Healthy obesity: Difference between revisions

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== What is Healthy Obesity? ==
== What is Healthy Obesity? ==


Although [[obesity]] is a major risk factor for cardiovascular disease and type 2 diabetes mellitus, about a third of obese individuals maintain healthy cardiometabolic profiles; this phenotype of '''healthy obesity''' may be linked to the location of [[adipocyte|adipose tissue]] and the metabolic characteristics of the fat. Some data also suggest that weight loss by healthy obese subjects may have an adverse impact on their favorable cardiometabolic profile. <ref>Lee CM ''et al.'' (2008) Indices of abdominal obesity are better discriminators of cardiovascular risk factors than BMI: a meta-analysis ''J Clin Epidemiol'' 61:646-53 PMID 18359190</ref> <ref>Wildman RP (2009) Healthy obesity ''Curr Opin Clin Nutr Metab Care'' 12:438-43 PMID 19474713</ref>
Although [[obesity]] is a major risk factor for cardiovascular disease and type 2 diabetes mellitus, about a third of obese individuals maintain healthy cardiometabolic profiles; this phenotype of '''healthy obesity''' may be linked to the location of [[adipocyte|adipose tissue]] and the metabolic characteristics of the fat. Some data also suggest that weight loss by healthy obese subjects may have an adverse impact on their favorable cardiometabolic profile. <ref>Lee CM ''et al.'' (2008) Indices of abdominal obesity are better discriminators of cardiovascular risk factors than BMI: a meta-analysis ''J Clin Epidemiol'' 61:646-53 PMID 18359190</ref> <ref name = Wildman>Wildman RP (2009) Healthy obesity ''Curr Opin Clin Nutr Metab Care'' 12:438-43 PMID 19474713</ref>




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'''Proposed Mechanistic Determinants of the Healthy Obese Phenotype'''
'''Proposed Mechanistic Determinants of the Healthy Obese Phenotype'''


[[Adipocyte|Adipose tissue]] is an endocrine organ, releasing several inflammatory cytokines and expressing endocrine hormone receptors. The location of adipose tissue, the histological characteristics of adipose tissue and its metabolic activity may be more relevant than its total mass with regards to the healthy obese phenotype, and  they may play a role in determining the cardiometabolic health of obese individuals <ref>(Wildman, 2009)</ref>.
[[Adipocyte|Adipose tissue]] is an endocrine organ, releasing several inflammatory cytokines and expressing endocrine hormone receptors. The location of adipose tissue, the histological characteristics of adipose tissue and its metabolic activity may be more relevant than its total mass with regards to the healthy obese phenotype, and  they may play a role in determining the cardiometabolic health of obese individuals <ref name =Wildman/>.


''Adiponectin and Healthy Obesity''
''Adiponectin and Healthy Obesity''


[[Adiponectin]] is a protein hormone which is secreted into the bloodstream from adipose tissue and modulates several metabolic processes, including fatty acid catabolism and glucose regulation. The level of adiponectin in the bloodstream is inversely correlated to the percentage of body fat in adults. It is associated with the suppression of metabolic processes that can lead to obesity, type 2 diabetes mellitus and non-alcoholic fatty liver disease (NAFLD). Diabetics tend to have reduced levels of the hormone and levels of adiponectin are significantly increased with weight loss. Other metabolic effects of adiponectin  are: decreased gluconeogenesis and increased glucose uptake; lipid catabolism; protection from endothelial dysfunction; insulin sensitivity, and control of energy metabolism. Hypoadiponectinaemia, therefore, is an independent risk factor for [[metabolic syndrome]] and type 2 diabetes mellitus– two conditions associated with an unhealthy metabolic profile of obese individuals.
[[Adiponectin]] is a protein hormone which is secreted into the bloodstream from adipose tissue and modulates several metabolic processes, including fatty acid catabolism and glucose regulation. The level of adiponectin in the bloodstream is inversely correlated to the percentage of body fat in adults. It is associated with the suppression of metabolic processes that can lead to obesity, type 2 diabetes mellitus and [[non-alcoholic fatty liver disease]] (NAFLD). Diabetics tend to have reduced levels of the hormone and levels of adiponectin are significantly increased with weight loss. Other metabolic effects of adiponectin  are: decreased [[gluconeogenesis]] and increased glucose uptake; lipid catabolism; protection from endothelial dysfunction; insulin sensitivity, and control of energy metabolism. Hypoadiponectinaemia, therefore, is an independent risk factor for [[metabolic syndrome]] and type 2 diabetes mellitus– two conditions associated with an unhealthy metabolic profile of obese individuals.


There is an inverse relationship between [[body mass index]] (BMI) and concentrations of adiponectin in both humans and animals. However, in ''ob/ob'' mice - mutant mice that eat excessively and become obese - overexpression of adiponectin in adipose tissue increased plasma adiponectin concentrations, keeping them in a physiological range. This increase  resulted in significant weight gain and reduced hyperglycaemia and amended metabolic abnormalities. These findings suggest a role of variable plasma adiponectin concentrations in the pathophysiology of the healthy obese phenotype. Data from one recent study shows that lack of suppression of adiponectin concentrations is independently associated with the metabolically healthy profile of certain obese individuals <ref name = Aguillar-Salinas >(Aguillar-Salinas  ''et al.'' 2008)</ref>.
There is an inverse relationship between [[body mass index]] (BMI) and concentrations of adiponectin in both humans and animals. However, in ''ob/ob'' mice - mutant mice that eat excessively and become obese - overexpression of adiponectin in adipose tissue increased plasma adiponectin concentrations, keeping them in a physiological range. This increase  resulted in significant weight gain and reduced hyperglycaemia and amended metabolic abnormalities. These findings suggest a role of variable plasma adiponectin concentrations in the pathophysiology of the healthy obese phenotype. Data from one recent study shows that lack of suppression of adiponectin concentrations is independently associated with the metabolically healthy profile of certain obese individuals <ref name = Aguillar-Salinas >(Aguillar-Salinas  ''et al.'' 2008)</ref>.


One study found that 20% of individuals with a BMI greater than 40kg/m2 had adiponectin concentrations on average higher than those of subjects with a normal BMI. Obese women and men with adiponectin concentrations higher than 12.49mg/l and higher than 8.07 mg/l respectively, were more likely to be metabolically healthy. These results were proven to be significant in a logistic regression model after controlling the effect of insulin, age, and waist circumference. Thus some obese individuals have plasma adiponectin concentrations similar to those of normal BMI subjects, and it is thought this is a contributing factor to the metabolically healthy obese phenotype <ref name=Aguillar-Salinas/>.  
One study found that 20% of individuals with a BMI greater than 40kg/m2 had adiponectin concentrations on average higher than those of subjects with a normal BMI. Obese women and men with adiponectin concentrations >12.49mg/l and >8.07mg/l respectively, were more likely to be metabolically healthy. These results were proven to be significant in a logistic regression model after controlling the effect of insulin, age, and waist circumference. Thus, some obese individuals have plasma adiponectin concentrations similar to those of normal BMI subjects, and this may contribute to the metabolically healthy obese phenotype <ref name=Aguillar-Salinas/>.  





Revision as of 06:49, 1 November 2011

What is Healthy Obesity?

Although obesity is a major risk factor for cardiovascular disease and type 2 diabetes mellitus, about a third of obese individuals maintain healthy cardiometabolic profiles; this phenotype of healthy obesity may be linked to the location of adipose tissue and the metabolic characteristics of the fat. Some data also suggest that weight loss by healthy obese subjects may have an adverse impact on their favorable cardiometabolic profile. [1] [2]


Why is Healthy Obesity Worthwhile investigating?

Investigating why H.O can't be regarded as simply obesity e.g. treatment problems, some weight losing methods actually detrimental to H.O individual

Waste of money to treat all H.O individuals as simply obese?


The Cause of Healthy Obesity?

Proposed Mechanistic Determinants of the Healthy Obese Phenotype

Adipose tissue is an endocrine organ, releasing several inflammatory cytokines and expressing endocrine hormone receptors. The location of adipose tissue, the histological characteristics of adipose tissue and its metabolic activity may be more relevant than its total mass with regards to the healthy obese phenotype, and they may play a role in determining the cardiometabolic health of obese individuals [2].

Adiponectin and Healthy Obesity

Adiponectin is a protein hormone which is secreted into the bloodstream from adipose tissue and modulates several metabolic processes, including fatty acid catabolism and glucose regulation. The level of adiponectin in the bloodstream is inversely correlated to the percentage of body fat in adults. It is associated with the suppression of metabolic processes that can lead to obesity, type 2 diabetes mellitus and non-alcoholic fatty liver disease (NAFLD). Diabetics tend to have reduced levels of the hormone and levels of adiponectin are significantly increased with weight loss. Other metabolic effects of adiponectin are: decreased gluconeogenesis and increased glucose uptake; lipid catabolism; protection from endothelial dysfunction; insulin sensitivity, and control of energy metabolism. Hypoadiponectinaemia, therefore, is an independent risk factor for metabolic syndrome and type 2 diabetes mellitus– two conditions associated with an unhealthy metabolic profile of obese individuals.

There is an inverse relationship between body mass index (BMI) and concentrations of adiponectin in both humans and animals. However, in ob/ob mice - mutant mice that eat excessively and become obese - overexpression of adiponectin in adipose tissue increased plasma adiponectin concentrations, keeping them in a physiological range. This increase resulted in significant weight gain and reduced hyperglycaemia and amended metabolic abnormalities. These findings suggest a role of variable plasma adiponectin concentrations in the pathophysiology of the healthy obese phenotype. Data from one recent study shows that lack of suppression of adiponectin concentrations is independently associated with the metabolically healthy profile of certain obese individuals [3].

One study found that 20% of individuals with a BMI greater than 40kg/m2 had adiponectin concentrations on average higher than those of subjects with a normal BMI. Obese women and men with adiponectin concentrations >12.49mg/l and >8.07mg/l respectively, were more likely to be metabolically healthy. These results were proven to be significant in a logistic regression model after controlling the effect of insulin, age, and waist circumference. Thus, some obese individuals have plasma adiponectin concentrations similar to those of normal BMI subjects, and this may contribute to the metabolically healthy obese phenotype [3].


Location of Adipose Tissue

Both central adiposity and ectopic fat (fat found in lean tissue) are thought to be associated with the role of fat location in healthy obesity. Some studies have found that healthy obese individuals have smaller waist circumferences or lower levels of abdominal visceral fat (VAT) than metabolically unhealthy individuals. This is not surprising as central visceral fat is drained into the portal circulation and contributes to insulin resistance and dyslipidaemia, two factors associated with cardiovascular risk and metabolic disturbances [2]. However, other studies produced data suggesting otherwise, and found that there were no differences in central obesity between healthy and at-risk obese individuals.

High levels of subcutaneous adipose tissue (SAT) have been found in some studies to be protective against atherosclerosis, independent of levels of VAT, suggesting a role for SAT in the healthy obese phenotype. However, other studies have found that high levels of SAT and VAT contribute to elevated CVD risk factors, and no differences in SAT levels were found between healthy and at-risk obese individuals. This could be due to the suggested modifying effects of VAT on SAT's effects on metabolic profile; high levels on SAT contribute to development of the metbolic syndrome when paired with loe VAT levels, but seem to be protective when paired with high levels of VAT [2].


Victoria Catherine Pickard 19:57, 31 October 2011 (UTC)

Criticism of Current Data - Does the Healthy Obesity Phenotype Actually Exist?

Investigating whether or not H.O is a genuine phenotype or has this subgroup emerged as a result of methodological/ measurement issues? Are these people healthy and truely obese/ are they obese yet truely healthy?

Conflicting findings of meta-analyses from NEJM and American heart journal etc. the impact of adjusting for physical activity and the role of other parameters. eg. lack of any the metabolic syndrome criteria & no insulin resistance counts as healthy. non metabolic morbidity.

or if that overlaps too much with someone else's section I could cover:

the role of ethnicity: A higher proportion of black healthy obese? Possible underlying mechanism?

Losing weight can be harmful for the healthy obese: (Gaesser 1999)Tijmen van Slageren 18:38, 24 October 2011 (UTC)


Conclusions

References

  1. Lee CM et al. (2008) Indices of abdominal obesity are better discriminators of cardiovascular risk factors than BMI: a meta-analysis J Clin Epidemiol 61:646-53 PMID 18359190
  2. 2.0 2.1 2.2 2.3 Wildman RP (2009) Healthy obesity Curr Opin Clin Nutr Metab Care 12:438-43 PMID 19474713 Cite error: Invalid <ref> tag; name "Wildman" defined multiple times with different content
  3. 3.0 3.1 (Aguillar-Salinas et al. 2008)