Obesity Prevention - Science topic

Actually, Mothers should help them in the beginning. So, after few trying they will prepare their breakfast easily

Just do this with fun

being active and choosing healthy foods has health benefits for everyone—no matter your age or weight. It’s important to choose nutrient-dense foods and be active at least 150 minutes per week

Please take a look at this useful link.

Health care workers often fail to take care of their own health. Some experience burnout or compassion fatigue periodically especially in the mental health field. Health care workers are at high risk due to their contact with patients who may have various diseases. Thus, not only are hand washing and other protocols important it is imperative that these workers periodically take time off to relax and decompress.

You can use Cohen's d (or Hedge's g) for before-after comparisons as well, but you need to adjust the SE for the within-pair correlation of measurements and the two time points.

You may find these papers helpful:

I hope the above papers will facilitate your project.

We are working in this question since the last two years with different accelerometers and different intensity but, at the moment, we don't have any publication.

NCCS pune has this cell line I aslo got from that source only.

You may look for a validated scale developed by Gould (1990). 

Gould SJ (1990) Health consciousness and health behavior: the application of a new health consciousness scale. American journal of preventive medicine, Department of Marketing, Rutgers, State University of New Jersey, New Brunswick 08903. 6(4): 228–237.

Here are some more articles that you may use to modify/adapt health consciousness scale.

Hope they help.

There are plenty of studies. If You are constructing dietary plan and exercise program You should be careful because of all the changes in physiology in individuals with down syndrome. You should be aware of lower relative peakVO2, reduced catecholamine response to exercise, chronotropic incompetence and limited cardiac output at peak exercise intensities and other factors that are demanding different exercise intervention. (e.g. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3012449/  ,

http://europepmc.org/abstract/med/8776225 )

Of course the same goes for nutritional intervention.

Some literature You might find helpful:

Kind regards,

Jan Homolak

Fexaramine reduced diet-induced weight gain, body-wide inflammation and hepatic glucose production, while enhanced thermogenesis and promoted browning of white adipose tissue (WAT) in diet induced obesity (DIO) mice. Its effects in humans are not known yet.

Dear colleague,

To determine the availblity and accessibility of food in a community; you can use HFSA ( house hold food secur and access qiestionaire) from  

Hi,

Usually, the "classical" way to validate a scale in another language is to:

1. Peaople who are fluent in both language revised a first translation of the scale, resolving translation difficulties by consensus.

2. Second, external expert(s) in the field is asked to examine the translation of each specific item.

3. Additional expert(s) independently back-translated the questionnaire into English, which allows to detect additional inconsistencies in translation.

The final French version is the administred to a sufficently large group of subject and Factor analysis is performed (Exploratory, Confirmatory or both, depending.)

Best,

S.

I think that lipid profile is necessary  to diagnose metabolic syndrome too.

I too have been watching the extent of World Cup junk food sponsorship with interest.  The promotion of the MacDonald's sponsorship started a month prior to the event with country named burgers a month, our major supermarkets running cross promotions aimed at children with discount CocaCola and soccer balls, and Gatorade TVCs aimed at children. www.businessinsider.com.au/gatorade-world-cup-commercial-2014-5 as well as the infield, App, naming rights, etc advertising.

Healthway, the Western Australian Health Promotion Foundation, established on hypothecated funding from cigarette taxes, has developed effective co-sponsorship guidelines for food and alcohol related sponsorships (attached).

Also, the Public Health Association of Australia has fairly rigorous guidelines. Unfortunately the Dietitians Association does not --as yet. Not sure what happened to my font but will send anyway as writing this on an IPad.

 

Poetically, "a rose by any other name or label would smell the same." When I was growing up there were a few kids that were overweight. None in my public school were obese. I cannot recall one classmate or for that matter anyone I heard of or saw that was autistic. Why, temporally speaking, would that be? Kids then were more active. We walked to school or rode our bikes. (Like the Dutch where it is uncommon to see obesity). Our food tasted like food; it was healthier; fruit and vegetables were not picked before they were ripe and had nutrient value. Tomatoes tasted like tomatoes. Fish was not farm fed, nor beef grain fed. (In many parts of the world where food has not become "lifeless", obesity is uncommon." Perhaps, just a thought, obesity and overweight are the body's response to not getting the nutritional value that is needed i.e., a compensatory mechanism like up-regulation of receptors in the setting of a deficiency (soluble transferring receptor ↑ in the setting of iron deficiency".

Now add in the propensity to feed many families with the high carb composition of fast foods. Toss in television and the contribution of sitting on one's duff and stuffing our mouths while watching high anxiety episodes of serial killers, etc. Think about the brain-washing of our society's media where everything is oriented towards buy this, eat that, drive this i.e., it's all about getting, taking in, possessing. We now live in a world where TV shows about diners, drive-ins, cooking high caloric meals flourish. We even have TV shows that highlight obese characters. News programs interview one obese person after another. America, the land of the free and the home of the brave has become the land of entitlements, what's in it for me, and a meal of burgers, fries, and soft drink for only $5.

So what do you think? Labeling obesity as a disease will change anything? Perhaps when healthcare premiums are dramatically less with ideal weight, BMI or waist circumference that will change. Perhaps when are city planners make every third street a bicycle only or a shared bicycle-pedestrian street that will change. Perhaps when we move water from areas that flood every year and create a new great lakes system in the SouthWest and grow organic crops, and mandate grass-fed beef that will change; and when citizens demand less brutality and violence-oriented TV (note second-hand stress now in the news) that will change.

The chances of the above happening are next to nothing. Sadly, our American society and elsewhere are "emulating" the decadence that characterized the fall of the Roman empire. But who knows, the story is not over until the "fat lady sings."

I will provide below a critical summary and assessment of the major reasonably effective pharmacological interventions for obesity reduction and treatment, with limitations noted. I also briefly discuss the much cited recent results from the University of Louisville team under Kira Taylor and locate their role and impact more modestly than as hailed in the uncritical popular medical literature. Finally, I conclude with a look forward and suggest that to date our progress is insufficient to halt the worst of the adverse impact on mortality and morbidity that is indisputably projected to be the wages of obesity across the globe from the furiously accelerating diabesity pandemic.

GASTRIC/PANCREATIC LIPASE INHIBITOR CLASS:

- Orlistat (Xenical/Alli) which blocks fat absorption from the gut, and remains the only drug currently approved by the FDA for long-term management of obesity. use in the clinical practice is limited by gastrointestinal side effects, mainly steatorrhea. Recently, however, even the safety of orlistat has come under scrutiny, following reports of serious events in obese patients, and in 2010, the FDA revised the label for orlistat to include safety information about severe liver injury, while orlistat has now even been associated with kidney and pancreas injuries [1].

- Cetilistat (Cametor) [In Phase III]: highly lipophilic benzoxazinone inhibitor of gastrointestinal (GI) and pancreatic lipases with plausible evidence of efficacy and non-inferior to orlistat [1,2].

NA-DA CLASS: these are noradrenaline (NA) + dopamine (DA) releasing agents

- Phentermine (Ionamin/Duromine)

- Methamphetamine (Desoxyn)

- DCR-Phentermine, a new experimental diffuse-controlled release formulation of phentermine (DCR-phentermine)

Efficacy and safety were shown in a small 12-week RCT [4] [ ], and decreased obesity was accompanied by reductions in waist circumference, LDL and total cholesterol; and although adverse effects were typical of the sympathomimetics no drug-related increases in systolic or diastolic blood pressure were observed. These preliminary results suggest that DCR-phentermine offers greater efficacy than many new experimental candidates awaiting approval. And although the issue of drug dependence could be raised, recent data found that abrupt cessation of phentermine in obese subjects on long-term phentermine therapy did not provoke either withdrawal or drug craving [5].

SYMPATHOMIMETIC CLASS:

These primarily target energy expenditure via the basal metabolic rate (BMR), with modest efficacy but not widespread use.

- Phendimetrazine (Tepanil/Bontril)

- Diethylpropion (Tenuate/Apisate)

- Benzphetamine (Didrex)

NA + 5-HT REUPTAKE INHIBITOR CLASS

Act centrally to enhance satiety

- Sibutramine (Reductil, Meridia) [Withdrawn 2010, due to increased heart attacks and strokes, based on controversial data from the SCOUT (Sibutramine Cardiovascular OUTcome) study [6]. Note: this author (C. Kaniklidis) has critically appraised the SCOUT study and found it fatally flawed methodologically, being performed in a subject population expressly contraindicated from sibutramine treatment both in the European Summary of Product Characteristics (SPC) and the US (FDA) Product Label, and thus represents an illicit off-label clinical trial in an inappropriate patient population. Bizarrely, despite the fact that the final results of the SCOUT trial did not show any increased cardiovascular mortality, sibutramine was withdrawn from the US market by FDA in October 2010. Based on best evidence-based review, critical appraisal, and assessment of methodological quality (I use the Heyland MQS metric), this author would conclude that the withdrawal was premature, in error and against the evidence.

CANNABINOID CB1 ANTAGONIST CLASS

- Rimonabant (Accomplia) [US: not approved but under development/EU. Efficacy and safety shown in the RIO-Europe, the RIO-North America, the RIO-Diabetes, and the RIO-Lipids RCTs. It has been withdrawn due to increased anxiety and depressive symptoms and suicidal ideation, and I would further argue its efficacy has now been challenged by the CARDIO-REDUSE RCT.

SSA/NA-DA CLASS: (Sugar Sulfamate Anticonvulsant) + NA-DA releasing agent)

- Topiramate (Topamax)/phentermine (Qnexa/Qsymia)

With efficacy and safety demonstrated in a number of clinical trials, especially the two, large, one-year Phase III pivotal trials OB-302 and OB-303, and the CONQUER RCT. It appears to be the most effective new generation antiobesity agent, and highly probably also superior to orlistat, rimonabant and sibutramine. To date, it manifestly satisfies the European regulatory requirements for anti-obesity drug approval; yet despite this, it has been withdrawn from the European market by the EMA in October 2012, due to adverse effects on heart rate, adverse psychiatric events, as well as concerns about fetal toxicity, and the birth defect issue is as yet resolved. It continues to be available in the US, with appropriate safety warnings.

DA REUPTAKE INHIBITOR/OPIOID ANTAGONIST CLASS

- Bupropion/naltrexone (Contrave)

The efficacy and safety of Contrave has been determined in four pivotal, 56-week, multicenter RCTs (NB-301, NB-302, NB-303 and NB-304 [7], and in the COR- and COR-2 trials. The efficacy approximates that of sibutramine or rimonabant, and appears to ranks below Qnexa in terms of weight loss efficacy, but above lorcaserin (Lorqess/Belviq) [8]. After resubmission of its NDA to the FDA in Dec 2013, the FDA is now expected to render a decision on Contrave by Jun 10, 2014, awaiting completion of the FDA sponsored Light Study RCT, with completion due in 2017. Based in interim reported findings, this author expects FDA approval.

SEEROTONIN 2C AGONIST CLASS

- Lorcaserin (Lorqess/Belviq), with safety and activity demonstrated in three RCTs: BLOOM, BLOSSOM and BLOOM-DM. Monotherapy yields very modest benefit, 3–4% more body weight loss compared to placebo after 1 year of treatment [BLOOM-DM].

SA-DA CLASS: Sulfonamide Anticonvulsant (SA)+DA Reuptake Inhibitor

- Zonisamide (Zonegran)+bupropion (Empatic)

In phase III awaiting FDA approval. However, Orexigen recently placed a hold on its clinical development, so the arrival of the Phase III trial results is uncertain. Nonetheless, Empatic appears to show more promise in delivering weight loss than bupropion+naltrexone (Contrave), but the lingering unanswered question is whether the anticonvulsant component (zonisamide) has any potential for fetal toxicity.

NA-DA-SSRI CLASS: (Reuptake inhibitor of noradrenaline, dopamine and serotonin)

- Tesofensine now in Phase III is a " triple monoamine reuptake inhibitor", of dopamine, norepinephrine, and serotonin, structurally similar to the dopamine reuptake inhibitor cocaine, and originally developed as an anti-parkinsonian agent, and with anti-obesity mode of action similar to that of sibutramine. Efficacy established in Phase I and II trials, but with cardiovascular safety as yet not satisfactorily demonstrated.

GLP1 AGONIST CLASS: Glucagon-like peptide-1 agonist

GLP-1 is released post-prandially, retards gastric emptying, and mediates satiety, and in general it appears that long-acting GLP-1 agonists like exenatide and liraglutide enhance insulin release, with accompanying body weight loss. The major entry is:

- Liraglutide (Victoza) with safety and efficacy established in the DURATION-6 trial [9, and with emerging GLP-1 agonists albiglutide, a GLP-1 receptor agonist, and taspoglutide, a GLP-1 analogue being explored although not yet in regulatory pipeline.

EMERGING STRATGEIES

Given the fact that plasma ghrelin levels correlate with hunger scores, with ghrelin release increasing following dieting, ghrelin may be a critical contributor to relapse to increased food intake and weight gain after dieting, so ghrelin receptor antagonists appear biologically and molecularly attractive, especially in the form of what's called GOAT (ghrelin-O-acyl transferase) antagonists. These are awaiting clinical testing. Another avenue of pursuit appeared to be the satiety hormone PYY (processed into PYY3–36), and although infusion of PYY3–36 in humans decreases 24-h caloric intake, the magnitude of effects have been so far disappointing. A third avenue centers around amylin released, along with insulin, from pancreatic β cells; amylin increases satiation via neuronal receptors, thus influencing part of the neural circuit that mediates satiation. Pramlintide (Symlin) is an approved anti-diabetic agent drug and also a novel human amylin peptide derivative, and I note that in a recent meta-analysis [10] of pramlintide treatment in diabetic and in obese subjects, it demonstrated modest weight loss after treatment for at least 16 weeks. Also being explored is a heterogeneous group of compounds targeting reduction of fat mass by increasing energy expenditure (especially modulating the basal metabolic rate (BMR)) or by redistributing adipose tissue, and these include angiogenesis inhibitors, beta-3 receptor agonists, sirtuin-I activators, and diazoxide among others like oxyntomodulin (OXM), pramlintide, obinepitide, leptin-based candidates, and dozens of others in various stages of clinical trial and investigation.

THE UNIVESITY OF LOUISVILLE ADIPOSITY-GENE STUDY

A genomic approach has recently been suggested by the University of Louisville collaboration with NHLBI’s CARe Project (Candidate Gene Association Resource) [13] via the identification of five genes - culled from a meta-analysis of ~2100 cardiovascular-related genes in individuals of European descent (n=50,00) from 22 cohorts - associated with increased WHR (waist-to-hip ratio) independent of overall obesity, two specific to women, and three shared across males and females, with special focus on the SHC1 gene strongly associated with abdominal fat through insulin receptor activation. This is intriguing research but it remains preliminary and not yet achieving even proof-of-concept stage let only human clinical trial stage, since the potential biological significance of these newly discovered loci are suggested and extrapolated only at the in vivo preclinical level, through the observation that mice lacking the SHC1 protein live longer and are leaner than their wild-type counterparts. It remains for clinical demonstration whether SHC1 is indeed effectively druggable and targetable at clinically relevant levels, and no pharmacological candidates for modulation (whether activation of inhibition) are yet available or even researched. Furthermore, without a two-stage study design which the investigators admit not conducting, the effect estimates themselves may be inflated.

Finally, the investigators admit that not all of these discovered genes have clear rationale in adiposity, so we still require the mature ex vivo and clinical demonstration that modulation of any of these genes can actually significantly disrupt the biological pathways that affect adiposity development.

MORE STILL NEEDED

Yet despite an increasingly more sophisticated understanding of the pathophysiology of obesity, accompanied by a broad spectrum of candidate interventions, I would conclude that we are still poorly in control of both (1) underlying etiological and molecular pathways, and (2) of the fundamental patho-behavioral drivers of human obesity and its demonstrable high degree of resistance to durable and clinical relevant weight loss gains: to date, we barely break 10% gains and the grim epidemiology of the diabesity (obesity + diabetes) pandemic (which I have elsewhere discussed [11,12] shows that we are effectively losing the battle with gains insufficient to stem the tide which unrelentingly is assured to bring the foremost and highest levels of morality and morbidity than that from even the leading cancers combined. We need new approaches to obesity that will deliver more than just modest incremental gains, and we concomitantly need to focus additional resources on prevention and not just therapeutics if we hope to avoid a global catastrophe that, regrettably as always, will disproportionately hit hardest the less developed and underserved regions (as I document in my "Cancer, Culture and Cooperation in the Middle East" paper). This will require international cross-cultural cooperative collaborations with governments and businesses under a collective umbrella of academia and leading research institutes, something that is still relatively unfocused and unintegrated to this day. But all of us medical and public health researchers have a stake and a role to play in fostering this sooner rather than later.

REFERENCES

1. M.A. Weir, M.M. Beyea, T. Gomes, D.N. Juurlink, M. Mamdani, P.G. Blake, R. Wald, A.X. Garg, Orlistat and acute kidney injury: an analysis of 953 patients. Arch Intern Med 2011; 171, 703–704.

2. Kopelman P, Bryson A, Hickling R et al. Cetilistat (ATL-962), a novel lipase inhibitor: a 12-week randomized, placebo-controlled study of weight reduction in obese patients. Int J Obes (Lond) 2007;31:494–499.

3. Kopelman P, de Groot HG, Rissanen A., et al. Weight Loss, HbA1c Reduction, and Tolerability of Cetilistat in a Randomized, Placebo-controlled Phase 2 Trial in Obese Diabetics: Comparison With Orlistat (Xenical). Obesity 2010; 18:108–115.

4. Kang JG, Park CY, Kang JH, Park YW, Park SW. Randomized controlled trial to investigate the effects of a newly developed formulation of phentermine diffuse-controlled release for obesity. Diabetes Obes Metab 2010; 12: 876–882.

5. Hendricks EJ, Greenway FL, Westman EC, Gupta AK. Blood pressure and heart rate effects, weight loss and maintenance during long-term phentermine pharmacotherapy for obesity. Obesity (Silver Spring) 2011; 19: 2351–2360.

6. James WP, Caterson ID, Coutinho W, Finer N, Van Gaal LF, Maggioni AP, et al., SCOUT Investigators. Effect of sibutramine on cardiovascular outcomes in overweight and obese subjects. N Engl J Med 2010; 363: 905–917.

7. Contrave FDA Briefing Document. NDA 200063. December 7, 2010. At:

committeesmeetingmaterials/drugs/endocrinologica

ndmetabolicdrugsadvisorycommittee/ucm235671.pdf.

8. Heal DJ, Gosden J, Smith SL. A review of late-stage CNS drug candidates for the treatment of obesity. Int J Obes (Lond) 2013; 37(1):107-17.

9. Buse JB, Nauck M, Forst T, et al. Exenatide once weekly versus liraglutide once daily in patients with type 2 diabetes (DURATION-6): a randomised, open-label study. Lancet 2013; 381, 117–124.

10. Singh-Franco, D., et al. (2011). The effect of pramlintide acetate on glycemic control and weight in patients with type 2 diabetes mellitus and in obese patients without diabetes: a systematic review and meta-analysis. Diabetes Obes. Metab. 13, 169–180.

11. Kaniklidis C. Diabetes Prevention - Promise and Limitations: A Review. [publication pending]. Available on ResearchGate at: https://www.researchgate.net/publication/236235056_Diabetes_Prevention_-_Promise_and_Limitations_A_Review.

12. Kaniklidis C. The Obesity Paradox - and commentary on the Flegal JAMA Study. [publication pending]. Available on ResearchGate at: https://www.researchgate.net/publication/236165156_The_Obesity_Paradox_-_and_commentary_on_the_Flegal_JAMA_Study.

13. Yoneyama S, Guo Y, Lanktree MB, et al. Gene-centric meta-analyses for central adiposity traits in up to 57 412 individuals of European descent confirm known loci and reveal several novel associations. Hum Mol Genet 2014 Jan 6.