Science topic

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).
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Dear colleagues,
May I ask, What are the most important factors that affect the feeling of hunger?
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Physiological and behavioral factors, gastrointestinal factors, disease-associated factors, and environmental factors that initiate the hunger center can affect the feeling of hunger.
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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 ?
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The following RG link is also very good:
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Dear Colleagues,
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?
Thanks
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Healthy plant-based foods may lower risk and severity of COVID-19.
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Dear collogues,
May I ask, What are the best natural herbs for obesity management?
Thanks
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Dear,
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.
Regards.
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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.
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Maternal obesity increases risks of pregnancy complications such as gestational diabetes, preeclampsia, preterm birth, and birth trauma, which have been shown to be associated with offspring neurodevelopment.
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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?
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yes , in deed , infantile obesity is very difficult to manage especially those which attributed to genetic cause
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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?
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What are the conceptual bases for personalised nutrition?
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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?
Thank you!
An update:
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.
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TRIPHALA - An excellent ayurvedic colon cleaner manufactured in India .
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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.
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For mice models you can use plant based oils like olive oil, safflower oil, corn oil or animal based fats like lard, beef tallow in a composition providing 20-60% of total energy. There are many related studies.
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Hi friends,
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.
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I agree with Kabelo Mokgalaboni.
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Please some one suggest me some quality peer review Jounals on Obesity and hyperlipidemia which donot ask for article processing fees.
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Please go to the website of these journals, to note for their impact factor, requirements for publications, publication cost and match it with how much you can spend on publication depending on whether you can afford it, or your institution may pay it, or the granting authority for the research you have done can pay it.
Many journals may waive off the publication charges for third world countries.
  • Journal of Obesity.
  • Obesity Research & Clinical Practice.
  • International Journal of Obesity.
  • Iranian Journal of Diabetes and Obesity.
  • The Open Obesity Journal.
  • Obesity Management.
  • Obesity Wiley Online Library.
  • Obesity journal.
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Dear statisticians,
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!
Kirsten.
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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.
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Refer reported concentration of high-fat diet to study obesity Djebbar Ahmed Abdelhammid
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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.
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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.
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For example: Cardiometabolic risk factors (Hypertension, Obesity, Dyslipidemia and fasting hyperglycemia) as outcomes
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It depends on your research question. For example: Do risk factors (Hypertension, Obesity, Dyslipidemia, fasting hyperglycemia) increase the incidence of heart attacks? If you want to compare those 4 risk factors, you need to have enough participants in all groups. So your sample size will be e.g. 4x 20 individuals.
Here you have the best program to determine sample size: https://www.psychologie.hhu.de/arbeitsgruppen/allgemeine-psychologie-und-arbeitspsychologie/gpower.html. You will find many tutorials on how to use it on youtube.
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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,
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Physics of the Human Body Lose Weight for Good
The best book for losing weight without dieting. Do not let them fool you. 90% of weight loss books are a con or are based on pointless diets. This is a scientific method that works perfectly, that has been calibrated over years and approved by different committees of doctors in physics. This is the only book that applies the laws of physics to weight loss.
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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
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Obesity cam be determined by the use of BMI criteria.. taking weight as well as height of the person in consideration. Considering weight only is not a good idea
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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.
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Obesity is a disease per se and is also a risk factor for all other disease as well. The main risk factor for obesity is sedentary lifestyle and over eating.
The life style modifications need to be inculcated since childhood and adolescence and it will help in long run.
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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?
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Hi Monika,
Maybe it's too late you already have the answer but I experience it also and I was surprised! :) I believe it can also help other people in the future :) When you try to isolate total RNA from the adipose tissue I recommend you to remove fat layer after homogenization. Normally, if you experienced 4 phase after chloroform it means that you used quite big amount of tissue and there was a lot of fat layer. So, it is important to remove fat layer by pipet as much as you can before adding chloroform. To achieve this separation correctly, you should do a centrifugation right after homogenization process. 2-3 mins at max speed. I'm using 200ul tips to remove fat layer and it is working so well! Rest of the protocol same than regular RNA isolation procedure.
Good luck Monika Nanda and others.. :)
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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? 
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Many scientific studies have shown that inflammation (chronic) is a fundamental and common underlying factor in all major degenerative diseases, including weight gain and difficulty in losing weight.
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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...  
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Hi,
always used only high-fat diet, or high- proten or high -fiber ,according to experimental models from previous studies. But usually we use one or the other.
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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.
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See in the references, there are links to different databases
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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!
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Thank you!
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Hi!
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!
Fiona
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Following answers
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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,
2. Infertility,
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,
8. Acne
9. Dark pigmentation of skin around the neck etc.
BUT
What are the actual reasons works behind development of that dangerous disease?
Is it curable?
How can it be prevented?
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Polycystic ovarian disease (PCOD) is widely dependent on genetic, environmental, lifestyle and ethnicity factors including body weight. Weight loss improves the endocrine profile and increases chances of ovulation and pregnancy.
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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.
-Jordan
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Hi, Jordan,
According to the answer of Marie, You can also submit preferencially rats To fructose diet (65%) or high fat diet or cafeteria diet in order to induce obesity and insulin resistance. That's the good model for the study of insulin resistance !!!!
Regards !
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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?
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Super nutrition - You mean Food Suppliment like Vitamines / Minerals / anti-oxidants .
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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.
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According to Birgitta Haga Gripsrud I would really like to know why so many people harm themselves by using so much mobile phone, watching TV, waste their microbiom by eating industrial sugar, industrial meat, fast food etc. or by taking pills which are not useful just because any physicain prescribes etc... We definitely need more self-authorization in handling our health-skills. Therfore a lot of new science and teaching is needed!
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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.
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Welcome and thank for you
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what are the genes that I can detect to determine the ones who have genetic predisposition to become thin and underweight, and how I can help them depending on their gens?
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Please take a look at this useful RG link.
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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?
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Dear Prof Rodolfo Vega Candelario,
Thank you very much for contributing an important question to this discussion. I myself is not specialised in any medical specialties. So it will be good if we could invite some experts to this question.
What percentage of microcirculation in the coronary can be revealed by Coronary Angiography, Electrocardiogram, Echocardiography and Cardiac PET?
Is there any preventative measures to reduce the risk?
Best regards
Ligen
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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?
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Although restriction of diet often results in initial weight loss, more than 80 per cent of obese dieters fail to maintain their reduced weight. Obese people may regain weight after dieting due to hormonal changes.
It means that even though our weight is reduced, hunger hormones persist to be released in a way by which individual gain weight again.
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I am a beginner and having a hard time finding statistics reference for obesity/pancreatic cancer.
please help
Thank you
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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?
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I personally think those who are overweight or obese are deprived of fibre and complex carbohydrates in their diets. Moreover, they mainly focus on taking only simple sugars and carbohydrates in their diet. Adding a good amount of fruits and raw vegetables will increase the fibre as well as will be full of antioxidants which will help them from certain diseases. Where as intake of Vitamin C in our diets is highly recommended for better immunity. Fibre provides us with satiety and will therefore, elongate the transit time of next meal.
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The B.M.I for adult male and female.
Childhood obesity.
Obesity and overweight for children under five years of age.
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Obesity in children is a big problem in Malta. I am researching literature on the subject to further my studies.
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Please also have a look at this useful RG discussion thread.
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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:
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Health policy, education policy etc. in every country should now include active promotion of healthy lifestyle in the media. As part of this policy, informational, educational and activating programs for sports, healthy eating, preventive health check etc. should be finalized from state funds. The governments of countries should consider introducing additional taxation of confectionery enterprises and thus funds for health policy programs could be significantly increased. Obesity is a serious problem that should be taken into account in the current pro-social policies for the promotion of healthy living co-financed from state finance funds.
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Hello,
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)?
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Sorry I just bumped into your question. We have a long experience doing both of these assays in our lab, measuring them in plasma and reading the plates (384-well) with the FluoStar Omega reader. What is it that you need to know? The type of sample, the assay to use or the parametres to set in the reader?
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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 ?
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that is depend on the constituents of food protein and its contents of essential and non essential amino acids and their percent
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I am working on diet induced obesity
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This is a very important aspect of disease prevention which needs to be pursued rigorously.
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).
Best regards
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true, we have a three pronged attack of AGE breaker, preventing the progression of developing AGE's/ALE's & AOPP.
this could be an ideal combination for chronic inflammatory conditions. This would take care of FAO also.
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Why is polycystic ovary syndrome (PCOS) rising all over the world?
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PCOS is heavily linked to insulin resistance. With the rise of non-communicable diseases globally including type 2 diabetes and metabolic syndrome, the incidence of PCOS is expected to also increase considerably.
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Health benefits for sugar reduction exist
What maximum sugar levels in food should be allowed?
Should we even ban sugar outright?
Thoughts?
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You don't need to post any blogs telling about how bad sugar is. There are thousands of such blogs available which described about the sugar. But who gave anyone right to ban sugar? Its decision of people to decide what is right and wrong for you. I want to eat sugar all the time and will do that, and if I am self aware, i will not eat it. So you can do. But I don't support such thing. And I am also not much interested to argue on this topic which is related much to choice of people.
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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??
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Inactivity due to any reason + foods rich in non-healthy content + genetics all are culprits. Limiting discussion and blaming only one factor is no the answer here. So I believe the disease causation is multifactorial and be taken like this.
Regards
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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.
Thank you,
J. S. Shapiro
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I'm just reading about the scandal too. Many thanks and best wishes.
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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.
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I think normal daily consumption dose not require any alkaline diets because organism already adopted in daily conditions. If you start alkaline diet it means you will change normal acid base balance which will require daily intervention.
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Function of leptin is same or different in physiological and pathological condition (obese)
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Is any relation to insulin plasma concentration
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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.
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Keto flu can be avoided by consuming more electrolytes and fats, adding more salt to diet, drinking chicken broths, doing moderate exercise and staying hydrated. Moreover, addition of prebiotics and probiotics to diet are also helpful in avoiding the keto flu.
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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 ?
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Hi,
The following article might answer your query
Impact of Obesity on Treatment of Chronic Hepatitis C . HEPATOLOGY 2006;43:1177-1186.
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Hello,
what do you think about gut microbiota and its role in obesity ?
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This is an interesting article for your question
Adv Nutr. 2016 Nov 15;7(6):1080-1089. doi: 10.3945/an.116.012914. Print 2016 Nov.
Gut Microbiota in Obesity and Undernutrition.
de Clercq NC1, Groen AK2,3, Romijn JA2, Nieuwdorp M2,4,5.
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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"
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Excess fat in the body stimulates the division of cells more than normal, which leads to cancer,
Read more on the theme of the site: https://mawdoo3.com
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What is the highest HbA1C that you have seen?
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Upper limits of any measure in laboratories depend upon technology use and we normally use a term called linearity range
for example my lab's A1c upper linearity range is 14.5 and values above are reported as >14.5
similarly there is another concept dealing with how low a analyte concentration can be measured and that is termed Diagnostic sensitivity, like my kit do not measures < 4.0 so this is the diagnostic range
Finally both linearity range and diagnostic sensitivity can be manipulated if you are having the requisite calibrators where you can target the range you want/think your value is.
if u think your value could be like AIC=20% than u must use a calibration curve targeting that range.
Regards
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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.
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I would imagine that your education program for young adults will cover key points such as awareness of the role of physical activity, diet and nutrition in obesity prevention/treatment, and the health implications of obesity such as cardiovascular disease, sleep apnea and diabetes risks.
Further, since you have a young target audience, I would expect coverage of the intermediate process variables such as endurance for sports, recreation, work and study.
Therefore, I would document your key educational objectives and incorporate these into the pre/post-test, taking care to include plausible but incorrect answer items as part of the set.
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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?
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I have diabetes because my mother was also diabetic. However; I am fine only with low carb diet and no medecine at all. It is not easy ; especially in the beguining. However diet not only solved my diabetes problem but also made my immunity system stronger. I feel much healtier now than when I had diabetes fifteen years ago.
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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? �
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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!
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Hi Yanuar
I've found lots of old papers in rats. Handling rats is always easier, their brain and bodies are x10 times larger, everything is easier with them. But since genetically modified animals are usually mice, they have become the species-of-use in the last two decades.
Optogenetics and pharmacogenetics can be done in rats as well, provided you get viral vectors designed for rats, which is not so difficult.
Both species are similar but not identical. Both are rodents, and good models for studying interesting issues for humans, I don't find advantages in mice or rats relative to their similarity to humans.
Good luck
Fernando
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Obesity is becoming a common problem in almost all developed countries. From life style to medicated and non-medicated medicines are all available in market?
What is your best advice to curb this menace in evolution?
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The state must invest in the promotion of health and preventive medicine.
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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.
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You may need to pray to God for divine direction on this aspect of life. He'll definitely Lead you through this part with outstanding testimony.
Also, you may also ask for expert advice from your lecturers/supervisors or colleagues to share ideas on areas you're caught your interest in public health.
Thank you.
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Any help is much appreciated.
Thanks! /Anne
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Thank you Sibylle! That is perfect! I will look into both of these sources! Wishing you all the best! / Anne
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It is very interesting I should like to mention it in my future research.
Thanks,
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).
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Dr Claudio Could you please explain what exactly you want so we might help you here,
Regards
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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
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I hope this link will help you
regards
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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.
Thank you
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My answer is from the neuro-biological point of view but I also think that the psychological aspects are as important.
The key aspect of these disorders is that they are enduring, relatively immutable conditions that represent a baseline substrate of impaired addictedness, of deficiencies, or distortions that limit the capacity to adapt successfully to stress. That means that the genetic factors in their relationship with the environment can modulate the relationship between the stress effects on the person’s health. But genes do not code a specific psychiatric disorder, nor any symptom, but they do code for proteins and epigenetic regulators responsible for this information processing in brain circuits. So the vulnerability is genetic. The effects of the enviroment (like the stress) affects the neurotrophines levels. Therefore, the neurotrophines that are involved in different mental problems (Ex: major depressive episode association with eating symptoms ). An association between MDE and polymorphism of the brain derived neurotrophic factor (BDNF) gene was also reported. The family of neurotrophins contains four proteins: nerve growth factor (NGFB), brain-derived neurotrophic factor (BDNF) and neurotrophins 3 and 4/5 (NTF3 and NTF4/5) and they play important roles in proliferation, differentiation and maintenance of neurons in the central and peripheral nervous system. An association between Eating Disorders(ED) and polymorphism of the BDNF gene was reported. The Val66Met polymorphism (rs6265) of the BDNF gene is proved to be associated with binge eating dissorder or anorexia.
Evidence show that the sympathetic nervous system, the Hypothalamo-Pituitary-Adreno-medullary (HPA) axis and the inflammatory response system form a major chain reaction released by the immune complex. The interaction established among these systems and the central autonomic network which includes both prefrontal and limbic cerebral structures form an internal regulation system through which the brain controls visceromotor, neuroendocrine, and behavioral responses that are critical for adaptability and health, thus explaining the diversity of psychosomatic symptoms starting with a slight nausea sensation and ending with severe insomnia. The serotonin transporter (5-HTT), encoded by the SLC6A4 gene, may also have an important role in eating disorders. The promoter region contains a functional insertion/deletion polymorphism with two common alleles that have been designated the short (*S) and long (*L) alleles. Meta-analysis showed that the *S allele could represent a moderate but significant risk factor that increases the vulnerability for ED.
Because 5-HT is decreased just like in depression, ED are treated using antidepressants, serotonin reuptake inhibitors being the most frequently prescribed. High doses of SSRIs are usually prescribed in eating disorders. Information about genetic variations of cytochrome P450 could facilitate pharmacotherapy by preventing the administration of high doses in poor metabolizers and identify rapid metabolizes who may require higher doses for efficacy.
So in conclusion, there are several genes with an essential role in the regulation of eating behavior and could be involved in the etiology. The stress factors can act on these genes via 3 ways (HPA axis activation, inflammation and kynurenin pathway) and the person affected cand develop simptoms. Kynurenin patway can be involved in depression/ anxiety/ obesity and also in ED. Clinically, ED can be treated using antidepressants (SSRIs) considering genetic alterations in the serotonin receptor and psychotherapy (CBT, CARe model,...).
PS: Prof. S. Stahl had a nice lecture on this topic with nice slides and my only hope is that my comment here is clear enought to help you on this topic.
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 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?
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After consumption of CHO, there is an increased uptake of the ingested glucose into the active muscle. If insulin concentration also increases there is a reduction of lipolysis and as a result of these two actions fat oxidation is decreased. This suppression of fat oxidation following CHO ingestion can last for several hours .Consequently, an individual consuming CHO before and/or during exercise will likely oxidize less fat and more CHO during and after the exercise session
References
1. Horowitz JF, Mora-Rodriguez R, Byerley LO and Coyle EF. Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise. Am J Physiol Endocrinol Metab 273: E768-E775, 1997. 22.
2. Howley ET, Bassett DR and Welch HG. Criteria for maximal oxygen uptake: review and commentary. Med Sci Sports Exerc 27: 1292-1301, 1995.
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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.
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Over heating is not much problem is Sub-Saharan countries but mostly countries in this area which are all developing are facing double burden of malnutrition. That is obesity in cities and towns and under-nutrition in rural areas.
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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.
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We can base on the literature to see why and how Paleo diet is developed. From the original publication ( ), Paleolithic diet was decided to capture the diet characteristics of our remote ancestors at Stone Age, with high intake and variety of fruit and vegetables, large amount of lean meat and no grains and dairy products. The reason why Paleo diet is developed is due to the evolutionary discordance hypothesis, which suggests the high prevalence of chronic diseases in the modern society is due to the changes of diet and physical activity patterns from our ancestors at Stone Age. Hence the focus of the diet is to minic the diet pattern of our ancestor instead of just avoiding glucose. Apart from the food groups I have mentioned, Paleo diet do not suggest processed food such as processed meat, soft drinks, etc.
Regarding to the efficacy of Paleo diet, a meta-analysis of randomized controlled trial concluded that Paleo diet may result in statistically significant short-term improvement in waist circumference and triglycerides ( ). However, it is important to note that the emerged sample size in the meta-analysis is still quite low (n = 159) and some studies warrant the long-term compliance to Paleo diet and its consequence (e.g. ). Hence according to the current limited evidence, I would not suggest people to follow Paleo diet for obesity, diabetes and hypertension, as more studies are needed to clarify its long term relationship and safety.
For your question about Food4Me and Paleo diet, Food4Me is a study on personalized nutrition, which considers the interaction between genes and nutrition (http://www.food4me.org/about/aims-and-objectives). Hence it is not related to Paleo diet.
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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.
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5% weight loss can be a good indicator, but it depends on the characteristics of your subjects and the health outcomes you concern.
Below is a relevant article for discussion:
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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).
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?
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I spent some time in eastern Africa as an environmental officer, my home was in Nairobi. On an assignment to Uganda, I ran across an old Brit MD and we discussed heart and vascular disease. He commented that the local diet was high in fat but that the prevalence of heart disease was low but had increased following the establishment of sugar plantations and refineries.
The fat may impact the ability of the endothelial cell to generate NO and the sugar generate ROS, thus pro inflammatory transcription factors, hence upregulation of ICAM-1
See, for example: Mitochondrial Reactive Oxygen Species Mediate Lysophosphadylcholine-induced Endothelial Cell Activation, by Xinyuan Li, et al.
Dr Edo McGowan
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Fat induced hepatic injury.
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Yes according to a recent work done by my collaborator. Nonpublished yet.
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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.
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J Clin Med Res. 2016;8(2):105-110
Influence of Body Composition on Lung Function and Respiratory Muscle Strength in Children With Obesity Dirceu Costa Juniora, Fabiana S. Peixoto-Souzab, Poliane N. Araujob, Marcela C. Barbalho-Moulinc, Viviane C. Alvesb, Evelim L. F. D. Gomesb, Dirceu Costa
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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?
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Obesity in mice can arise from either monogenic disorders or from complex interactions between genetic background, maternal-fetal environment, learned behaviors and external environmental variables such as diet composition, ambient temperature, threats from predators, and so on.
High-Fat Diet Formula:
HFD that consists of 58% fat, 25% protein and 17% carbohydrate, lard (13%), cholesterol (1%), vitamin, and minerals (0.6%) as a percentage of total kcal ad libitum, respectively, was administered every (5 ).Food intake was calculated every day and bodyweight was measured once in every two days.
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I'm evaluating these factors.
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Reference range and short- and long-term biological variation of interleukin (IL)-6, IL-17A and tissue necrosis factor-alpha using high sensitivity assays.
Todd J, Simpson P, Estis J, Torres V, Wub AH.
Cytokine. 2013 Dec;64(3):660-5. doi: 10.1016/j.cyto.2013.09.018. Epub 2013 Oct 12.
Serum IL-1beta levels in health and disease: a population-based study. 'The InCHIANTI study'.
Di Iorio A, Ferrucci L, Sparvieri E, Cherubini A, Volpato S, Corsi A, Bonafè M, Franceschi C, Abate G, Paganelli R.
Cytokine. 2003 Jun 21;22(6):198-205
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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.
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Leonardo:
You have already received some fine feedback from the various contributors to this forum, so let me try to address your excellent question from an evidence-based perspective, based on an internal review I recently completed for a regulatory authority [pending publication].
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MYTHS AND REALITY RE OBESITY AND HUNGER
It is true that we have robust evidence that under conditions of scarcity, the poor and the hungry react more impulsively towards food rewards [Claassen 2016]. This is known as obesogenic eating behavior. NOTE, however, that this want-driven behavior does NOT wholly account for an obesity-hunger connection, as both economic development and socioeconomic class play critical roles [Pampel 2012a] [Dinsa 2012].
Landmark data from several studies across 67 countries [Pampel 2012a] representing all the regions of the world examined how economic development, socioeconomic status (SES), and obesity were related. They found that:
(1) Across the board, obesity rose with a nation’s economic development
(2) But socioeconomic status (SES) modulated the dynamics so that in lower-income countries, people with higher socioeconomic status (SES) were MORE likely to be obese, however and conversely, in high-income countries, those with higher SES were LESS likely to be obese, this observation being known as the REVERSAL HYPOTHESIS.
It appears therefore that in lower-income countries, higher socioeconomic status (SES) often leads to consuming high-calorie food and avoiding physically demanding activities, but in higher-income countries, individuals with higher socioeconomic status (SES) more typically respond with healthy eating and regular physical activity and exercise, and this was further confirmed in a study drawing from data from 17 nations [Pampel 2012b] where it was found that activities like reading, attendance at cultural events and films were associated just as much as exercise with a lower BMI, while people who participated in activities like significant watching TV, attendance at sporting events, and shopping, had higher BMI (this phenomenon sometimes referred to by the query: "Does Reading Keep You Thin?").
And if we look more specifically at the youth-to-early-adulthood transition, an intergenerational study [Scharoun-Lee 2011] found a nuanced picture, that men with a middle-class upbringing and lifestyle were almost as likely to be obese as those brought up in working-poor households who however were now working in lower-status jobs, while for women, the relationships varied by race: For white females, all socioeconomic status (SES) groups had a greater risk of obesity compared with the most advantaged, but in sharp contrast, among black women only those from working-poor households who now had lower-status jobs were at increased obesity risk compared with the most advantaged group.
These results show that risk of obesity affects different socioeconomic status (SES) groups differently, with additional variation by gender, by race, and by a country's economic development status [Newton 2017]., confirmed also in the large five-country WHO COSI (Childhood Obesity Surveillance Initiative) cross-sectional study [Lissner 2016]. And this teaches us that without subtle adjustments for socioeconomic status (SES), economic development, age, gender and race, all generalizations are necessarily suspect, and there is no single neat correlation between obesity and hunger, although the concept of eating in the absence of hunger (EAH) that I discuss in detail below has shown itslef to be the most productive and fertile avenue of investigation, with validated / cross-confirmed results as described.
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EATING IN THE ABSENCE OF HUNGER (EAH)
The form of disinhibited obesogenic eating behavior that is most relevant to the question of the connection between obesity and hunger is well-studied through hundreds of studies and clinical trial and is known as EATING IN THE ABSENCE OF HUNGER (EAH), which refers to the consumption of palatable foods in a sated state, that is in the absence of perceived physiological hunger [Kral 2007], and so constitutes a failure to self-regulate intake that then leads to overconsumption. It has been proposed that eating in the absence of hunger (EAH) promotes excess weight gain in youth, and has been widely - and correctly - construed as an indicator of disinhibited eating, making it one of the behavioral pathways implicated in the etiology of childhood obesity, predisposing youth to develop obesity. [Faith 2006] [Birch 2003].
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CONTRIBUTORS TO EATING IN THE ABSENCE OF HUNGER (EAH):
SOCIOCULTURAL PRESSURES, DIET, GENETICS
Across numerous studies, eating in the absence of hunger (EAH) has emerged as a robust endophenotype for child and adolescent obesity [Shomaker 2011] [Shomaker 2013]. In addition, sociocultural pressures linking to body image (like parental feeding restriction, family pressure towards thin body type, and in girls especially media pressure) may contribute to natural history of disinhibited eating behaviors during adolescence [Reina 2013]. It's also been argued that overweight boys are less susceptible than girls to social desirability effects, and that in girls, the desire not to be seen overeating itself might inhibit the expression of EAH [Moens 2007].
And we also know that greater increases in cortisol in response to psychosocial stress are related to dysregulated eating and higher body mass, especially in older children [Francis 2013], and that consumption of high-glycemic index (GI) carbohydrates may increase hunger and promote overeating relative to consumption of items with a lower glycemic index GI), suggesting strongly that consumption of whole grain and lower-GI cereals instead of highly refined cereals may be dietary change that may help prevent overeating [Roberts 2000].
In addition, eating in the absence of hunger (EAH) appears to be moderately heritable [Fisher 2007], with some provisional evidence that 16p11.2 deletion - where the 16p11.2 genotype is consistently associated with obesity - may influence certain specific obesity-associated disinhibited eating behaviors, namely:
(1) EAH due to external trigger and
(2) EAH due to boredom [Gill 2014].
EAH, on average, increases as children age, but children with overweight or obese parents consume more energy during the EAH paradigm, and consequently show the greatest increases in EAH over time compared to children without overweight parents [Francis 2007] [Faith 2006].
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EATING IN THE ABSENCE OF HUNGER (EAH): THE DYNAMICS
In a systematic review [Lansigan 2015] of 19 robust studies (six prospective, 12 cross-sectional, one behavioral-intervention), it was found that consistent evidence supported increased levels of EAH among overweight and obese versus normal weight children, both cross-sectionally and prospectively, with two studies supporting a genetic component to EAH [Birch 2003] [Faith 2006], as we noted above.
In two landmark studies [Hill 2008], it was found that the majority (over 90%) of children ate snacks when these snacks were offered, despite having just eaten a meal, strongly indicative of the power of sweet snacks to reinstate eating in the sated state, that is, EAH. And as the investigators observe, the amount of food consumed in the EAH task is significantly associated with adiposity, the thinnest subjects eating less than those who are normal weight, who in turn ate less than the overweight or obese.
LESSON: In boys, this demonstrates that EAH is a behavioural phenotype that is NOT specific to overweight or obese children, but instead shows a graded association with adiposity, and as I noted above, the weaker results in girls likely indicate the influence of social desirability constraining the expression of food cue responsiveness.
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EXTERNAL TRIGGERS VERSUS EMOTIONAL TRIGGERS
The subtype of eating in the absence of hunger (EAH) in response to EXTERNAL triggers (EAH-EXT) is thought to be more prevalent [Moens 2007], in contrast to another subtype of EAH, namely eating in the absence of hunger (EAH) in response to EMOTIONAL triggers (EAH-EMOT) which is thought to overlap more with disordered eating behaviors that begin to emerge during adolescence [Shomaker 2011], that is, EAH in response to negative emotions (EAH-NEG-EMOT) which is more closely aligned with adolescent disordered eating behaviors (e.g., loss of control or binge eating) that often involve eating to cope with negative affect [Tanofsky-Kraff 2007].
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THE PATHOLOGY OF EATING IN THE ABSENCE OF HUNGER (EAH)
There are plausible hypotheses as to the pathodynamics at work here: since adipose tissue is active and secretes several hormones related to energy maintenance, overweight or obese individuals may engage in greater levels of EAH driven by a hormonally-based, diminished satiety response [Klok 2007] [Henry 2008]; and EAH can also be seen as a behavioral trait where children don't completely compensate for excess calories consumed, thus progressing to weight gain [Kral 2012].
Further, there is a familial - independently of genetic - component related to childhood eating in the absence of hunger (EAH), as it's been observed that parents who use food as a way to help regulate their child’s emotions - PARENTAL FOOD REGULATION - may be unconsciously promoting EAH [Liang 2016], and in addition children of parents who themselves exhibit a disinhibited eating style (one marked by eating in response to external cues), have been found to be more likely to engage in EAH, so collectively these findings suggest that eating in the absence of hunger (EAH) may be a learned behavior in part, as witness also in that TV food advertisement exposure was associated with higher caloric consumption of recently advertised foods, the effect modified by a Fat Mass and Obesity Associated Gene (FTO), the rs9939609 single nucleotide polymorphism, increasing linearly with each additional FTO risk allele even after controlling for BMI [Gilbert-Diamond 2017] [Emond 2017] [Rutters 2010] [Faith 2006].
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REFERENCES
[Birch 2003] Birch LL, Fisher JO, Davison KK. Learning to overeat: maternal use of restrictive feeding practices promotes girls' eating in the absence of hunger. Am J Clin Nutr 2003; 78: 215–220.
[Claassen 2016] Claassen MA, Klein O, Corneille O. Poverty & obesity: how poverty and hunger influence food choices. European Health Psychologist 2016; 18(Supp.).
[Dinsa 2012] Dinsa GD, Goryakin Y, Fumagalli E, Suhrcke M. Obesity and socioeconomic status in developing countries: a systematic review. Obes Rev. 2012 Nov; 13(11):1067-79.
[Emond 2017] Emond JA, Tovar A, Li Z, Lansigan RK, Gilbert-Diamond D. FTO genotype and weight status among preadolescents: Assessing the mediating effects of obesogenic appetitive traits. Appetite. 2017 Oct 1;117:321-329.
[Faith 2006] Faith MS, Berkowitz RI, Stallings VA, Kerns J, Storey M, Stunkard AJ. Eating in the absence of hunger: a genetic marker for childhood obesity in prepubertal boys? Obesity 2006; 14: 131–138.
[Fisher 2007] Fisher JO, Cai G, Jaramillo SJ, Cole SA, Comuzzie AG, Butte NF. Heritability of hyperphagic eating behavior and appetite-related hormones among Hispanic children. Obesity 2007;15:1484-1495.
[Francis 2007] Francis LA, Ventura AK, Marini M, Birch LL. Parent overweight predicts daughters' increase in BMI and disinhibited overeating from 5 to 13 years. Obesity 2007;15:1544-1553.
[Francis 2013] Francis LA, Granger DA, Susman EJ. Adrenocortical regulation, eating in the absence of hunger and BMI in young children. Appetite. 2013 May; 64:32-8.
[Gilbert-Diamond 2017] Gilbert-Diamond D, Emond JA, Lansigan RK, et al. Television food advertisement exposure and FTO rs9939609 genotype in relation to excess consumption in children. International journal of obesity (2005). 2017;41(1):23-29.
[Gill 2014] Gill R, Chen Q, D'Angelo D, Chung WK. Eating in the absence of hunger but not loss of control behaviors are associated with 16p11.2 deletions. Obesity (Silver Spring). 2014 Dec;22(12):2625-31.
[Henry 2008] Henry BA, Clarke IJ. Adipose tissue hormones and the regulation of food intake. Journal of neuroendocrinology. 2008;20(6):842–9.]
[Hill 2008] Hill C, Llewellyn CH, Saxton J, et al. Adiposity and 'eating in the absence of hunger' in children. Int J Obes (Lond). 2008 Oct; 32(10):1499-505.
[Klok 2007] Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007;8(1):21–34.
[Kral 2007] Kral TV, Faith MS. Child eating patterns and weight regulation: a developmental behaviour genetics framework. Acta Paediatr Suppl 2007;96:29-34.
[Kral 2012] Kral TVE, Allison DB, Birch LL, Stallings VA, Moore RH, Faith MS. Caloric compensation and eating in the absence of hunger in 5- to 12-y-old weight-discordant siblings. Am J Clin Nutr. 2012;96(3):574–83.
[Lansigan 2015] Lansigan RK, Emond JA, Gilbert-Diamond D. Understanding eating in the absence of hunger among young children: a systematic review of existing studies. Appetite. 2015 Feb; 85:36-47.
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Constantine Kaniklidis
Director, Medical Research, No Surrender Breast Cancer Foundation (NSBCF)
Oncology Reviewer, Current Oncology [journal]
Society for Integrative Oncology (SIO)
European Association for Cancer Research (EACR)