of folic acid daily are more likely to conceive with assisted reproductive technology (ART) than those whose daily intake is less than 400 µg.

Vitamin D. Vitamin D may affect fertility through receptors found in the ovaries and endometrium. An extremely low vitamin D level (< 20 ng/mL) is associated with higher risk for spontaneous miscarriage risk. Some reports suggest that women with adequate vitamin D levels (> 30 ng/mL) are more likely to conceive after ART when compared with those whose vitamin D levels are insufficient (20-30 ng/mL), or deficient (< 20 ng/mL). These findings, however, are inconclusive.

Carbohydrates. Dietary carbohydrates affect glucose homeostasis and insulin sensitivity, and by these mechanisms can affect reproduction. The impact is most pronounced among women with polycystic ovary syndrome (PCOS). In women with PCOS, a reduction in glycemic load improves insulin sensitivity as well as ovulatory function. Whole grains have antioxidant effects and also improve insulin sensitivity, thereby positively influencing reproduction.

Omega-3 supplements. Omega-3 polyunsaturated fatty acids lower the risk for endometriosis. Increased levels of omega-3 polyunsaturated fatty acids are associated with higher clinical pregnancy and live birth rates.

Protein and dairy. Some reports suggest that dairy protein intake lowers ovarian reserve. Other reports suggest improved ART outcomes with increased dairy intake. Meat, fish, and dairy products, however, can also serve as vehicles for environmental contamination that may adversely affect the embryo. Fish, on the other hand, has been shown to exert positive effects on fertility.

Dietary approach. In general, a Mediterranean diet is favored (high intake of fruits, vegetables, fish, chicken, and olive oil) among women diagnosed with infertility.

Recommendations

A well-balanced diet, rich in vegetables and fruits, is preferred for infertile women and should provide the required micro- and macronutrients. It remains common for patients consume a wide variety of vitamin, mineral, and micronutrient supplements daily.^[4] Supplements should not replace food sources of vitamins and trace elements because of differences in bioavailability (natural versus synthetic), and inaccuracy of label declarations may result in suboptimal intake of important nutrients.^[5,6] Furthermore, naturally occurring vitamins and micronutrients are more efficiently absorbed.

With respect to overall diet, women are advised to follow a caloric intake that won’t contribute to being overweight or obese. Obesity is on the rise among younger people, including children. Obese women have a lower chance of conceiving and are less likely to have an uncomplicated pregnancy.^[7] Proper weight can be maintained with an appropriate diet and regular exercise.

Finally, women must abstain from substances that are potentially harmful to pregnancy (eg, smoking, alcohol, recreational drugs, high caffeine intake).

Causes of Infertility

ovulatory defect,
tubal occlusion,
low sperm counts), and many

Factors lower the chance of pregnancy

older age,
lower ovarian reserve,
endometriosis

Factors can’t be altered

age and
ovarian reserve

Modifiable Factors:

body weight and
lifestyle habits

REFERENCES

SOURCE

http://Peter Kovacs. Food and Fertility: What Should Women Consume When Trying to Conceive? – Medscape – Dec 06, 2018.

Read Full Post »

Live 2:30-4:30 PM Mediterranean Diet and Lifestyle: A Symposium on Diet and Human Health: October 19, 2018

Posted in Acute coronary syndrome, Cancer - General, Cancer Prevention: Research & Programs, congestive heart failure, Epigenetics and Cardiovascular Risks, Heart Failure (HF), interventional oncology, Obesity, Scientific & Biotech Conferences: Press Coverage, Scientific Publishing, tagged application to nutrition, balanced life, dietician, healthy diet, healthy eating, lifestyle, mediteranean diet, Mediterranean Diet, New York University, Nutrition, phytochemicals, preventive healthcare, wellness on October 20, 2018| Leave a Comment »

Live 2:30-4:30 PM Mediterranean Diet and Lifestyle: A Symposium on Diet and Human Health: October 19, 2018

Reporter: Stephen J. Williams, Ph.D.

2:30 Mediterranean Diet, Intangible Heritage and Sustainable Tourism?

Prof. Fabio Parasecoli, PhD.

Nutrition and Food Department, New York University

We focus on more of the cultural aspects and the relevance of this diet to tourism in Italy where there is a high rate of unemployment. The diet is interesting from a touristic standpoint as the diet have the perspective of the different ingredients inherent in Italy. The mediterranean diet food pyramid totally different than US. How do we explain to consumers these medical concepts; for example in China, Germany they are using different ways to explain the benefits of this diet.

A Cultural Formation

a way of life, for tourism there is the way of life people want to adopt (easiest way to do this is go to the Mediterranean and learn the lifestyle)
so for example Olive Garden for marketing purposes sent a few chefs for half a day training so the image of learning to cook in the mediterranean diet style can be very powerful communicative tool
2003 UNESCO Convention for Safeguarding the Culturing Heritage: protecting landscapes but then decided to protect other intangible heritage like oral, language, oral traditions like transmitting recipes, social and festive events (how do we cook how do we grow tomatoes, wheat etc)
UNESCO: promoted France Gastronomic, Mediterranean Diet, and traditional Mexican Cuisine (Mayan)
defined Greece, Italy, Morroco then included Cyprus Crotia and Portugal in the Mediterranean diet
has it been used for promotion: no UNESCO did not use this since does not safeguard the culture
(gastrodiplomacy); like Korea and kimchie; included in the list of cultural cuisine but can create tourist bubbles as you tourism places like hotels don’t always use; for reasons of economy or safety or accessibility , local food
Centrality of Territorio: food consumed from tourist should come from the area

Sustainable Tourism: a form of tourism where have the intention to get to know the place;

have to think in three ways

environmental
social
cultural

how do we make a circular economy so no waste; for example certain companies using food waste to make other products

Tourism clusters made of many groups; he is working on a way to jump start these networks in Nigeria;

Sustainable Food Supply Chain Tourism can be used as way to engage people and promote the diet

Question: are there regions where people are not adopting the diet because of taste, preferences

Yes there is always a problem with accessibility, affordability, trade issues and regional acceptance. For instance in Australia a big push back against the Mediterranean diet. Medical professionals need to work with communication experts and media experts in developing ways to communicate the benefits since “no one wants to be preached at” and “as economies get richer people want to be more modern and try new things”

In Nigeria we are working with many different industries like transportation, engineers, the IT industry and chefs to build a scalable model

3.00 Italy as a Case Study: Increasing Students’ Level of Awareness of the Historical, Cultural, Political and Culinary Significance of Food

Prof. Lisa Sasson

Nutrition and Food Department, New York University

Started a program at NYU to understand food from a nutritionist and historical point of view as a cultural heritage in Italy, but when students came back students mentioned it changed their food shopping habits

they described diet as wine, pasta, and olive oil

Artisional Production: understanding the taste and flavor; she wanted them to learn about the food culture and educate their tastes

Food Memories: how we pass on recipes and food aromas, food tastes. The students were experienced food in a unique way for the first time, experiencing what cheese, quality oil other foods when fresh tastes like. Artisional foods may be expensive but need only a little of it because the tastes and flavors are so potent due to the phytochemicals

Within six months students:

increased consumption of weekly wine consumption with meals
increased consuming satisfying meals
increased time consuming meals

In the womb the fetus is actually acquiring sense of taste (amniotic fluid changes with mother diet; can detect flavor chemicals)

Student Perceptions after a study Abroad Program

eating foods local and seasonal
replacing butter with quality olive oil
using herbs
very little sugar
unsweetened beverages
limiting red meats
fish a couple of times a week
dairy in moderation
no processed foods

Eating and Dining for Americans is a Challenge: The students ate well and satisfying meals but ate alot but did not gain weight

3:30 Italian Migration and Global Diaspora

Dr. Vincenzo Milione, PhD

Director of Demographics Studies, Calandra Institute, City University of New York

for a PDF of this presentation please click here: sbarro handout.

Dr. Millione used the U.S. Census Bureau Data to estimate the growth of the Italian diaspora descendants in host countries in the Americas and to determine the mixed global ancestry of Italian descendants.

Italian emigration to the US happened in two waves

Wave 1: early 1900 peaking between 1901 and 1911 (turn of century)
Wave 2: 1951-1971 (post WWII)

This pattern was similar between North and South America although South American had first Italian immigration; in 1860 we got rid of slavery so many jobs not filled new orleans

Developing a mathematical model of Italian diaspora: the model is centered on the host country population dynamics but descendants are separated into first generation and multi generation

Model dependent on:

birth and death rates
first generation population growth
multi generational population growth
emigration from host country over time

He was able to calculate an indices he termed Year of Italianization Change (YIC): the year the growth of the multi generation supercedes the first generation immigrant population

Country	Year of Italianlization Change (YIC)
Brazil	1911
Uruguay	1915
Argentina	1918
USA	1936
Venezuela	1963
Canada	1968
Australia	1988

note: as a result there is an increasing loss of language and traditional customs with host country cultural adaptation among the native born descendants

In addition, over the last 20 years Italian-American population growth demonstrates that Italian-American self-identity in the United States has increased. The census data identified two ancestries of the respondent. In mixed ancestry Italian-American respondents to the extent they identify Italian first demonstrating the strong Italian-American identity.

The foreign born Italian Americans mirror the immigration pattern of Italian immigration from Italy until 1980 where more Italian Americans self identify as foreign born in other countries and not in Italy

Summary

over 5 million Italians have emigrated from Italy from 1980 to present
most went to North and South America but many went to other global countries
the Italian immigration to the different countries in the Americas varies over the period of mass emigration when the growth of multi generational Italian descendants is greater then first generation Italians (Year of Italianization Change) goes from 1911 in Brazil to 1988 in Australia
Immigrants to the USA was not just from Italy but from almost all nations globally over all geographical continents
Italina immigrants descendants greatly grew after 1930 with appreciable increase with other ethnicities such that 61% of Italian Americans are mixed ancestry in 2014: to date mixed ancestry represents 98% of Italian Americans
younger italian americans more likely to have mixed ancestry with Central and South America, Asian and African ethnicities

over time during immigration eating habits has changed but more research is needed if and how the italian recipes and diet has changed as well

4:15 Conclusions

Prof. Antonio Giordano, MD, PhD.

To follow or Tweet on Twitter please use the following handles (@) and hashtags (#):

@ handles

# hashtags

#health

#nutrition

Please see related articles on Live Coverage of Previous Meetings on this Open Access Journal

Real Time Conference Coverage for Scientific and Business Media: Unique Twitter Hashtags and Handles per Conference Presentation/Session

LIVE – Real Time – 16th Annual Cancer Research Symposium, Koch Institute, Friday, June 16, 9AM – 5PM, Kresge Auditorium, MIT

Real Time Coverage and eProceedings of Presentations on 11/16 – 11/17, 2016, The 12th Annual Personalized Medicine Conference, HARVARD MEDICAL SCHOOL, Joseph B. Martin Conference Center, 77 Avenue Louis Pasteur, Boston

Tweets Impression Analytics, Re-Tweets, Tweets and Likes by @AVIVA1950 and @pharma_BI for 2018 BioIT, Boston, 5/15 – 5/17, 2018

BIO 2018! June 4-7, 2018 at Boston Convention & Exhibition Center

LIVE 2018 The 21st Gabay Award to LORENZ STUDER, Memorial Sloan Kettering Cancer Center, contributions in stem cell biology and patient-specific, cell-based therapy

HUBweek 2018, October 8-14, 2018, Greater Boston – “We The Future” – coming together, of breaking down barriers, of convening across disciplinary lines to shape our future

Read Full Post »

Live 12:00 – 1:00 P.M Mediterranean Diet and Lifestyle: A Symposium on Diet and Human Health : October 19, 2018

Posted in Apoptosis, Biological Networks, Gene Regulation and Evolution, Cancer - General, Cancer and Current Therapeutics, Epigenetics and Cardiovascular Risks, Epigenetics and Environmental Factors, Genomic Expression, Health Economics and Outcomes Research, Heart and Brain Disease in Women, Immune Modulatory, interventional oncology, Left Main Coronary Artery Disease (LMCAD), Li-fraumeni syndrome., Micronutrients, Nutrigenomics, Nutritional Supplements: Atherogenesis, Obesity, Pharmacotherapy of Cardiovascular Disease, REAL TIME Conference Coverage Twitter's Hashtags and Handles per Presentation/session, Scientific & Biotech Conferences: Press Coverage, TP53 - Germline mutations, Uncategorized, tagged application to nutrition, Cancer, cancer prevention, Diabetes, diet, disease prevention, environment, Epidemiology, epigenetic, gastric cancer, healthcare, healthy eating, mediteranean diet, Nutrition, RB2, retinoblastoma gene, TP53, World Health Organization on October 19, 2018| Leave a Comment »

Live 12:00 – 1:00 P.M Mediterranean Diet and Lifestyle: A Symposium on Diet and Human Health : October 19, 2018

Reporter: Stephen J. Williams, Ph.D.

12.00 The Italian Mediterranean Diet as a Model of Identity of a People with a Universal Good to Safeguard Health?

Prof. Antonino De Lorenzo, MD, PhD.

Director of the School of Specialization in Clinical Nutrition, University of Rome “Tor Vergata”

It is important to determine how our bodies interacts with the environment, such as absorption of nutrients.

Studies shown here show decrease in life expectancy of a high sugar diet, but the quality of the diet, not just the type of diet is important, especially the role of natural probiotics and phenolic compounds found in the Mediterranean diet.

The WHO report in 2005 discusses the unsustainability of nutrition deficiencies and suggest a proactive personalized and preventative/predictive approach of diet and health.

Most of the noncommunicable diseases like CV (46%) cancer 21% and 11% respiratory and 4% diabetes could be prevented and or cured with proper dietary approaches

Italy vs. the US diseases: in Italy most disease due to environmental contamination while US diet plays a major role

The issue we are facing in less than 10% of the Italian population (fruit, fibers, oils) are not getting the proper foods, diet and contributing to as we suggest 46% of the disease

The Food Paradox: 1.5 billion are obese; we notice we are eating less products of quality and most quality produce is going to waste;

growing BMI and junk food: our studies are correlating the junk food (pre-prepared) and global BMI
modern diet and impact of human health (junk food high in additives, salt) has impact on microflora
Western Diet and Addiction: We show a link (using brain scans) showing correlation of junk food, sugar cravings, and other addictive behaviors by affecting the dopamine signaling in the substantia nigra
developed a junk food calculator and a Mediterranean diet calculator
the intersection of culture, food is embedded in the Mediterranean diet; this is supported by dietary studies of two distinct rural Italian populations (one of these in the US) show decrease in diet
Impact of diet: have model in Germany how this diet can increase health and life expectancy
from 1950 to present day 2.7 unit increase in the diet index can increase life expectancy by 26%
so there is an inverse relationship with our index and breast cancer

Environment and metal contamination and glyphosate: contribution to disease and impact of maintaining the healthy diet

huge problem with use of pesticides and increase in celiac disease

12:30 Environment and Health

Dr. Iris Maria Forte, PhD.

National Cancer Institute “Pascale” Foundation | IRCCS · Department of Research, Naples, Italy

Cancer as a disease of the environment. Weinberg’s hallmarks of Cancer reveal how environment and epigenetics can impact any of these hallmarks.

Epigenetic effects

gene gatekeepers (Rb and P53)
DNA repair and damage stabilization

Heavy Metals and Dioxins:( alterations of the immune system as well as epigenetic regulations)

Asbestos and Mesothelioma: they have demonstrated that p53 can be involved in development of mesothelioma as reactivating p53 may be a suitable strategy for therapy

Diet, Tomato and Cancer

looked at tomato extract on p53 function in gastric cancer: tomato extract had a growth reduction effect and altered cell cycle regulation and results in apoptosis
RBL2 levels are increased in extract amount dependent manner so data shows effect of certain tomato extracts of the southern italian tomato ( )

Antonio Giordano: we tested whole extracts of almost 30 different varieties of tomato. The tomato variety with highest activity was near Ravela however black tomatoes have shown high antitumor activity. We have done a followup studies showing that these varieties, if grow elsewhere lose their antitumor activity after two or three generations of breeding, even though there genetics are similar. We are also studying the effects of different styles of cooking of these tomatoes and if it reduces antitumor effect

please see post https://news.temple.edu/news/2017-08-28/muse-cancer-fighting-tomatoes-study-italian-food

To follow or Tweet on Twitter please use the following handles (@) and hashtags (#):

@ handles

# hashtags

#health

#nutrition

Please see related articles on Live Coverage of Previous Meetings on this Open Access Journal

Real Time Conference Coverage for Scientific and Business Media: Unique Twitter Hashtags and Handles per Conference Presentation/Session

LIVE – Real Time – 16th Annual Cancer Research Symposium, Koch Institute, Friday, June 16, 9AM – 5PM, Kresge Auditorium, MIT

Real Time Coverage and eProceedings of Presentations on 11/16 – 11/17, 2016, The 12th Annual Personalized Medicine Conference, HARVARD MEDICAL SCHOOL, Joseph B. Martin Conference Center, 77 Avenue Louis Pasteur, Boston

Tweets Impression Analytics, Re-Tweets, Tweets and Likes by @AVIVA1950 and @pharma_BI for 2018 BioIT, Boston, 5/15 – 5/17, 2018

BIO 2018! June 4-7, 2018 at Boston Convention & Exhibition Center

LIVE 2018 The 21st Gabay Award to LORENZ STUDER, Memorial Sloan Kettering Cancer Center, contributions in stem cell biology and patient-specific, cell-based therapy

HUBweek 2018, October 8-14, 2018, Greater Boston – “We The Future” – coming together, of breaking down barriers, of convening across disciplinary lines to shape our future

Read Full Post »

Omega-3 fats Supplements Effect on Cardiovascular Health: EPA and DHA has little or no effect on Mortality or Cardiovascular Health

Posted in Atherogenic Processes & Pathology, Cardiovascular Research, Frontiers in Cardiology and Cardiovascular Disorders, Nutrition, Nutritional Supplements: Atherogenesis, Nutritional Supplements: Atherogenesis, lipid metabolism, Obesity, Plant extract, tagged (long-chain omega-3 (LCn3), docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), from plants (alpha-linolenic acid (ALA), omega-3 polyunsaturated fatty acids on July 24, 2018| Leave a Comment »

Omega-3 fats Supplements Effect on Cardiovascular Health: EPA and DHA has little or no effect on Mortality or Cardiovascular Health

Reporter: Aviva Lev-Ari, PhD, RN

Cochrane Database Syst Rev. 2018 Jul 18;7:CD003177. doi: 10.1002/14651858.CD003177.pub3. [Epub ahead of print]

Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease.

Abdelhamid AS¹, Brown TJ, Brainard JS, Biswas P, Thorpe GC, Moore HJ, Deane KH, AlAbdulghafoor FK, Summerbell CD, Worthington HV, Song F, Hooper L.

Author information

Abstract

BACKGROUND:

Researchers have suggested that omega-3 polyunsaturated fatty acids from oily fish (long-chain omega-3 (LCn3), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), as well as from plants (alpha-linolenic acid (ALA)) benefit cardiovascular health. Guidelines recommend increasing omega-3-rich foods, and sometimes supplementation, but recent trials have not confirmed this.

OBJECTIVES:

To assess effects of increased intake of fish- and plant-based omega-3 for all-cause mortality, cardiovascular (CVD) events, adiposity and lipids.

SEARCH METHODS:

We searched CENTRAL, MEDLINE and Embase to April 2017, plus ClinicalTrials.gov and World Health Organization International Clinical Trials Registry to September 2016, with no language restrictions. We handsearched systematic review references and bibliographies and contacted authors.

SELECTION CRITERIA:

We included randomised controlled trials (RCTs) that lasted at least 12 months and compared supplementation and/or advice to increase LCn3 or ALA intake versus usual or lower intake.

DATA COLLECTION AND ANALYSIS:

Two review authors independently assessed studies for inclusion, extracted data and assessed validity. We performed separate random-effects meta-analysis for ALA and LCn3 interventions, and assessed dose-response relationships through meta-regression.

MAIN RESULTS:

We included 79 RCTs (112,059 participants) in this review update and found that 25 were at low summary risk of bias. Trials were of 12 to 72 months’ duration and included adults at varying cardiovascular risk, mainly in high-income countries. Most studies assessed LCn3 supplementation with capsules, but some used LCn3- or ALA-rich or enriched foods or dietary advice compared to placebo or usual diet.Meta-analysis and sensitivity analyses suggested little or no effect of increasing LCn3 on all-cause mortality (RR 0.98, 95% CI 0.90 to 1.03, 92,653 participants; 8189 deaths in 39 trials, high-quality evidence), cardiovascular mortality (RR 0.95, 95% CI 0.87 to 1.03, 67,772 participants; 4544 CVD deaths in 25 RCTs), cardiovascular events (RR 0.99, 95% CI 0.94 to 1.04, 90,378 participants; 14,737 people experienced events in 38 trials, high-quality evidence), coronary heart disease (CHD) mortality (RR 0.93, 95% CI 0.79 to 1.09, 73,491 participants; 1596 CHD deaths in 21 RCTs), stroke (RR 1.06, 95% CI 0.96 to 1.16, 89,358 participants; 1822 strokes in 28 trials) or arrhythmia (RR 0.97, 95% CI 0.90 to 1.05, 53,796 participants; 3788 people experienced arrhythmia in 28 RCTs). There was a suggestion that LCn3 reduced CHD events (RR 0.93, 95% CI 0.88 to 0.97, 84,301 participants; 5469 people experienced CHD events in 28 RCTs); however, this was not maintained in sensitivity analyses – LCn3 probably makes little or no difference to CHD event risk. All evidence was of moderate GRADE quality, except as noted.Increasing ALA intake probably makes little or no difference to all-cause mortality (RR 1.01, 95% CI 0.84 to 1.20, 19,327 participants; 459 deaths, 5 RCTs),cardiovascular mortality (RR 0.96, 95% CI 0.74 to 1.25, 18,619 participants; 219 cardiovascular deaths, 4 RCTs), and it may make little or no difference to CHD events (RR 1.00, 95% CI 0.80 to 1.22, 19,061 participants, 397 CHD events, 4 RCTs, low-quality evidence). However, increased ALA may slightly reduce risk of cardiovascular events (from 4.8% to 4.7%, RR 0.95, 95% CI 0.83 to 1.07, 19,327 participants; 884 CVD events, 5 RCTs, low-quality evidence), and probably reduces risk of CHD mortality (1.1% to 1.0%, RR 0.95, 95% CI 0.72 to 1.26, 18,353 participants; 193 CHD deaths, 3 RCTs), and arrhythmia (3.3% to 2.6%, RR 0.79, 95% CI 0.57 to 1.10, 4,837 participants; 141 events, 1 RCT). Effects on stroke are unclear.Sensitivity analysis retaining only trials at low summary risk of bias moved effect sizes towards the null (RR 1.0) for all LCn3 primary outcomes except arrhythmias, but for most ALA outcomes, effect sizes moved to suggest protection. LCn3 funnel plots suggested that adding in missing studies/results would move effect sizes towards null for most primary outcomes. There were no dose or duration effects in subgrouping or meta-regression.There was no evidence that increasing LCn3 or ALA altered serious adverse events, adiposity or lipids, although LCn3 slightly reduced triglycerides and increased HDL. ALA probably reduces HDL (high- or moderate-quality evidence).

AUTHORS’ CONCLUSIONS:

This is the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date. Moderate- and high-quality evidence suggests that increasing EPA and DHA has little or no effect on mortality or cardiovascular health (evidence mainly from supplement trials). Previous suggestions of benefits from EPA and DHA supplements appear to spring from trials with higher risk of bias. Low-quality evidence suggests ALA may slightly reduce CVD event risk, CHD mortality and arrhythmia.

PMID:

30019766

DOI:

10.1002/14651858.CD003177.pub3

SOURCE

https://www.ncbi.nlm.nih.gov/pubmed/30019766

Read Full Post »

Curation of selected topics and articles on Role of G-Protein Coupled Receptors in Chronic Disease as supplemental information for #TUBiol3373

Posted in Alzheimer's Disease, Autoimmune Inflammatory DIseases, Biological Networks, Biological Networks, Gene Regulation and Evolution, Bone Disease and Musculoskeletal Disease, Ca2+ triggered activation, Cancer - General, Cancer and Current Therapeutics, CANCER BIOLOGY & Innovations in Cancer Therapy, Cell Biology, Cell Biology, Signaling & Cell Circuits, Chronic Thromboembolic Pulmonary Hypertension (CTEPH) and Pulmonary Arterial Hypertension (PAH), Crohn's disease, Curation, Etiology, Frontiers in Cardiology and Cardiovascular Disorders, interventional oncology, Obesity, Pharmacotherapy and Cell Activity, tagged #TUBiol3373, Alzheimer Disease, Amyloid aggregates, cardiovascular and lung disease, Cardiovascular and Metabolic Diseases, chronic diseases, Chronic Obstructive Lung Disease (COPD), G Protein coupling, G-protein coupled receptors (GPCR), ovarian cancer on May 2, 2018| Leave a Comment »

Curation of selected topics and articles on Role of G-Protein Coupled Receptors in Chronic Disease as supplemental information for #TUBiol3373

Curator: Stephen J. Williams, PhD

Below is a series of posts and articles related to the role of G protein coupled receptors (GPCR) in various chronic diseases. This is only a cursory collection and by no means represents the complete extensive literature on pathogenesis related to G protein function or alteration thereof. However it is important to note that, although we think of G protein signaling as rather short lived, quick, their chronic activation may lead to progression of various disease. As to whether disease onset, via GPCR, is a result of sustained signal, loss of desensitization mechanisms, or alterations of transduction systems is an area to be investigated.

From:

Molecular Pathogenesis of Progressive Lung Diseases

Author: Larry H. Bernstein, MD, FCAP

Chronic Obstructive Lung Disease (COPD)

Inflammatory and infectious factors are present in diseased airways that interact with G-protein coupled receptors (GPCRs), such as purinergic receptors and bradykinin (BK) receptors, to stimulate phospholipase C [PLC]. This is followed by the activation of inositol 1,4,5-trisphosphate (IP3)-dependent activation of IP3 channel receptors in the ER, which results in channel opening and release of stored Ca²⁺ into the cytoplasm. When ER Ca2+ stores are depleted a pathway for Ca²⁺ influx across the plasma membrane is activated. This has been referred to as “capacitative Ca²⁺ entry”, and “store-operated calcium entry” (3). In the next step PLC mediated Ca²⁺ i is mobilized as a result of GPCR activation by inflammatory mediators, which triggers cytokine production by Ca²⁺ i-dependent activation of the transcription factor nuclear factor kB (NF-kB) in airway epithelia.

In Alzheimer’s Disease

Important Lead in Alzheimer’s Disease Model

Larry H. Bernstein, MD, FCAP, Curator discusses findings from a research team at University of California at San Diego (UCSD) which the neuropeptide hormone corticotropin-releasing factor (CRF) as having an important role in the etiology of Alzheimer’s Disease (AD). CRF activates the CRF receptor (a G stimulatory receptor). It was found inhibition of the CRF receptor prevented cognitive impairment in a mouse model of AD. Furthermore researchers at the Flanders Interuniversity Institute for Biotechnology found the loss of a protein called G protein-coupled receptor 3 (GPR3) may lower the amyloid plaque aggregation, resulting in improved cognitive function. Additionally inhibition of several G-protein coupled receptors alter amyloid precursor processing, providing a further mechanism of the role of GPCR in AD (see references in The role of G protein-coupled receptors in the pathology of Alzheimer’s disease by Amantha Thathiah and Bart De Strooper Nature Reviews Feb 2011; 12: 73-87 and read post).

In Cardiovascular and Thrombotic Disease

Adenosine Receptor Agonist Increases Plasma Homocysteine

and read related articles in curation on effects of hormones on the cardiovascular system at

Action of Hormones on the Circulation

In Cancer

A Curated History of the Science Behind the Ovarian Cancer β-Blocker Trial

Further curations and references of G proteins and chronic disease can be found at the Open Access journal https://pharmaceuticalintelligence.com using the search terms “GCPR” and “disease” in the Search box in the upper right of the home page.

Read Full Post »

Benefits of Fiber in Diet

Posted in Autoimmune Inflammatory DIseases, Cell Biology, Cell Biology, Signaling & Cell Circuits, Chemical Biology and its relations to Metabolic Disease, Gut Microbiome and Obesity, Human Immune System in Health and in Disease, Lipid metabolism, Metabolomics, Microbiology, Micronutrients, Nutrition, Nutrition and Phytochemistry, Nutrition Disorders, Obesity, Population Health Management, Population Health Management, Nutrition and Phytochemistry, Protein-energy malnutrition, Signaling & Cell Circuits, tagged Dietary fiber, enzyme, gut bacteria, inflammation, microbiome, Obesity on March 14, 2018| Leave a Comment »

Benefits of Fiber in Diet

Reporter and Curator: Dr. Sudipta Saha, Ph.D.

UPDATED on 1/15/2019

This is How Much Daily Fiber to Eat for Better Health – More appears better in meta-analysis — as in more than 30 g/day

by Ashley Lyles, Staff Writer, MedPage Today

January 14, 2019

In the systematic review, observational data showed a 15% to 30% decline in cardiovascular-related death, all-cause mortality, and incidence of stroke, coronary heart disease, type 2 diabetes, and colorectal cancer among people who consumed the most dietary fiber compared to those consuming the lowest amounts.

Whole grain intake yielded similar findings.

Risk reduction associated with a range of critical outcomes was greatest when daily intake of dietary fibre was between 25 g and 29 g. Dose-response curves suggested that higher intakes of dietary fibre could confer even greater benefit to protect against cardiovascular diseases, type 2 diabetes, and colorectal and breast cancer.

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(18)31809-9.pdf

Eating more dietary fiber was linked with lower risk of disease and death, a meta-analysis showed.

According to observational studies, risk was reduced most for a range of critical outcomes from all-cause mortality to stroke when daily fiber consumption was between 25 grams and 29 grams, reported Jim Mann, PhD, of University of Otago in Dunedin, New Zealand, and colleagues in The Lancet.

By upping daily intake to 30 grams or more, people had even greater prevention of certain conditions: colorectal and breast cancer, type 2 diabetes, and cardiovascular diseases, according to dose-response curves the authors created.

Quantitative guidelines relating to dietary fiber have not been available, the researchers said. With the GRADE method, they determined that there was moderate and low-to-moderate certainty of evidence for the benefits of dietary fiber consumption and whole grain consumption, respectively.

Included in the systematic review were 58 clinical trials and 185 prospective studies for a total of 4,635 adult participants with 135 million person-years of information (one trial in children was included, but analyzed separately from adults). Trials and prospective studies assessing weight loss, supplement use, and participants with a chronic disease were excluded.

Food is digested by bathing in enzymes that break down its molecules. Those molecular fragments then pass through the gut wall and are absorbed in our intestines. But our bodies make a limited range of enzymes, so that we cannot break down many of the tough compounds in plants. The term “dietary fiber” refers to those indigestible molecules. These dietary fibers are indigestible only to us. The gut is coated with a layer of mucus, on which sits a carpet of hundreds of species of bacteria, part of the human microbiome. Some of these microbes carry the enzymes needed to break down various kinds of dietary fibers.

Scientists at the University of Gothenburg in Sweden are running experiments that are yielding some important new clues about fiber’s role in human health. Their research indicates that fiber doesn’t deliver many of its benefits directly to our bodies. Instead, the fiber we eat feeds billions of bacteria in our guts. Keeping them happy means our intestines and immune systems remain in good working order. The scientists have recently reported that the microbes are involved in the benefits obtained from the fruits-and-vegetables diet. Research proved that low fiber diet decreases the gut bacteria population by tenfold.

Along with changes to the microbiome there were also rapid changes observed in the experimental mice. Their intestines got smaller, and its mucus layer thinner. As a result, bacteria wound up much closer to the intestinal wall, and that encroachment triggered an immune reaction. After a few days on the low-fiber diet, mouse intestines developed chronic inflammation. After a few weeks, they started putting on fat and developing higher blood sugar levels. Inflammation can help fight infections, but if it becomes chronic, it can harm our bodies. Among other things, chronic inflammation may interfere with how the body uses the calories in food, storing more of it as fat rather than burning it for energy.

In a way fiber benefits human health is by giving, indirectly, another source of food. When bacteria finished harvesting the energy in the dietary fiber, they cast off the fragments as waste. That waste — in the form of short-chain fatty acids — is absorbed by intestinal cells, which use it as fuel. But the gut’s microbes do more than just make energy. They also send messages. Intestinal cells rely on chemical signals from the bacteria to work properly. The cells respond to the signals by multiplying and making a healthy supply of mucus. They also release bacteria-killing molecules. By generating these responses, gut bacteria help to maintain a peaceful coexistence with the immune system. They rest on the gut’s mucus layer at a safe distance from the intestinal wall. Any bacteria that wind up too close get wiped out by antimicrobial poisons.

A diet of fiber-rich foods, such as fruits and vegetables, reduces the risk of developing diabetes, heart disease and arthritis. Eating more fiber seems to lower people’s mortality rate, whatever be the cause. Researchers hope that they will learn more about how fiber influences the microbiome to use it as a way to treat disorders. Lowering inflammation with fiber may also help in the treatment of immune disorders such as inflammatory bowel disease. Fiber may also help reverse obesity. They found that fiber supplements helped obese people to lose weight. It’s possible that each type of fiber feeds a particular set of bacteria, which send their own important signals to our bodies.

References:

https://www.nytimes.com/2018/01/01/science/food-fiber-microbiome-inflammation.html

https://www.ncbi.nlm.nih.gov/pubmed/29276171

https://www.ncbi.nlm.nih.gov/pubmed/29276170

https://www.ncbi.nlm.nih.gov/pubmed/29486139

https://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/fiber/art-20043983

https://nutritiouslife.com/eat-empowered/high-fiber-diet/

http://www.eatingwell.com/article/287742/10-amazing-health-benefits-of-eating-more-fiber/

http://www.cookinglight.com/eating-smart/nutrition-101/what-is-a-high-fiber-diet

https://www.helpguide.org/articles/healthy-eating/high-fiber-foods.htm

https://www.gicare.com/diets/high-fiber-diet/

Read Full Post »

Higher BMI (Obesity Marker): Earlier onset of incident CVD followed by Shorter overall Survival – Men and women of all ages

Posted in Frontiers in Cardiology and Cardiovascular Disorders, Obesity on March 5, 2018| Leave a Comment »

Higher BMI (Obesity Marker): Earlier onset of incident CVD followed by Shorter overall Survival – Men and women of all ages

Reporter: Aviva Lev-Ari, PhD, RN

Men and women of all ages with a higher BMI were found to have both an earlier onset of incident CVD followed by shorter overall survival, Sadiya Khan, MD, of Northwestern University Feinberg School of Medicine in Chicago, and colleagues wrote in JAMA Cardiology.

Among middle-aged men, there were 13,457 incident CVD events total, with the highest percentage attributed to fatal or nonfatal myocardial infarctions. This incidence rate of CVD events increased accordingly with BMI range, with the highest seen in those who were morbidly obese. Compared with men who died due to non-CVD related causes — the most common of which was cancer — men who weighed more had a significantly higher rate of experiencing their first CVD event.

When compared to middle-aged men of normal weight, those in higher BMI categories had an increased incidence of CVD:

Overweight: adjusted competing HR 1.21 (95% CI 1.14-1.28)

Obese: 1.67 (95% CI 1.55-1.79)

Morbidly obese: 3.14 (95% CI 2.48-3.97)

Similar event rates were seen among middle-aged women of a higher BMI, as well:

Overweight: HR 1.32 (95% CI 1.24-1.40)

Obese 1.85 (95% CI 1.72-1.99)

Morbidly obese: 2.53 (95% CI 2.20-2.91)

Both men and women had a longer time to first CVD event if they were of normal weight by around 7.5 year and 7.1 years, respectively, when compared with people with morbid obesity.

The researchers noted that the morbidly obese category likely saw the highest rate of CVD events mainly due to a five-fold increase in the incidence of congestive heart failure events. These patterns were also seen in the younger and older age groups.

Although the notion of the “obesity paradox” — when people with a higher BMI might actually live longer after CVD onset compared to those of normal weight — has been described in some prior studies, the researchers noted that their findings suggest that “this occurs because of a trend toward earlier onset of disease in individuals who are overweight and obese.”