I have never been skinny...

except mentally while pregnant. I will explain, gaining a whopping 60 pounds during my first pregnancy I whole-heartedly convinced myself that Kate Moss was a model of MY prepregnancy self. Hmmm...delusions aside, I know it it hard to keep and maintain one's health. The following is my attempt at finding additional motivation.

Nutrition, Obesity, and Atherosclerotic Cardiovascular Disease: a Trifecta of Energy Homeostasis
The prevalence of obesity has propelled its causation and treatment to the forefront of medical vernacular and concern. This concern pertains to obesity’s contribution to numerous other disease states and comorbidities. Specifically concerning is its association in accelerating atherosclerosis and cardiovascular death. Atherosclerosis is characterized by the deposition of plaque in the form of fatty substances such as cholesterol in the innermost layer of the arterial wall. Such an association is demon
strated through the increase in hypertension, diabetes, and dyslipidemia. The role of nutrition in diminishing obesity and subsequently the associated atherosclerosis is ever increasing as non-surgical and preventative methods are emphasized. While numerous research studies are examining this relationship, the following review highlights three studies that researched the role of specific nutrient factors in contributing and controlling obesity and atherosclerosis.

Biological Basis
Energy homeostasis pertains to the ability to maintain a stable biological state regardless of adjustments in nutrition or environmental changes. The biological mechanisms that contribute to this physiological regulation consist of organ systems, organs, hormones, microbes, molecules, and cells. These mechanisms function by integration of intake and expenditure and subsequent (re)allocation of energy. For example, during periods of energy deficiency, the brain’s neuronal pathways cause appetite to increase while metabolic rate declines (Flier et.al, 2007). . The endocrine and nervous system also regulate digestion and energy extraction. This combination causes efficient recovery of lost weight when access to energy is restored. This energy storage is of vital importance as 78% of a body’s energy stores is in the form of fats (Johnson, 2010). However, maladaptive responses to this relationship caused by excess storage due to excess energy consumption results in obesity.

This excess energy consumption pertains to malnutrition, defined by an excess or an deficiency of nutrients (Johnson, 2010). The subsequent connection between nutrition, obesity, and atherosclerotic cardiovascular disease is a result of mounting evidence relating how nutrition affects obesity levels and how obesity affects atherosclerosis. The research articles that are reviewed in the following discourse identified the nutritional component as integral to obesity treatment and prevention.

Research Findings
Research by Haiming et. al. (2008), in the identification of lipokine, documented an increase in lipogenesis enabled resistance in adipose tissue to the “systemic effects of dietary lipid exposure” (Haiming et. al., 2008). This resistance was documented through the tissue lipid profiles of mice. These mice were deficient in specific fatty acid binding proteins (FABPs) that resulted in significant improvements in their resistance levels. Those deficient in FABP2 had improved insulin sensitivity. Those with combined deficiency in both FABP4 and FABP5 had “profound” systemic metabolic regulation and were resistance to atherosclerosis and obesity (Haiming et. al., 2008).

Further analysis by Valavanis et. al. (2010) sought to identify obesity as a cardiovascular disease risk factor. Researched initially examined 24 genetic variants and 38 nutritional variants to study the etiology of obesity through a dataset of 2,341 participants. Two artificial neuron networks (ANNs) were used to analyze data pertaining to the participants’ risk factors in accordance to their BMI. Eighteen nutritional variants were identified as components of obesity as a risk factor. The primary nutritional factor was determined as cholesterol-intake in food. Additional factors include vitamin A-total intake, omega 3-intake in supplements, and vitamin B12- intake in food.

Stepien et al. (2011) sought to evaluate the high protein diet (HPD) as a strategy against obesity. Eighty Wistar rats were studied in varying dietary feeding modes and mRNA levels were measured in the liver, adipose tissues, kidneys, and muscles. Energy expenditure was measured by calorimetry. Significant results in organs were only observed in the liver where decreased mRNA encoding glycolysis and lipogenesis enzymes and increased mRNA encoding gluconeogenesis enzyme lowering and stabilization occurred. This was coupled by calorimetry that resulted in a reduction in glucose oxidation and stable fat oxidation.

Public Health Application
Within a public health context, Valavanis’ 18 nutritional variants and Stepien’s high protein diet have a greater applicability than Haiming’s lipokine identification. This applicability pertains to the incorporation of nutritional factors such as vitamin A or omega-3 supplementation into obesity treatment and prevention that is not readily adhered in regards to removal of FABPs. For example, nutritional program implementation could utilize Valavanis and Haiming’s data to create possible weight loss or management programs that are high in protein, low in cholesterol, high in vitamin A and B12, and encourage supplementation of omega-3s and vitamin A. Prevention programs utilizing existing school lunch programs, corporate meal providers, senior meal centers, etc. could incorporate these dietary guidelines. Undoubtedly, current guidelines would be hard to change based on data extrapolated from mice and rats, but pilot test programs within these existing providers may be effective. The current obesity pandemic warrants such efforts in research and implementation.




References
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Berg, A., Scherer, P. (2005) Adipose Tissue, Inflammation, and Cardiovascular Disease, Circulation Research, 96, 939-949. doi: 10.1161/01.RES.0000163635.62927.34
Flier, J.S., & Maratos-Flier, E. (2007). What fuels fat. Scientific American, 297, 72–81.
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Haiming, C., Gerhold, K., Mayers, J., Wiest, M., Watkins, S., and Hotamisligil, G. (September 2008) Identification of a Lipokine, a Lipid Hormone Linking Adipose Tissue to Systemic Meatbolism. Cell , 134, 6, 933-944. doi:10.106/j.cell.2008.07.048
Johnson, M.D.  (2010). Human Biology:  Concepts and current issues.  San Francisco. CA:  Pearson Benjamin Cummings.
Katagiri, H., Yamada, T., & Oka, Y. (2007). Adiposity and cardiovascular disorders disturbance of the regulatory system consisting of humoral and neuronal signals. Circulation Research, 101, 27–39.  
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Stepien, M., Gaudichon, C., Fromentin, G., Even, P., Tome, D., Azzout- Marniche, D. (February 2011) Plos One, 6, 2.
Valavanis, I., Mougiakakou, St., Grimaldi, K., Nikita, K. (2010) A multifactorial analysis of obesity as CVD risk factor: Use of neural network based methods in a nutrigenetics context. Bio Med Central Bioinformatics 11, 453.