American food is in a state of crisis. Obesity and diabetes are on the rise, food costs are skyrocketing, family farms are in decline and our agricultural environment is in jeopardy. Ingredients (2009) explores a thriving local food movement as our world becomes a more flavorless, disconnected and dangerous place to eat. Discovering better flavor and nutrition, Ingredients is a journey that reveals the people behind the movement to bring good food back to the table and health back to our communities.

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Fat, Sick & Nearly Dead

100 pounds overweight, loaded up on steroids and suffering from a debilitating autoimmune disease, Joe Cross is at the end of his rope and the end of his hope. In the mirror he saw a 310 lb man whose gut was bigger than a beach ball and a path laid out before him that wouldn’t end well— with one foot already in the grave, the other wasn’t far behind. FAT, SICK & NEARLY DEAD (2010) is an inspiring film that chronicles Joe’s personal mission to regain his health.

With doctors and conventional medicines unable to help long- term, Joe turns to the only option left, the body’s ability to heal itself. He trades in the junk food and hits the road with juicer and generator in tow, vowing only to drink fresh fruit and vegetable juice for the next 60 days. Across 3,000 miles Joe has one goal in mind: To get off his pills and achieve a balanced lifestyle.

While talking to more than 500 Americans about food, health and longevity, it’s at a truck stop in Arizona where Joe meets a truck driver who suffers from the same rare condition. Phil Staples is morbidly obese weighing in at 429 lbs; a cheeseburger away from a heart-attack. As Joe is recovering his health, Phil begins his own epic journey to get well.

What emerges is nothing short of amazing – an inspiring tale of healing and human connection.
Part road trip, part self-help manifesto, FAT, SICK & NEARLY DEAD defies the traditional documentary format to present an unconventional and uplifting story of two men from different worlds who each realize that the only person who can save them is themselves.

The Obesity Epidemic Lecture

Public Lecture at Cardiff Metropolitan University, Wales 

This open lecture was given  on 7 February 2012 by the nutritionist Zoë Harcombe.

In the UK, obesity has increased ten fold since the 1970′s. Clearly it cannot increase ten fold again or 250% of us will be overweight. However, the prediction of the Foresight report is that 90% of today’s children will be overweight or obese by 2050. We cannot allow this to happen.

We want to be slim more than anything else in the world, so why do we have an obesity epidemic?

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Red Wine Compound May Fight Obesity

Kee-Hong Kim found that piceatannol, a compound found in red wine and several fruits, blocks immature fat cells from growing. (Purdue Agricultural Communication photo/Tom Campbell)

A compound found in red wine, grapes and other fruits, and similar in structure to resveratrol, is able to block cellular processes that allow fat cells to develop, opening a door to a potential method to control obesity, according to a Purdue University study.

Kee-Hong Kim, an assistant professor of food science, and Jung Yeon Kwon, a graduate student in Kim’s laboratory, reported in this week’s issue of the Journal of Biological Chemistry that the compound piceatannol blocks an immature fat cell’s ability to develop and grow.

While similar in structure to resveratrol – the compound found in red wine, grapes and peanuts that is thought to combat cancer, heart disease and neurodegenerative diseases – piceatannol might be an important weapon against obesity. Resveratrol is converted to piceatannol in humans after consumption.

“Piceatannol actually alters the timing of gene expressions, gene functions and insulin action during adipogenesis, the process in which early stage fat cells become mature fat cells,” Kim said. “In the presence of piceatannol, you can see delay or complete inhibition of adipogenesis.”

Over a period of 10 days or more, immature fat cells, called preadipocytes, go through several stages to become mature fat cells, or adipocytes.

“These precursor cells, even though they have not accumulated lipids, have the potential to become fat cells,” Kim said. “We consider that adipogenesis is an important molecular target to delay or prevent fat cell accumulation and, hopefully, body fat mass gain.”

Kim found that piceatannol binds to insulin receptors of immature fat cells in the first stage of adipogenesis, blocking insulin’s ability to control cell cycles and activate genes that carry out further stages of fat cell formation. Piceatannol essentially blocks the pathways necessary for immature fat cells to mature and grow.

Piceatannol is one of several compounds being studied in Kim’s laboratory for its health benefits, and it is also present in different amounts in red grape seeds and skin, blueberries, passion fruit, and other fruits.

Kim would like to confirm his current finding, which is based on a cell culture system, using an animal model of obesity. His future work would also include determining methods for protecting piceatannol from degrading so that concentrations large enough would be available in the bloodstream to stop adipogenesis or body fat gain.

“We need to work on improving the stability and solubility of piceatannol to create a biological effect,” Kim said.



Jung Yeon Kwon, Sang Gwon Seo, Yong-Seok Heo, Shuhua Yue, Ji-Xin Cheng, Ki Won Lee, and Kee-Hong Kim. Piceatannol, Natural Polyphenolic Stilbene, Inhibits Adipogenesis via Modulation of Mitotic Clonal Expansion and Insulin Receptor-dependent Insulin Signaling in Early Phase of Differentiation. J Biol Chem 2012; 287: 11566-11578.



Designer Probiotics Could Reduce Obesity

Specially designed probiotics can modulate the physiology of host fat cells say scientists writing in Microbiology. The findings could lead to specialised probiotics that have a role in the prevention or treatment of conditions such as obesity.

Scientists from the Alimentary Pharmabiotic Centre (APC), Cork, University College Cork and Teagasc, in Ireland engineered a strain of Lactobacillus to produce a version of a molecule called conjugated linoleic acid (CLA). When this engineered bacterial strain was fed to mice, the researchers found that the composition of the mice’s fat tissue was significantly altered, demonstrating that ingesting live bacteria can influence metabolism at remote sites in the body.

CLA is a fatty acid that is produced in different versions by different bacteria. One type, called t10, c12 CLA, has been shown to be associated with decreased body fat in humans and other animals. t10, c12 CLA also has the ability to inhibit the growth of colon cancer cells and induce their death. However, this type of CLA is only produced by certain types of bacteria including Propionibacterium acnes – a skin bacterium that can cause acne.

In this study, an enzyme-encoding gene from P. acnes was transferred to the Lactobacillus strain allowing it to produce t10, c12 CLA. Lactobacillus strains are common inhabitants of the normal gut flora and are often found in probiotic products. The researchers found that the level of t10, c12 CLA in the mice’s fat tissue quadrupled when they were fed this recombinant probiotic. Thus, this study demonstrates that gut microbes have an impact on host metabolism, and in particular fat composition.

Dr Catherine Stanton, from Teagasc who led the study explained the significance of the results. “CLA has already been shown to alleviate non-alcoholic fatty liver disease that often accompanies obesity. Therefore, increasing levels of CLA in the liver by ingestion of a probiotic strain is of therapeutic relevance,” she said. “Furthermore, fat is not an inert layer around our bodies, it is active and proinflammatory and is a risk factor for many diseases, including cancers. The work shows that there is potential to influence this through diet-microbe-host interactions in the gut.”

The same group of researchers previously found that microbially produced CLA was able to reduce the viability of colon cancer cells by 92%. “It is possible that a CLA-producing probiotic may also be able to keep colon cancer cells in check. All our findings to date demonstrate that the metabolism of gut bacteria can modulate host cell activity in ways that are beneficial to the host,” explained Dr Stanton. “We need to further investigate the effects of CLA-producing bacteria on human metabolism, but our work so far certainly opens up new possibilities for the use of probiotics for improvement of human health.”


Rosberg-Cody E, Stanton C, O’Mahony L, Wall R, Shanahan F, Quigley E, Fitzgerald G, Ross P. Recombinant lactobacilli expressing linoleic acid isomerase can modulate the fatty acid composition of host adipose tissue in mice. Microbiology 2011; 157 (Pt 2): 609-15.


This is a trailer of the film Microwarriors: The Power of Probiotics (Health Point Productions).


Treating Obesity Via Brain Glucose Sensing


The past two decades have witnessed an epidemic spread of obesity-related diseases in Western countries. Elucidating the biological mechanism that links overnutrition to obesity could prove crucial in reducing obesity levels. In the July 26 issue of PLoS Biology, Dr. Dongsheng Cai and his research team at Albert Einstein College of Medicine describe a pathway that directs the brain to sense the body’s glucose dynamics, and they find that a defect of this glucose sensing process contributes to the development of obesity and related disease. Importantly, the team also found that correction of this defect can normalize the whole-body energy balance and treat obesity.

The hypothalamus in the brain plays a key role in controlling energy and body weight balance. To maintain balance between energy intake and energy expenditure, the hypothalamus constantly gauges the whole-body’s energy levels by sampling circulating hormones (e.g. insulin and leptin) as well as nutrients (e.g., glucose). Although we know quite a bit about the hormonal pathways in the hypothalamic regulation of feeding, the mechanisms for hypothalamic nutrient sensing are much less clear. Moreover, a causal link between a nutrient sensing defect and obesity remains to be established. The team led by Dr. Cai discovered a novel role of a protein complex, hypoxia-inducible factor (HIF), in hypothalamic glucose sensing and whole-body energy balance in mice.

HIF is a nuclear transcription factor which induces hypoxia response. When tissue oxygen level is low, HIF is activated to promote cellular metabolic adaption and survival. Recent research has appreciated the involvement of HIF in the metabolism of tumor cells. “However, an intriguing but unexplored question is whether HIF can be important for the regulation of whole-organism metabolism, and if so, which tissue and cells are responsible.” says Cai, who is an expert in neuroendocrinology and metabolism.

Cai and his group examined HIF in the hypothalamus and, surprisingly, found that it can be activated by glucose and that this regulation was associated with appetite control in mice. In identifying the cellular and molecular basis, the team found that in response to glucose, HIF acts in a unique group of hypothalamic nutrient-sensing neurons to induce expression of POMC gene – a gene which has been known to play a key part in hypothalamic control of feeding and body weight. Most excitingly, the team demonstrated the therapeutic potential of targeting hypothalamic HIF to control obesity. By enhancing the hypothalamic HIF activity via gene delivery, mice become resistant to obesity despite the condition of nutritional excess.

“It was an exciting discovery,” explains Cai, “Our study is the first to show that beyond its classical oxygen-sensing function in many cells, HIF in the hypothalamic neurons can sense glucose to control the whole-body balance of energy intake and expenditure which is critical for body weight homeostasis.” Overall, this study reveals a crucial role for neuronal HIF in bridging the brain’s glucose sensing with the brain’s regulation of body weight and metabolic physiology. These findings also highlight a potential implication for developing neuronal HIF activators in treating and preventing obesity and related diseases.



Zhang H, Zhang G, Gonzalez FJ, Park S-m, Cai D.  Hypoxia-Inducible Factor Directs POMC Gene to Mediate Hypothalamic Glucose Sensing and Energy Balance Regulation. PLoS Biol 2011; 9 (7):  e1001112. doi:10.1371/journal.pbio.1001112



Does Food Act Physiologically Like A ‘Drug Of Choice’ For Some?

Reducing variety in food choices may represent an important strategy for those trying to lose weight.

Variety is considered the “spice of life,” but does today’s unprecedented level of dietary variety help explain skyrocketing rates of obesity? Some researchers think it might.

According to ASN Spokesperson Shelley McGuire, PhD: “We’ve known for years that foods- even eating, itself- can trigger release of various brain chemicals, some of which are also involved in what happens with drug addiction and withdrawal. And, as can happen with substance abusers, tolerance or “habituation” can occur, meaning that repeated use (in this case, exposure to a food) is sometimes accompanied by a lack of response (in this case, disinterest in the food). The results of the study by Epstein and colleagues provides a very interesting new piece to the obesity puzzle by suggesting that meal monotony may actually lead to reduced calorie consumption. The trick will be balancing this concept with the importance of variety to good nutrition.”

Studies have shown that many people become disinterested in a particular food when they are repeatedly exposed to it. This response, called habituation, can decrease caloric intake in the short-run. Conversely, when presented with a variety of foods, caloric intake can increase. The “food addiction hypothesis” purports that some people may overeat because they are insensitive to the normal habituation response and thus need even more exposure to a food to trigger a disinterest. However, there has been no rigorous research investigating whether healthy-weight and overweight individuals have different habituation responses, and little is known about what patterns of food exposure are most powerful in triggering habituation. To help close these research gaps, researchers studied long-term habituation in obese and nonobese women. Their results, and an accompanying editorial by Nicole Avena and Mark Gold, are published in the August 2011 issue of The American Journal of Clinical Nutrition.

Sixteen nonobese [BMI (in kg/m2) < 30] and 16 obese (BMI  30) women were randomly assigned to 1 of 2 groups: the “weekly group” participated in weekly experimental food exposure sessions for 5 wk, whereas the “daily group” were studied daily for 5 consecutive days. During each 28-min experimental session, subjects were asked to complete a variety of tasks after which they were “rewarded” by being given a 125-kcal portion of macaroni and cheese. Participants could work for as much food as they wanted. The researchers then evaluated total energy intake.

Whereas weekly food exposure increased total caloric intake by approximately 30 kcal/d, daily exposure decreased energy consumption by ~100 kcal/d. This supports long-term habituation in terms of caloric intake. Very few differences were found between how obese and nonobese individuals responded.

The authors concluded that reducing variety in food choices may represent an important strategy for those trying to lose weight. Moreover, having a person even remember that they have eaten a certain food recently may be effective in this regard. In their accompanying editorial, Avena and Gold compare physiologic components of the food addiction hypothesis to the body’s addictive responses to drugs. They also ponder whether school-lunch planners and public health officials should note that diversity in the menu is not necessarily a virtue” but might instead “be associated with promoting excess food intake and increased body mass index.” Provocative food for thought.



Epstein LH, Carr KA, Cavanaugh MD, Paluch RA, Bouton ME. Long-term habituation to food in obese and nonobese women. Am J Clin Nutr 2011; 94: 371–6.