Obesity - Science topic
A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).
Questions related to Obesity
Health impacts of saturated fat seems to be contentious. Reports showing negative effects are numerous but inferences of some reports showing positive effects cannot be neglected at all. Based upon latest findings and summing up them with past research conclusions, what can be the best suggestion for common people today ?
A plant-based diet is a diet based on fruits, vegetables, whole grains, and legumes while a vegan diet is strictly against all animal products. Whats your openion about PBD and vegan and their effects on our health?
In context of a planned research program on obesity prevention, we would like to invite obesity and weight loss support groups from several European groups as consultants. These are not always easy to find, do any of you have contacts or links to such organisations? This would give a more patient centered profile for entire project.
Obese women have an increased risk of pregnancy-related complications, including hypertension, gestational diabetes, and blood clots. Maternal obesity is also known to be associated with increased rates of complications in late pregnancy such as cesarean delivery, and shoulder dystocia.
With the increase in studies examining the effects of infant growth and/or diet on later onset obesity I would be interested to hear what areas clinicians think are missing in this growing area of research. If given the opportunity what area of infant diet and/or growth would clinicians examine in looking at later onset obesity?
Obesity is simply defined as an excess of body fat. Peripheral (general) obesity is defined by finding a body mass index (BMI) = Wt(kg)/Ht (M2) of 30 and more. According to BMI, there are three grades of obesity, grade I obesity with BMI of 30-35, grade II obesity with BMI of 35-40 and grade III (morbid obesity) with BMI of 40 and more. On the other hand, abdominal (visceral) obesity is commonly assessed by measuring waist circumference (WC). It is usually confirmed with the finding of WC of 102 cm and more in men and 88 cm and more in women although there are population-based variations in these WC limits. Which is more harmful in terms of health complications, peripheral or abdominal obesity?
When we grow older, it is seems that we are more easily to have constipation. What are your suggested preventive measures in treating this condition?
As I have the physiological condition of anorexia nervosa/morbid obesity, I have to adopt the anorexic Luigi Cornaro diet of eat-but-little. And I think my problem of constipation is a result of my eating habit.
My solution for this problem is, don't wait for the spontaneous bowel movements, try to have two or more bowel movements within one day, one in the early morning when I just get up, the other one in the later afternoon to evening. In this way, I can effectively prevent constipation.
Need suggestion for High Fat Diet/Cafeteria diet of Indian food type for induction of Obesity in laboratory animals.I want to study specifically about Binge eating disorder.
I am looking to find out the top scientists and their clusters who are working in the field of Hyperlipidemia, Obesity and Lipid research. Please suggest me best methods to find out.
For my bachelor's thesis (Health Sciences), I am looking into the relationship between Eating Behaviour and Sensory Processing Sensitivity (a (personality) trait). My research question is therefore: What is the relationship between Eating Behaviour and Sensory Processing Sensitivity?
I have a sample of 150 participants, and I am doing a cross-sectional association survey study.
Eating Behaviour can be measured with the Adult Eating Behaviour Questionnaire, consisting of 35 5-point Likert scale items, that form 8 subscales. Those eight are my dependent variables.
Sensory Processing Sensitivity can be measured via the Highly Sensitive Person Scale, consisting of 27-items 7 point Likert scale, that form three subscales. The independent variables (four) are the total score for Sensory Processing Sensitivity, and it's three subscales.
After excluding participants who completed less than 80 % of both questionnaires, I have 0.26% missing items, only 23 out of 9000 items. As I will need to compute subscores with these items, I do not want these data points to remain missing/zero. As a method of imputation, I was considering mean imputation (so for each missing, imputing the mean of this specific item). I have read that this is not the best recommended method since it does not take into account relationships between variables, but the method is OK when you have very little missing data.
What type of missing imputation would you recommend me to do? The other option I'm considering is multiple imputation.
Please let me know your thoughts, I would be so grateful!
Thanks so much in advance!
Dear colleagues in a study which aims to test the effect of a medicinal plant on obesity, I want to know if there is a protocol for rapidly inducing obesity in rats.
In most of the communities especially are owned by lower socioeconomic status.Diet contains more of carbohydrate than protein and fat. More carbohydrate after catabolism produce more saturated fatty acids. This may disturb the level of LDL( high ) lead to atherosclerosis.
Obesity is big risk factor for many diseases including diabetes, stroke and cardiovascular diseases, so properly management is essential like 5 A, s, Ask, Assess, Advise, Agree, and Assist, you can check my video with full presentation with all information about obesity,
Obesity should be defined by a person's health - not just their weight, says a new Canadian clinical guideline.
It also advises doctors to go beyond simply recommending diet and exercise.
Instead, they should focus on the root causes of weight gain and take a holistic approach to health.
The guideline, which was published in the Canadian Medical Association Journal on Tuesday, specifically admonished weight-related stigma against patients in the health system.
"The dominant cultural narrative regarding obesity fuels assumptions about personal irresponsibility and lack of willpower and casts blame and shame upon people living with obesity," the guideline, which is intended to be used by primary care physicians in diagnosing and treating obesity in their daily practice, states.
Ximena Ramos-Salas, the director of research and policy at Obesity Canada and one of the guideline's authors, said research shows many doctors discriminate against obese patients, and that can lead to worse health outcomes irrespective of their weight.
"Weight bias is not just about believing the wrong thing about obesity," she told the BBC. "Weight bias actually has an effect on the behavior of healthcare practitioners."
5 August, BBC
Obesity puts people at risk for a whole host of conditions, including Type 2 diabetes, high blood pressure and sleep problems. But is obesity itself a disease?
Doctors are divided on the issue. Some say obesity is indeed a disease, with causes beyond eating too much and exercising too little, and consequences that harm the body like any medical condition. In addition, they say referring to obesity as a disease would improve care for patients, and ensure treatments are covered by insurance plans.
Others argue obesity is a risk factor for health problems, but not a disease itself. They say calling obesity a disease would stigmatize a huge population, and categorize some people as "sick" who actually may be healthy.
How can we harvest more RNA from adipose tissue which contains a lot of fat/lipid? Do we need any special reagent kits? Will we extract more total RNA from adipose tissue of one DIO (diet-induced obesity) mouse than that of one lean control mouse?
Basically, most of the literature declared that obesity will cause to up-regulation of inflammatory markers and macrophage infiltration in fat tissue. My question is that body weight loss other pathologic condition will decrease the inflammation and macrophage content of fat tissue?
I was wondering whether high-fat diet or high-sugar-high-fat diets are more commonly used for diet induced obesity in rodents? And the reasoning behind using one or the other.
When i do a pub-med search i see more hits for 'high-fat diet' for rodents, although there are many different terms for a high-sugar-high fat diet, so its hard to say. I would have expected that HFHS would be more effective.
I'm interested in which is the most effective at inducing obesity, and in particular i'm interested in the effect of the quality of the diet on inducing overeating behaviour. (i'm not planning on conducting experiments, rather looking at the findings in the literature). In general, I'm hoping to get impressions of 'experts in the field' as to what researchers generally use and why...
I'm looking for a dataset that includes basal metabolic rate (BMR) as a function of different attributes such as age, height, weight, fat mass, fat free mass, ethnicity, etc. Please let me know if you know of any related database or articles.
In the clinical world, GLP1 agonists and SGLT2 inhibitors are not commonly co-prescribed, though given the benefit of weight loss, cardiovascular benefits, and blood glucose control in patients with insulin resistance as well as obesity, should this be more commonly used? Thank you!
I would like to calculate the FCR for a diet-induced obesity experiment in rats. Since I have many nutrients/groups, I am calculating the food intake (FI) in kcal, not in grams of food. Has anybody ever calculated the FCR in kcal or knows a valid formula for it? I am not sure whether estimating the FCR as kcal/g of weight gain would be correct, since both the FI and the weight gain need to be in similar units. Some of the works I have been reading are not discerning between foods, and estimate the FCR as FI (g) / weight gain (g).
Many thanks in advance!
As per available records, PCOD develops due to imbalance of the two female hormones (estrogen and progesterone) where estrogen taking the upper hand.
Common symptoms are:
1. Menstrual irregularities,
3. Increased risk of Endometrial (inner lining of the uterus) cancer,
4. Increased risk of Breast cancer,
5. Insulin resistance,
6. Obesity and increase in weight (mainly around the waist),
7. Unwanted excess hair growth on face and body,
9. Dark pigmentation of skin around the neck etc.
What are the actual reasons works behind development of that dangerous disease?
Is it curable?
How can it be prevented?
I am interested in exploring the contribution of obesity in murine wound healing without the characteristic hyperglycemia of diabetic mice.
I have considered the use of an obese diabetic mouse raised on high fat diet, and then later attempting to suppress the hyperglycemia, but I fear that the mouse *ever* having high blood glucose levels may affect the long-term function of the immune and regenerative cells.
I am looking into Non-obese diabetic (NOD) mice, but an obese non-diabetic would be great.
Thank you for your time. Any advice would be welcome.
How can we obtain balanced full nutrition by just eating simple foods like bread and eggs?
There is something neglected in the common energy and nutrition balance equation for weight management.
The common understanding on energy and nutrition balance is that, it is the difference between energy/nutrition intake and energy/nutrition expenditure:
Energy/nutrition balance = energy/nutrition input – energy/nutrition output
When the intake exceeds the expenditure, there is a positive balance, which results in weight gain. When the intake is below the expenditure, there is a negative balance and weight loss results.
But most people on weight management know by experience that this equation doesn't work.
As a fundamental cellular homeostasis management program, Autophagy deals with harmful or surplus cellular contents such as protein aggregates, dysfunctional/long-lived organelles, intracellular pathogens, and storage nutrients (glycogen and lipid droplets) and recycles them as source of energy/nutrition:
So should we revise the energy/nutrition balance equation as:
Energy/nutrition balance = energy/nutrition input + recycled energy/nutrition from autophagy – energy/nutrition output?
Our health and physical/mental well-being is very important to our family, to the community and to the nation. If we fall in sickness, we will be the burden of our family, our community and to the nation.
So to be responsible for our family, our community and our nation, we should take good care of ourselves.
We evaluated patients from public and privative health care before and after bariatric surgery (pdf paper below). The presence or absence of advanced hepatic fibrosis was evaluated by NAFLD Fibrosis Score, a non-invasive method that uses age, BMI, AST/ALT ratio, albumin, platelet count and the presence or absence of hyperglycemia or diabetes. The characteristics of the two groups were compared.
Were analyzed 40 patients with a mean age of 34.6±9.5 years for private network and 40.6± 10.2 years for public. The study sample, 35% were treated at private health system and 65% in the public ones, 38% male and 62% female. Preoperatively in the private network one (7.1%) patient had advanced liver fibrosis and developed to the absence of liver fibrosis after surgery. In the public eight (30.8%) patients had advanced liver fibrosis preoperatively, and at one year after the proportion fell to six (23%).
The non-alcoholic fatty liver disease in its advanced form is more prevalent in obese patients treated in the public network than in the treated at the private network and bariatric surgery may be important therapeutic option in both populations.
Here I give two examples:
One is asked by Dr Alka Rani in the thread:
Another is "Why then do experimental animals not survive on diets lacking essential amino or fatty acids?", asked by Dr C.A. (Kees) Kan in the thread:
These questions have helped me to understand the importance of microbiome to our health.
Do you have encountered any good questions in researchGate that inspires and enlightens you?
People in attempt of losing weight always experience weight cycling: the repetitions of losing and gaining weight multiple times through their lives, or the so-called “Yo-Yo Effect”. What do you think are the causes of Yo-Yo Effect, and how to overcome them?
Excess weight is a serious concern worldwide which prones the individual to several complications like heart diseases and strokes, high blood pressure, diabetes, certain types of cancer, kidney disease, sleep apnea and fatty liver disease to list as few. According to WHO, more than 1.9 billion adults aged 18 years and older were overweight in 2016, of which over 650 million adults were obese. According to you, what are some of the most effective exercises, diet plan and herbs that can aid in weight loss?
There are lots of misconceptions about obesity, and its relation to diseases. The so called obesity epidemic is overblown, as a 2006 Scientific American paper stated:
Obesity is not life threatening, and it is not necessary leading to illness.
In dealing with obesity, it is important to distinguish morbid obesity from non-morbid obesity.
The most prominent cause of obesity is infectious diseases and inflammation, and the term infectobesity was coined by Dr. Nikhil V. Dhurandhar in 2001:
The up-regulated autophagy (xenophagy) triggered by infectious diseases turns the eliminated pathogens and dysfunctional cell components into nutrition and energy, which contributed to obesity. So obesity is a side effect of our body’s protective reaction to illness.
Obesity is normally measured by BMI. Yet, the big contributor to BMI is the subcutaneous fat, which is protective and normally harmless. But one relatively small component of the obesity, the excessive visceral fat and ectopic fat that surround the organs or enter the organ tissues, are very dangerous, which contributes to morbid obesity, and is associated with numerous diseases.
To get rid of the ectopic fats that surround the organs or enter the organ tissues, so as to avoid morbid obesity, daily regular time restrictive eating is efficient, and one still can live a long and healthy life by doing so:
I am working on a project about the involvement of oxidative stress in obesity. Does anyone have experience with adiponectin and/or leptin measurement using microplate readers (FluoStar Omega in particular)?
Every athlete requires an adequate amount of protein. It’s not only good to increase lean muscle mass , it will also optimize anabolic hormone levels, increase metabolism relative to other nutrients and improve cardiovascular risk profiles.
So which are better protein supplements or protein in foods ?
AGEs, ALEs and AOPPs are involved in almost all chronic inflammatory diseases. Preventing their formation may be a major step in reducing the morbidity of various chronic inflammatory diseases.
Most of these can be used as supplements to standard medication (eg. Resveratrol, L-Carnosine, Alpha Lipoic Acid, Pyridoxamine and Benfotiamine).
Please share your views and research findings (especially the dosages).
Pt contends that weight gain happened due to inability to adequately exercise due to prior failed spinal surgery leaving pain, radiculopathy and Lt drop foot. Evaluating MD said no and stated "there is a myth that exerecise is the most effective means of decreasing weight, when the effect is the opposite. Weight gain/Obesity is usually due to caloric intake" Who is correct?? Great arguement in the office what say you??
I have an article on energy metabolism that I want to publish, and I'm not sure what journal would be appropriate for it. The article presents a new theory based on data from existing studies. It is not really a review, because it doesn't address a question that these previous studies asked. Can anyone suggest a journal that might publish such an article?
I am primarily interested in getting this idea into the medical databases. Getting a large amount of exposure is not that important.
If you want to know about the theory, it concerns "weight cycling" -- the strong tendency of dieters to regain the weight they have lost. My theory is that weight cycling is an evolutionary adaptation to seasonal food shortages.
J. S. Shapiro
The thought behind this diet is to cut out foods that cause your body to produce acid ; including meat, wheat, refined sugar, processed foods, dairy, eggs, canned food, packaged snacks, caffeine and alcohol. The Alkaline diet encourage of most fruits and vegetables, nuts, legumes, soybeans and tofu. These are foods that are alkaline; that have a pH value of 7 or above.
The ketogenic diet has gained popularity as a natural way to lose weight and improve health. The diet is very low in carbohydrates, high in fat and moderate in protein. While the diet is considered safe for most people, it’s associated with some unpleasant side effects.
Steatosis , occurs in more than 50% of patients with chronic hepatitis C, that is related to visceral adiposity and obesity. Moreover, Weight loss in patients with chronic hepatitis C may be associated with a reduction in steatosis and abnormal liver enzymes and an improvement in fibrosis. So my question May weight reduction provide a proper response for treatment of patients with chronic C ?
Obesity is the plague of current day era. Now some researchers even link it to cancer. As per medscape
" Excess body weight is responsible for about 4 percent of all cancer cases worldwide and an even larger proportion of malignancies diagnosed in developing countries, a new study suggests"
I have a project on obesity prevention campaign. this project is aimed to study the effectiveness of the campaign on the targets' knowledge on obesity and healthy lifestyle. hence, i would like to find the most suitable questionnaire that can be used for the pre and post test of the campaign. the target of the campaign will be female university students ranging from 18 to 24 years old.
Your ability to lose, gain or maintain your weight is dependent on genetic, environmental, and behavioral factors. But how much of a role does genetics play in weight loss versus eating a healthy diet? Is there any truth to genetics playing a substantial role in your ability to lose weight to improve health and overall body composition? Or the exercise and diet is the driving factor?
Can anyone provide papers or links to research conducted on the Prevalence of Obesity in Patients with Type 2 Diabetes Mellitus in The Middle East Countries during the Last Decade? �
Dear esteemed colleagues,
Does anyone have any insight why most of the neuroendocrine studies, i.e hypothalamus-pituitary-peripheral organs axis, are mostly studied in mice? I do know some studies were done in rat, and even there are some rat animal models (HFD, genetic models, streptozocin, etc) but to my knowledge this is overwhelmingly minor compared to mouse models.
Is there any particular reason, such as mice neuroendocrine system more closely mimics human's? Or is there any technical reason? Thank you!
My interest is on Weight Management. I have read a lot of articles on Anti-fat bias amongst Health professionals and I am finding it difficult to trace gaps in research.
It is very interesting I should like to mention it in my future research.
Dr. Claudio Blasi
(Blasi C. The Role of the Vagal Nucleus Tractus Solitarius in the Therapeutic Effects of Obesity Surgery and Other Interventional Therapies on Type 2 Diabetes. Obes Surg. 2016 Dec;26(12):3045-3057. Review. PubMed PMID: 27730463).
i have read several articles and there were contradictions. The main problem was about adipose tissue and obesity. As adipocyte grows, it would secrete MCP-1 or other adipokine that attract macrophages. Consequently attracted macrophages would secrete various inflammation cytokines such as TNF-alpha. Those cytokines would decrease insulin sensitivity in adipose tissue and muscle. On top of that it would also decrease ppar gamma gene expression and increase lipolysis. As a result concentration of free fatty acid increases. However, the obese are getting more fat and have a larger adipose tissue than lean subject or mouse. Can anyone solve this contradiction
I'm writing a paper where I'm establishing Binge Eating Disorder, Obesity and Stress. I'm looking for latest research around it.
Any feedback, paper link, insight around this topic will be appreciated.
It is known that the insulin level drops during sports in healthy people, despite a much higher glucose demand of skeletal muscles. Is this important for glucagon regulation and fat burn? How would a high continuing glucose ingestion during activity influence performance and fat burn utilisation?
People these days are becoming sick because of overeating and junk foods and bad food additives, and healthy people are those who eat small amounts. Most people are dying because of diseases linked to food consumption and their number is more than those who are dying of hunger.
Paleo diet method is one of the successful diet method for diabetic, obesity, HT. The main concept of this food method is simple as avoid glucose completely. And there is no restriction for the natural lipid and protein intake.
I am analysing the change in BMI between two groups. Although the results are statistically significant, I am struggling to find any sources that have evidence for what a clinically significant difference is?
Any advice/ direction to relevant sources would be gratefully recieved, thank you.
Please go through these 3 references:
1. An excerpt from wikipedia: (https://en.wikipedia.org/wiki/Lipid) reads:
"A few studies have suggested that total dietary fat intake is linked to an increased risk of obesity (Astrup, 2005; Astrup et al., 2008) and diabetes (Astrup, 2008). However, a number of very large studies, including the Women's Health Initiative Dietary Modification Trial, an eight-year study of 49,000 women, the Nurses' Health Study and the Health Professionals Follow-up Study, revealed no such links (Beresford et al., 2006; Howard et al., 2006). None of these studies suggested any connection between percentage of calories from fat and risk of cancer, heart disease, or weight gain."
2. Watch the video, Sugar the bitter truth by Robert H. Lustig, MD, UCSF professor of pediatrics in the division of endocrinology (https://www.youtube.com/watch?v=dBnniua6-oM).
3. Read this book by John Yudkin: http://www.teethforlife.co.za/images/Pure,%20White%20and%20Deadly%20-%20%20John%20Yudkin.pdf
Analogy: So is it logical to exonerate sugar and indict fat cholesterol as the major causes of heart diseases, increase in blood pressure, obesity, type 2 diabetes etc?
Forced inspiratory vital capacity (FIVC) and forced first-second inspiratory volume (FIVC) may be increased or descreased in obesity, asthma or both?
I could only find references about VIF1 in the performance evaluation of swimmers.
I'm currently working on a mouse model that becomes obese and glucose intolerant at the age of 7 months when fed standard chow. Since I'm primarily a reproductive biologist, I have a naive question: do I need to do a high fat diet experiment? My hypothesis is that then the mice might just become more obese and maybe at a younger age, but would this experiment be necessary? What crucial information could I gain by doing this experiment?
It is estimated that around 11,000 people die about obesity-related diseases every day around the world. While the number of deaths worldwide for hunger or malnutrition-related illness is around 24,000 per day. Obesity is fought by reducing food spending while to fight hunger in the world it is necessary to increase food spending.