These presentations draw on 27 volume of Advances in Strategic Management entitled “History and Strategy” that is available in pdf through your university library or via the Kindle Store. For details, click here. History and Srategy Book

Organizer: Steven Kahl; Dartmouth College (TUCK);
Organizer: Brian S. Silverman; U. of Toronto;
Participant: David A. Kirsch; U. of Maryland;
Participant: Huseyin Leblebici; U. of Illinois;
Participant: J Peter Murmann; Australian School of Business, UNSW;

Yale Rudd Centre for Food Policy and Obesity
http://www.yaleruddcenter.org/

Co-Founder and Director is commentator for the NY Times, Kelly D. Brownell, PhD. kelly dot brownell at yale dot edu

Source: http://www.smh.com.au/opinion/society-and-culture/we-should-stop-putting-blame-on-obese-people-20110118-19v78.html?skin=text-only

Colaguri et al. (incl. Caterson), 2010 published a paper called the cost of overweight and obesity in Australia in eMJA. The cost data that I used was based on an analysis of 5-year follow-up data from the Australian Diabetes, Obesity and Lifestyle study, collected in 2004?2005 and compared it to National Health Survey data of 2007-8 to make sure it was relevant. The study was for adults aged over 30 years.

Bio: http://www.unisanet.unisa.edu.au/staff/Homepage.asp?Name=caroline.mcmillen
Publications List: http://www.unisanet.unisa.edu.au/staff/Homepage.asp?Name=caroline.mcmillen#ResearchPublications
Interview audio file in dropbox

Catherine Suter
- The Victor Change Institute
- Spoke at Melbourne epigenetics conference in 2009 on the role of maternal nutrition (both overnutrition and malnutrition) in epigenetic reprogramming.
- I can find no research specifically related to obesity.

Bio & Selected Publications: : http://www.victorchang.edu.au/research/DrCatherineSuterPhD.cfm?cid=331
ABC Science show 2007: http://www.abc.net.au/catalyst/stories/s1900723.htm

Mark Vickers
- Auckland
- Primary interest is in the developmental origins of health and disease with a particular focus on the association between poor maternal nutrition and the development of obesity and type 2 diabetes in offspring.
- INTERESTING: They also have an interest in therapies aimed at reversing the metabolic disturbances that result from a suboptimal early life environment.

Bio and Selected Publications: http://www.liggins.auckland.ac.nz/uoa/markvickers

“obesity develops as a consequence of an interaction between prenatal under-nutrition and postnatal high-fat nutrition. This phenotype also shows significant alterations in POMC, NPY, AgRP and OBRb gene expression together with elevations in circulating levels of both plasma leptin and insulin. These findings are consistent with the predictive adaptive response hypothesis that neuroendocrine development during fetal life may be based on predictions about postnatal environmental conditions.” http://joe.endocrinology-journals.org/cgi/content/abstract/193/1/31 (in endnote)

Moshe Szyf
- University of Montreal
- mainly looking at epigenetics for cancer, commercialization of products.

website: http://www.medicine.mcgill.ca/pharma/mszyflab/

2. The outcome of this study indicates that polymorphisms in the FTO gene and near the MC4R gene do not have a role in regulating food intake and preference for specific food items: http://sirius.library.unsw.edu.au/V/MT6V3UTENBGRG4S94HMNFX98RHAE3M8QQ4TYREMT78KHBG86BF-22050?func=quick-3&short;-format=002&set_number=004881&set_entry=000008&format=999

3. Acquired preference for fatty foods is associated with obesity, independent of genetic background. Modification of fat preferences may be an important step in the prevention of obesity in the general population.: http://www.nature.com/ijo/journal/v26/n7/abs/0802014a.html

4. By using comparative measures within twin pairs we found that the amount of food consumed is the major contributor to obesity independent of genetic predisposition: http://www.ncbi.nlm.nih.gov/pubmed/19943715

Epigenetics
epigenetics has been defined as the study of heritable changes in gene expression that occur in the absence of a change in the DNA sequence itself

The epigenetic state of the DNA and the associated phenotype can sometimes be inherited in what is called the “transgenerational epigenetic inheritance”

DNA methylation
covalent histone modifications
chromatin folding
regulatory action of miRNAs and polycomb group complexes

Calorie restriction/dieting study: data show that both DNA methylation and gene expression are responsive to caloric restriction and provide new insights about the molecular pathways involved in body weight loss as well as methylation regulation during adulthood. The genes affecting differences included genes likely to be involved in metabolic pathways related to angiogenesis and cerebellar long-term depression. Title:Differential epigenomic and transcriptomic responses in subcutaneous adipose tissue between low and high responders to caloric restriction (endnote)
Conclusions: These

Chemical Exposure: Exposures are being held responsible for causing epigenetic changes that lead to a disease process. Exposure to heavy metals, bioflavinoids, and endocrine disruptors, such as bisphenol A and phthalates, has been shown to affect the epigenetic memory of an organism. Title: Epigenics in womens health care (endnote)

Genes and Diet

Evidence: Yung (2007) genetic epidemiology of obesity (in dropbox)

Some potential susceptibility genes, which relate to energy homeostasis, appetite, satiety, lipoprotein metabolism, and a number of peripheral signaling peptides, may be involved in variable responses to diets (138).

obesity-related genes “epiobesigenes”

Genes regulating energy homeostasis and thermogenesis include:
1. neuropeptide Y (NPY),
2. agouti-related protein (AGRP),
3. melanocortin path- way factors (MC4R),
4. uncoupling proteins (UCPs), and
5. fatty acid binding protein (FABP) (80, 138).

Diet intake control may be affected by genes encoding taste receptors and a number of peripheral signaling peptides, such as:
1. insulin (INS),
2. Leptin LEP,
MC4R: High-fat diet leads to a decreased methylation of the Mc4r gene in the obese BFMI and the lean B6 mouse lines: MC4R mice study (dropbox)
3. ghrelin (GHRL), and
4. cholecystokinin (CCK) (138).
5. The MC4R gene and the neuromedin beta gene (NMB) were identified as having an association with the control of eating behavior (142, 143).

Metabolism:

intermediate metabolism:
COX7A1
LPL,
CAV1,
IGFBP3,

Carbs and Protein
Clusters of a-amylase genes (AMY1A, AMY2A, and AMY2B), involved in the digestion of starch, and the insulin- like growth factor 1 gene (IGF1) may be linked to car- bohydrate and protein intakes (140, 141).
Fat

adipogenesis
FGF2,
PTEN,
CDKN1A
ESR1

Some genes have been identified and linked to variable responses to diet in the lipoprotein metabolism pathway, including:
apolipoprotein E (APOE),
apolipoprotein B (APOB),
apolipoprotein AIV (APOA4),
apolipoprotein CIII (APOC3),
low-density lipoprotein receptor (LDLR),
FABP,
LPL,
mi- crosomal transfer protein (MTP),
cholesteryl ester transfer protein (CETP), and
hepatic lipase (HPL) (144).

Inflamation
SOCS1/SOCS3