Tuesday, November 29, 2011

Hair Donation and Nutrition for Healthier Hair

Hair. Some call it their Crowning Glory. Being the perennial optimists, the Chinese named it 3000 Strands of Sorrow. Rapunzel wore hers in a lovely Braid of Golden Stairs. Medusa's head-turning tresses of Serpents could turn one stone cold. Buddhist monks shave their noggins as renouncement of worldliness. 
No matter which philosophy, style, length, colour one chooses, those little keratinized, filamentous threads growing out of the follicles on our scalp, at the approximate rate of 1/2 inch per month, have indeed been the originator of many, well, hairy tales! They regularly induce post haircut traumatic stress disorder; can be more powerful than WMD  in destructing one's self esteem; and yet, on occasions have been the source of artistic inspiration for drunkard uncles at my family wedding dinners (as evidenced by said uncle's keen observation & deep appreciation that "4th aunty's hairdo bears such striking resemblance to a perfect head of cauliflower").
But I shall not concern myself with such perplexing matters of the hair anymore, because I have decided to chop mine off, to be turned into a wig! You see, I have decided to shed my locks, for donation to Locks of Love, a public non-profit organization that makes hair prosthetics for financially disadvantaged children who have lost theirs due to diagnosed health conditions, or caused by the medical treatments they are undergoing for their illnesses. The hairpieces will go a long way in helping these children restore self esteem and confidence. I think that is really important, for what is health if one does not feel a sense of self worth! 
Nutrition is integral in maintaining good hair quality, and malnutrition often presents itself in weak, brittle hair or even pronounced hair loss. Obviously, no amounts of the most nutritious foods in the world can cause hair to sprout if your genome is more akin to that of a smooth, shiny globe than a rambutan! But barring preexisting conditions and dispositions, good nutrition should generally yield hair of higher quality.
Here are some tips I found on nutrition for better hair:
According to an article published by The American Hair Loss Association (1), good nutrition underscores hair growth. A malnourished person who is deficient in Protein, Vitamin A, Iodine and Iron is likely to experience unhealthy hair quality or loss. Additionally, consumption of sugar might be detrimental to the health of one's hair due to sugar's effects on Insulin, vis a vis Insulin's connection to the secretion of another hormone Testosterone. A substance known as dihydrotestosterone, which is a byproduct of Testosterone, is a common factor found in hair loss patterns.
In this area, I found offerings in Traditional Chinese Medicine too. Dr. Maoshing Ni, in his book "Secrets of Self Healing" (2), ascribed hair loss to "a decline of the vital kidney essence". Possible causes might be stress, physical and emotional strain, an unhealthy lifestyle including excessive sexual activity (I can hear loud protests here), and overindulgence in alcohol (more loud protests). Therefore, restoration of kidney essence is vital for healthy hair.
Integrating both western and eastern theories, Dr. Mao named a few vitamins and nutrients which are essential. Methysulfonylmethane (MSM) is a building block of strong hair. Biotin and B Complex contributes to hair growth while Vitamin E improves delivery of oxygen. Zinc is known to regulate endocrine function in relation to hair growth. Vitamin C increases blood circulation in the scalp. Silica is important for building strong hair. Amino Acids improve overall quality of hair. 
Further, Dr. Mao recommends including the following foods in our diets : organic vegetables; whole grains; walnuts, sesame seeds, sunflower seeds, pumpkin seeds; beets; mushrooms; fruits such as blueberries, cranberries, raspberries, blackberries, apples, pears, peaches; legumes such as black beans, mung beans; meat such as organic lamb, chicken and deep-sea fish. He also specifies the importance of eliminating or limiting processed foods, artificial additives, bleached flour, sugars, soft drinks (yes, even diet ones), spicy, deep fried and fatty foods.
Additionally, Evening Primrose Oil, Flaxseed and Fish Oils can act as precautionary measures for damaged hair and follicles. Other remedies include Gingko Biloba, Saw Palmetto, Green Tea, Chinese Arbovitae, Eclipa, Chinese Foxglove, Black Cohosh, Vitex, Ginger and Sesame.
With a few tips in our pockets, maybe some of you might join me in eating well and making similar hair donations; or perhaps you could help by forwarding this to someone who might be interested. I wish some of you many good hair days ahead; and to others, some happily hairless ones as well!
References:
1. American Hair Loss Association, http://blog.americanhairloss.org/hair-loss/nutrition-and-hair-loss/
2. Ni Maoshing, (2008), Secrets of Self Healing: harness nature's power to heal common ailments, boost your vitality, and achieve optimum wellness, Penguin Group (USA) Inc, Pp 304-7

Sunday, October 30, 2011

Possible Effects of Excessive Physical Exercise on Prepubescent Children

The ill effects of a sedentary lifestyle on children are well documented, and is a heavyweight contributing factor to childhood diabetes and obesity today. More often, we hear calls to steer our kids away from their attachments to TVs and computers, and to involve them in more athletic activities. Hence, it is rarer to find a child who is too active than one who is inactive, and even more of an anomaly for a mother to be concerned that her child might be overexercising.
So, can too much of a good thing really be bad for you? Make no mistake, I am certainly of the view that a physically active lifestyle for children and adults alike, together with balanced nutrition, is the answer to a healthy body. I do not, for one single moment, believe that inactivity is an option for anyone capable of physical movement, unless immobility is your goal later in life! But as important as exercise is, I believe that it can indeed be hurtful when it becomes too much or too strenuous, leading to injuries, endocrine disruptions, eating disorders, and can be especially detrimental to the development in children.
Children are not mini me's of adults. In fact, they are very physiologically variant from adults. Their metabolism, hormonal responses work differently; their musculoskeletal systems are still undergoing shifts, formation and growth at different rates; hence, making them susceptible to physiological disturbances brought on by excessive physical stress. Of special concern to prepubescent girls is the effect on their endocrine system. Control of growth and development leading to, and at menarche, involve complex interaction of many factors, including physical and metabolic demands of intensive athletic training.
Again, I want to emphasize that this does not indicate that children are not well suited to physical movement. On the contrary, in 2008, a study by The National Institute of Arthritis and Musculoskeletal and Skin Diseases concluded that jumping exercises performed for a duration of one year in pre puberty, led to increased bone densities in children, and such effects remained with the children up to 8 years after (1). In another study completed in February 2011, researchers of the same institute showed that although genetics govern skeletal growth, physical activity during a child's development can improve skeletal health dramatically, and such benefits were found to be greatest in activities that involved loading weight and intense impact (2). Studies also proved that the benefits of regular activity for children extended beyond musculoskeletal development, and in fact could enhance their cardiovascular fitness and insulin sensitivity (4). As such, it is without doubt that physical stimulation is required for healthy growth, but the challenge lies in finding the right balance between exertion and rest.
Rates of growth and sexual development through puberty in children depend on the actions of hormones such as Growth Hormones (GH), Insulin-like Factors (IF), Steroid Sex Hormones (SSH). The same hormones also influence metabolic processes during physical activity. For young girls, "Adrenarche", signifies the beginning of secretion of Androgens and generally takes place in girls between the ages of 6-8 years of age. "Gonadarche" usually follows about 2 years later. It denotes activation of the ovaries and is governed by GH, IF and SSH. "Menarche" marks the onset of menstruation (3).
Hormones released during these stages control later development in puberty as well as other bodily strictures, and exercise causes dramatic changes in hormonal and metabolite levels. Hence, it is important to manage physical activity to the extent that it does not interfere with the child's endocrine and metabolic systems in adverse manners. Excessive training in adolescence can delay menarche in girls, bring about amenorrhea and the suppression of the body's immune system (4).
According to an article published in the American Journal of Clinical Nutrition in 2000 (5), delayed puberty is most prevalent in elite female athletes, most notably gymnasts, dancers and long distance runners. Bone formation is governed by a combination of nutrition, weight bearing activity, and secretion of SSHs. Since over 90% of adult bone mineral is accrued during pubertal years, delaying the onset of puberty might cause a shortfall in bone mineralization. Hypoestrogenism (under production of estrogen) as a consequence of delayed sexual maturation can also negate the benefits of weight bearing exercises on skeletal development. In a group of prepubescent runners, subjects with delayed periods were found to have lower bone density compared to the runners with regular period within the normal range.

Contrary to the undesirable effects of excessive activity, the same study found moderate exercise to favour cardiovascular health and body composition. However, careful attention should be drawn especially to sports such as wrestling, gymnastics, dancing. Children involved in these activities require close monitoring due to the emphasis on strict weight control and the high energy requirements. In a comparative experiment conducted over 2 years between a group of swimmers training 8 hours per week and a group of gymnasts training 22 hours per week, the gymnasts were found to have considerably decreased growth velocities (i.e. they were shorter and had less body mass), although it might be worthy to note that the data connecting intense athletic training and sexual growth in female gymnasts were not conclusive. 
For the purpose of interpretation, it will be useful to account for variables such as intensity of training, individual state of health, genetic disposition, socioeconomic, psychological and emotional factors, nutrition etc. Furthermore, perturbations in pubertal development were uncommon among young women engaged in recreational exercise or adolescents who trained less than 15 hours per week. Hence, it is necessary to distinguish elite athletic training from non elite sporting activities because training time and intensity are integral factors for consideration. It has been shown that olympic athletes have dramatically later menarche than high school, college or club level athletes.
Findings by The Committee on Sports Medicine and Fitness from the American Academy of Pediatrics in 2000 (6) recommended that it would be more beneficial to engage children in a variety of sports rather than focusing on just one sport. Not only will specialisation deny children of the benefits of varied activity and widened range of skills, it also adds unnecessary physical, physiological and psychological demands from intense training. Moreover, repetitive stress of doing the same movement over and over, may create detrimental results. However, this pertains to high intensity and sports specialization. 
The committee also reported that "although child athletes have superior cardiac functional capacity compared to non-athletes, data suggests that myocardial function can be depressed, at least transiently, after intense exercise". This raises some questions on very intense exercise on young children, but much closer investigation on the specifics of this area would be required before jumping to conclusions 
Other undesirable outcomes of excessive stress of physical activity in the report included tissue breakdown, overuse injuries such as tendonitis, apophysitis, fractures etc. In addition, injuries to joint surfaces and the spine during development were said to be particularly damaging to growing children because of the long term implications. Also of special concern were disruptions to the epiphyseal growth centre, which entails parts of the bone that are still growing. Soft tissues surrounding the physeal plate i.e. growth plate, grow at a faster rate, therefore external stress might disrupt the growth plate itself rather than the softer ligaments round it, resulting in stunted growth and/or deformed bones. It is also important to know that thermoregulatory responses in children are different from that of an adult. Children sweat less and create more heat in response to exercise, therefore care should be taken in temperature control while engaging young children in physical activities.
A 2008 paper published in the Journal of Applied Physiology (4), postulated that children  rely heavily on aerobic metabolism for energy and have low anaerobic capacities. They also have an immature glucose regulatory system compared to adults. The higher proportion of slow twitch, fatigue resistant (type 1) fibres in their musculature makeup might account for their reliance on aerobic metabolism, and at the same time, heighten their need for the oxidative metabolism of fat for energy. Together with the smaller endogenous carbohydrates reserves within their bodies, children are not suited to highly intensive, exhaustive physical activity.
A study on the effects of moderate exercise on adolescents, between a first group of 180 children of ages 10-14 years and a second group of 190 children between ages 15-19 years, showed that the the former group utililised considerably more fat than the second group. Moreover, that phenomenon lasted even when carbohydrates were fed to both groups before exercise, proving the point that aerobic metabolism and hence, fat oxidation was comparatively more pronounced in youth; and that their metabolic mechanism will shift towards a more anaerobic mode as children grow. As such, prepubescent children might be more adapted to start physical activities that are aerobic in nature and of a moderate pace, and gradually move on to more anaerobic activities that are of high intensity for brief periods, as they progress into puberty and beyond.
Similar conclusions were echoed by Researchers at the University of Rennes in France in 2000 (3), who also found children to respond unfavourably to exhaustive resistance training. Yet in contrast, they responded well to prolonged exercises of moderate intensity. Furthermore, the same study showed that the capacity to store muscle glycogen is much lower in children than in adults. Hence, in picking an athletic activity, it would be pertinent to consider this physiological constraint in young children. Any activity of moderate intensity (70% maximal oxygen uptake) that lasts over an hour, is unsuitable to be performed by children, as depletion of carbohydrate storage occurs much sooner.
Here you can find the key guidelines issued by U.S. Department of Health and Human Sciences on recommended level of physical activity : http://www.hhs.gov/news/press/2008pres/10/20081007a.html


Sources:
  1. Simple Exercise in Children yields long-term Skeletal Benefit. (November, 2008). National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH. Retrieved October 30, 2011 from: http://www.niams.nih.gov/news_and_events/spotlight_on_research/2011/child_exercise_bone.asp
  2. Childhood Exercise leads to Sustained Improvements in Bone Mass. (February, 2011). National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH. Retrieved October 30, 2011 from: http://www.niams.nih.gov/news_and_events/spotlight_on_research/2011/child_exercise_bone.asp
  3. Boisseau Nathalie, Delamarche Paul. (2000). Metabolic and Hormonal Responses to Exercise in Children and Adolescents. Sports Medicine 2000 Dec; 30 (6). Pp 405-422.
  4. Riddell Michael C. (2008). The Endocrine Response and Substrate Utilization during exercise in Children and Adolescents. Journal of Applied Physiology . Volume 105. August, 2008. doi:10.1152/japplphysiol.00031.2008. Pp 725-733.
  5. Rogol Alan D, Clark Pamela A, Roemmich James N. (2000). Growth and Pubertal Development in Children and Adolescents: Effects of Diet and Physical Activity. American Journal of Clinical Nutrition. 2000. 72(supp). Pp 521S-8S.
  6. Intensive Training and Sports Specialization in Young Athletes. Committee on Sports Medicine and Fitness. (2000).106 (1):154. American Academy of Pediatrics. ISSN 0031 4005.

Sunday, October 9, 2011

Carbohydrate vs Protein quantity in our Diets, the corresponding Metabolic outcomes in Skeletal Muscle vs Fat Tissue, and the effects on Genetic Expression associated with some Human Pathologies

Is the High Carbohydrate or the High Protein Diet healthier? Time and again, this subject has been debated by health pundits and diet gurus alike. From my vantage point, it appears that individual preferences to that depends largely on one's specific goals and beliefs. Therefore, I wish to point out that in my examination of a much hackneyed subject, my interest pertains solely to two areas. First, I'm curious to know which food compound or combination favors the creation of proportionally leaner body mass. Second, the impact such food compounds might have on causing common pathological conditions and aging.
As it turns out, studies have proven that a higher intake of Carbohydrate compared to Protein, increased cellular activity in Fat tissue, as opposed to Muscle tissue (1). Furthermore, it was evidenced that a proportionally higher consumption of Carbohydrates, seemed to drive those Genes which are linked to diseases such as Inflammation, some Cancers, Dementia, Alzheimer's, Diabetes, much harder. At the same time, reduced Carbohydrate intake appeared to first deactivate a Gene connected with Cardiovascular diseases, and second, to have an effect on another Gene that has been related to the maintenance of youthfulness (2).
At first look, the battle seems to lean in favour of the High Protein Diet, but hang on, does it really? What defines a High Protein Diet? Although it is true that data supports lowering the Carbohydrate content in our diets, that in no way endorses excessive consumption of Protein. It is therefore imperative to note that in the studies referenced, dietary intake of Protein did not exceed 35% of total caloric intake. Also of equal importance to note, is that diets which are dangerously high in Protein might lead to a whole host of health problems as well.
So before we bet our bottom health dollar on either side of this Carbohydrate vs Protein tug of war, let's look at the studies and learn a little more on the workings of these Food Substances on our 1. Muscle and Fat cells; and 2. Gene Expression, where information derived from DNA is translated into materials which are either being used by our cells to perform its functions, or for its own structure.
Metabolic Activity in Muscle vs Fat Tissue, in response to diets which are proportionally different in Carbohydrate and Protein content.
In a joint study between the University of Chicago and the University of Illinois, diets which were lower in Carbohydrates, which comprised of 35% Carbohydrate, 35% Protein, 30% Fats, increased responsiveness of the hormone Insulin, within Muscle tissue. Since Insulin mediates intracellular signaling via its influences on certain enzymes related to protein synthesis, this diet effectively improved metabolic responses in Skeletal Muscle, thereby enhancing the production of Muscle cells.
Conversely, diets which were higher in Carbohydrates, comprising 60% Carbohydrate, 12% Protein, 28% Fats, induced elevated signaling on the same enzymes within Fat tissue, which implies that a diet which is chronically high in Carbohydrate load would create more metabolic activity, increased growth and division of Fat cells.
In short, the diet which was lower in Carbohydrates encouraged growth of Skeletal Muscle whereas the diet with increased Carbohydrates encouraged growth of Fat cells.
Genetic Activity leading to some Pathologies, in response to diets which are proportionally different in Carbohydrate vs Protein content.
Research was conducted at the Norwegian University of Science and Technology to observe how a higher Carbohydrate vs a lower Carbohydrate Diet affected Gene Expression. While one group of participants were fed increased quantity of Carbohydrates in diets consisting 65% Carbohydrates, 15% Protein, 20% Fats; a second group was fed reduced Carbohydrates in diets consisting 35% Carbohydrates, 35% Protein, 30% Fats. Even though the percentage of total Fats in the diets varied, Omega-3 and Omega-6 Fatty Acids were kept constant in both Diets.
In the First Group, it was observed that the Carbohydrate-rich diet triggered activity in our bodies' Inflammatory Genes, as well as a whole group of Disease-related Genes such as Diabetes, Cancer, Alzheimer's. On the other hand, when the second group was fed the Carbohydrate-reduced diet, a Gene that has been linked to causing Cardiovascular diseases, appeared to become inactivated. In addition, the reduced Carbohydrate diet seemed to have a positive effect on what scientists dubbed the "Youth Gene".
It is a well known fact that too much Carbohydrates in our diets will cause a spike in Insulin, which we know to be a hormone responsible for Glucose conversion in the blood stream. But according to the researchers of this study, it is “not as simple as regulation of Blood Sugar". It is in our interest to limit Insulin production because that defense response is indeed Inflammatory. In order to reduce Insulin secretion, it is advisable to control Carbohydrate consumption and to spread our dietary intake equally throughout the day into 5-6 meals.
Results of this study also showed that even a 6-day reduction of Carbohydrate load made a difference in Gene Expression, although the researchers were quick to point out that in order to make any real progress in decreasing our Genes' vulnerability, one would have to make this reduction a permanent feature of our diets.
Conclusion
In managing our diets with the perspective on staying healthy, I think it is most useful to first have the ability to think a little more about how our diets affect our biochemistry and physiology, and then decide for yourself which route you wish to take, rather than following diet fads and propaganda blindly.

I invite you to start looking at food in different light, to understand that the function of food is not limited to the providence of fuel for our bodies. If that was the case, then food would be a straightforward mathematical sum of caloric input vs output. But indeed, that would be oversimplification.
In fact, the broken down components of foods we ingest every day go on to interact with organic molecules in our bodies, setting off biochemical reactions and chains of genetic communication which resonate throughout every cell. These have tremendous impact on our bodily functions, and might eventually translate into disease formation. Although it is far fetched to say that foods can prevent illnesses, it is clear that by picking the right diet, we can at least reduce the likelihood that our genes might be put in disease-causing dispositions.
So what does a healthy diet look like? Well, as you might have guessed by now, the answer varies according to individual health conditions and goals. The truth is that most western diets today are heavily carbohydrate laden (approximately 65% of total caloric intake), hence reduction of Carbohydrates in general will be beneficial. However, I'd like to emphasize that the gist of the matter really lies in keeping our Carbohydrate intake in check, and ensuring the right proportions of Carbohydrates vs Protein vs Fat in our diets as much as possible. It does not mean piling on Protein indiscriminately, nor does it mean cutting Carbohydrates out completely from our diets, for that would be contraindicative, for a spectrum of reasons that merits separate discussion. (Note: Fruit and Vegetables are sources of Carbohydrates too).
Therefore, in light of the latest research, and barring any existing health conditions or special needs, it seems that maintaining the following proportions of 35% Carbohydrates, 35% Protein, 30% Healthy Fats, of our individual total daily recommended caloric intake, in each of the 5-6 meals that are well spread throughout the day, would be the smartest strategy, and that is my safest bet!
Sources:
  1. Devkota Suzanne, Layman Donald K. (2011). Increased Ratio of Dietary Carbohydrate to Protein shifts the focus of Metabolic Signaling from Skeletal Muscle to Adipose. Nutrition and Metabolism 2011, 8:13 doi:10.1186/1743-7075-8-13.
  2. Feed Your Genes. Norwegian University of Science and Technology. (September 19, 2011). Retrieved October 9, 2011 from : http://www.ntnu.edu/news/feed-your-genes

Sunday, September 18, 2011

Hormones, Brain Plasticity, and the Regulation of Metabolism

You may be familiar with Leptin and Ghrelin, and even know them as appetite-regulating hormones. But how do they work to make us raid the fridge at inappropriate times? Contrary to common beliefs, hunger does not always stem from our stomachs, and could all very well be in your head !
This study explains the behavior of such metabolic hormones causing rewiring within the brain’s appetite centre (synaptic plasticity); and hence, the brain's involvement with the physiology of energy regulation.
Understanding informational signaling within the brain, and how such signaling might affect energy balance and metabolism in our bodies.
Neurons are brain cells. They interact by synapsing (information transmitted across the gap between neurons), from the axon (one end) of one neuron to the dendrite (the other end) of an adjacent neuron. Information transmission can occur chemically via neurotransmitters and neuromodulators (molecules which act like messengers between neurons); or electrically (direct contact between two neurons); or by the release of gaseous substances. The specific type of signaling is determined by respective neuronal connections, the availability of receptors for different neurotransmitters, modulators and the various metabolic hormones. 
Our body's changing metabolic state affects the wiring and rewiring of metabolic circuits in the hypothalamus (located at the base of the brain, above the brain stem). Previous studies conducted on non human subjects revealed that short term fasting resulted in strong and quick remodeling of synaptic inputs : first, in key orexigenic (appetite inducing) neurons on the hypothalamus; and second, in the respective interneuronal modulators.
As such, it is a foregone conclusion that the hypothalamus is not hardwired but indeed, is capable of rewiring itself in response to different stimulus and inputs. In the same way, this synaptic plasticity (remodeling of synapses) within the hypothalamus, provides the pathway through which orexigenic (appetite inducing) and anorexigenic (appetite reducing) hormones such as Leptin, Ghrelin as well as Estradial (a form of estrogen), act to mediate energy homeostasis i.e. balance, and metabolism.
How is Leptin linked to metabolism?
There is a strong relationship between Leptin and Metabolism. Leptin is an anorexigenic (appetite reducing) hormone and modulates energy balance via its regulatory effects on neurons Neuropeptide Y (NPY), Proopiomelacortin (POMC), and Orexin. Here is what happens.
First, it was observed that lowered levels of Leptin during periods of fasting coincided with rapid rearrangements of synapses within the appetite centre of the brain. Second, Leptin has a suppressive effect on the functions of neurons Neuropeptide Y (NPY) and Orexin, thereby diminishing their ability to secrete Leptin receptors. Since receptors are imperative to the function of hormones, a change in the levels of Leptin receptors will in turn have adverse effects on the proper mechanism of the Leptin hormone.
Third, Leptin modulates feeding patterns via its effects on NPY and POMC. First, it is important to know that increased activity in NPY, and reduced activity in POMC, encourages feeding and fat conservation. Conversely, the reverse in activity of such neurons discourages eating and promotes lean body mass. Studies have shown lowered levels of Leptin to cause an increase in NPY and a corresponding decrease of POMC, consequently heightening hunger and weight gain. Thus, when Leptin was replaced in Leptin-deficient mice, their food intake decreased dramatically and triggered weight loss.
How does Ghrelin factor in?
Ghrelin is an orexigenic (appetite inducing) hormone; and hence, has the opposite effect that Leptin has on our appetite centres. While overnight food deprivation suppresses Leptin secretion, the same would induce an increase in levels of Ghrelin, triggering more synaptic current and rewiring of the appetite-regulating neurons of the brain.
It is also interesting to note that Ghrelin has been found to have the ability to bind to neurons which govern spatial learning and memory function. In this way, Ghrelin might be the linking pin between metabolism and the higher learning capabilities of the brain.
One Final Word.
Certainly, it is important to acknowledge that daily fluctuations of levels of these hunger- regulating hormones are intrinsic to us and are very vital to our survival. However, comprehension of the physiology of hunger signaling and energy metabolism underscores the importance of maintaining our body’s hormonal balance in areas where managing eating behaviours, and on a larger scale, weight management are concerned. 
Furthermore, it is my opinion that a well modulated hormonal state can bring us benefits that extend beyond eating patterns, such as emotional equilibrium; and that such a state might be be achieved through the influences of lifestyle choices, sufficient sleep, diet, exercise etc.
Source:
Horvath, Tamas L (2006). Synaptic Plasticity in Energy Balance Regulation. Obesity. Aug 2006. Vol 14. pp 228S-232S.

Friday, June 17, 2011

The Senobi Breathing Exercise helps Weight Loss in the Obese.

A proportionally more active parasympathetic system (commonly known as the rest and digest system) in comparison with the sympathetic system (commonly known as the flight or fight system), in addition to blunted secretion of various hormones, are well recognised as traits of overweight people. In a joint study conducted by Niigata University School of Medicine, and Niigata University Graduate School of Medical and Dental Sciences, the effectiveness of the Senobi Breathing Method as a means of creating weight loss, by revitalising the sympathetic system, was being tested and confirmed.
Developed by the researchers of this study, the Senobi Breathing method encompasses stretching and breathing, and is based on a customary stretch done in Japan during ancient times. Performing this exercise requires little resources as it only involves tiring one's hands, arms and shoulders by keeping them in raised positions, stretching the muscles on one’s neck as well as the back. In spite of its apparent simplicity, this breathing and stretching method proved to be effective in creating weight loss in the overweight.
What does Senobi Breathing do for our bodies in terms of weight loss?
In order to understand the physiological mechanisms of the Senobi Breathing Method, we must first know that poor postural alignment leads to extremely low basal metabolism in our bodies. Brown fat cells which are located on our erector spinae muscle (a deep muscle which runs along our spine) play an important role in fat combustion. Performance of the Senobi Breathing Method increases the skin temperature of this area, activating the brown fat cells located there, and hence, enhances fat combustion. Moreover, abdominal and thoracic (mid back) respiration, both which are elemental in the Senobi Breathing Method, have been previously proven to be instrumental in weight loss.
Who participated in this experiment?
A total of 40 pre-menopausal women aged 40 to 50 years were studied. 20 of them were of healthy weight whereas the other 20 were overweight (Overweight being defined as having a body mass index higher than 25 and body fat higher than 30%).
How do we perform Senobi Breathing?
This breathing method can be done either standing or sitting. 
In the standing position with one's feet placed hip width apart, the arms should be extended firmly towards the sky and shoulder width apart, with the palms facing each other. The neck and back are arched backwards such that one's chest points in the direction of the sky.
(Bittergourd Note: Draw abdomen in towards the spine in order to provide lower back support and avoid overexertion. It is also recommended that the exerciser keeps a slight bent in the knees). 
Holding the above position, perform 1 cycle of breathing, which includes 5 seconds of inhale followed by 5 seconds of exhale. Then repeat this breathing cycle 2 more times. This posture causes the scapulas (shoulder blades) to close, which allows for abdominal breathing. 
Following abdominal breathing, proceed with thoracic breathing. To facilitate thoracic breathing, assume all positions described in abdominal breathing except for a change in the arm positions. While lifting the arms above one’s head, intertwine fingers and turn the palms so that they face the sky. This action allows the scapulas to open, which in turn facilitates thoracic breathing. This breathing should also be completed for 3 cycles.
Both abdominal as well as thoracic breathing described above can also be performed while seated with the feet firmly planted on the floor, hip width apart. Perform both abdominal and thoracic breathing 3 times daily, as was the case in the experiment.
Outcome of the Experiment.
Measurement of autonomic nerve activity (parasympathetic vs sympathetic nerves) was done by a machine called the Body Checker Analyzer. In healthy women, there was no change in level of sympathetic activity before and after practicing the Senobi Breathing Method. However, results of overweight women showed significant increases in the level of sympathetic activity after only 1 minute of Senobi breathing.
Measurements of the concentration of hormones such as noradrenaline, estradiol as well as growth hormones were also taken from samples of urine. Little, or no change, on the levels of all hormones were observed in the healthy women group. On the other hand, significant increases in all 3 hormones were observed in the overweight women group.
After one month of performing Senobi breathing 3 times daily, significant weight loss was observed ONLY in the overweight women group.
Summary of the physiological changes and their implications on weight loss as a result of the performance of the Senobi Breathing Method.
  1. Revitalised sympathetic nervous system in overweight women as a result of leptin's signaling action on the Central Nervous System. Leptin is a major hormone involved in the regulation of hunger.
  2. Increased secretion of noradrenaline. First, noradrenaline plays a significant role in our feeding behaviour and has been proposed as a contributing neurotransmitter of the sympathetic nervous system. Second, noradrenaline increases fat burning and reduces visceral fat. After performance of the Senobi Breathing Method, levels of noradrenaline in overweight women were restored, and even exceeded that of the healthy women.
  3. Increased secretion of estradiol. Estradiol is a form of estrogen. Studies have shown decreased estrogen, together with decreased ovarian function, leads to obesity. Hence, increased estradiol levels in overweight women will encourage weight loss.
  4. Increased secretion of growth hormones. Abdominal adiposity is inversely related to the production of growth hormones in our bodies. In addition, studies have proven that growth hormones reduces visceral fat and low density lipoprotein (LDL) cholesterol in obese women. In this study, the overweight women showed an increase in growth hormones after performance of Senobi Breathing.
Finally, a word of caution. Before embarking on any of the exercises, it is best to check with your doctor to ensure suitability.


Source:
1. Sato, Kazunari., Kawamura, Toshihiko., Yamagiwa, Satoshi. (2010). The Senobi Breathing Exercise is recommended as first line treatment for Obesity. Niigata University School of Medicine, Niigata University Graduate School of Medical and Dental Sciences. Biomedical Research 31 (4). Pp 259-262.


Sunday, May 15, 2011

Research shows Iyengar Yoga's potential Therapeutic Effects on Major Diseases and Skin Aging through its ability to curtail Inflammation [Revised Version 2]

Prelude.
This is the year 2011. Regardless of whether you do yoga or not, I hope by now you'd know, at a bare minimum, that it benefits our health at some level. But, how many of us (including yoga aficionados like yours truly) can honestly say we understand the mechanisms of yoga's positive effects on our bodies? I chose this topic because I realized that, as an advocate for yoga, I've been intellectually lazy and hypocritical, to preach the health benefits of yoga, armed with only a vague understanding of the underlying biomechanisms. 
In this era, where education, abundant information and savvy consumerism rule, it's simply not enough to settle for vague ideas. I needed to see the hard science and tangible proof for what I believe. I trust that all of you, my smart friends, also aspire for the same clarity. Not only in matters relating to yoga, but to be diligent in all areas pertaining to your health.
Of course, even for the most educated amongst us, it's impossible to know everything. But what is more important than focusing on making the right decision every time, is to try and go in with your eyes wide open, instead of blindly following exercise trends that are being mass marketed by the fitness industry. It further aggravates me to see equally mindless trappings being popularized by some within the yoga circle. Indeed, it's important to recognize that not all yoga methods are created equal, and be able to discern among them. If you merely go along unthinkingly with popular herding instincts, you will likely end up with the same diseases and imbalances that are plaguing the common herd today. 
I'm not interested in promoting paranoia or intellectual pomposity. But somewhere between one extreme of obsessive research and excessive intellectualizing, and the other extreme of total apathy and disregard for hard facts, I'm sure we can strike the balance to make logical, reasonable and well-thought decisions when picking the best for our bodies. Remember : Health is wealth, so don't take it lightly!
Overview of Iyengar yoga's potential therapeutic effects on the human body.
In a study conducted at Ohio State University College of Medicine, entitled "Stress, Inflammation, and Yoga Practice" (1), regular and long term practice of Iyengar yoga was found to significantly reduce and control stress-induced inflammatory reactions in the human body. 
Chronic Inflammation has been intricately linked to many major illnesses such as cardiovascular diseases, type 2 diabetes, arthritis, osteoporosis, Alzheimer's disease, periodontal diseases, obesity, age related decline in bodily functions, as well as skin aging. Hence, the ability of Iyengar yoga in suppressing such inflammation may ultimately lead us to greatly improved health and youthful vitality.
What is chronic inflammation and its roles in diseases and skin aging?
Touted as the new poster child in health sciences today, chronic inflammation has been tightly connected with a multitude of diseases that are afflicting us in modern times. Essentially, inflammation is our bodies' response to infection, whereby defense cells move from our blood stream into invaded tissue to fight perceived threats to our bodies. Chronic inflammation is a low grade but persistent kind of inflammation.
As explained in a joint study “Interleukin-6 and Chronic Inflammation” between the University Hospital of Geneva and University of Geneva School of Medicine, this defense mechanism triggers the secretion of Cytokines, which are protein molecules involved in the communication between our cells, setting the stage for inflammation (2). Interleukin (IL)-6 is one such important cytokine being released in the process, and plays a protective role when secreted in short bursts and at limited levels during the acute phase of inflammation. However, As IL-6 production continues in a persistent and constant manner, acute inflammation soon transforms into chronic inflammation, turning IL-6 into highly detrimental proinflammatory factors (2).
Increased levels of IL-6 during chronic inflammation, has been consistently associated with cardiovascular diseases, osteoporosis, dementia, Alzheimer's, type 2 diabetes, Arthritis and cancer (2). In a separate study completed at Hallym University in Korea, it was also reported that elevated levels of ultraviolet-induced IL-6 caused inflammation in our skin cells and damaged the integrity of the skin matrix. Without a firm network, collagen and elastin fibers in our skin tissue begin to breakdown, eventually resulting in skin aging and the formation of wrinkles (3). 

Why specifically Iyengar yoga and not other forms of yoga? 
At this point, it is pertinent to emphasize that in this particular research study, the only form of yoga examined was the Iyengar method. Therefore, only the health benefits of Iyengar yoga, and not other forms of yoga, can be concluded from this study. In the report, Iyengar yoga was described as a form of Hatha yoga, which "combines body postures, or asanas, breath control or pranayama, and meditation." 
The report also states that Iyengar yoga was specifically chosen for the study because this practice "emphasizes the use of props to help students achieve precise postures safely and comfortably according to their body types and needs." Furthermore, inflammation in our bodies could result from even modest amounts of psychological stressors, anxiety and depression. Hence, Iyengar yoga was favored because "a restorative session was selected rather than a vigorous sequence in order to promote recovery from stressors."
What is Iyengar yoga?
Iyengar yoga is characterized by certain distinguishing features. First, there is strong focus on precise and correct anatomical alignment. Second, the prominent use of props in supported postures encourages relaxation in our muscle fibers, and hence lessen their tendency to resist stretching. Third, postures are sequenced in a certain manner to enhance cumulative therapeutic effects. Fourth, the concept of holding each posture longer creates deeper penetration of beneficial effects while at the same time, builds strength, endurance, and continuous refinement of the postures.
According to B.K.S. Iyengar (founder of Iyengar yoga), in Light on the Yoga Sutras of Patanjali (4), one of the many cornerstones of yoga is that the practitioner "knows his body and its orderly functions" and "possesses an excellent body with grace, strength, perfect complexion and lustre". It is therefore plain to see that good health and great skin were indeed one of the many original intents of yoga as envisioned by Mr. Iyengar.
Perhaps it should not be surprising to find immense health benefits from the practice of Iyengar yoga, although it is indeed gratifying and reassuring to learn the scientific explanation and see supportive evidence for it. 
Not only is this form of yoga grounded in technical precision and biomechanics, it also embodies philosophy and the beauty of human art form. Hence, it is an all-rounded practice requiring full engagement of the intellect as well as the physicality. To quote Mr. Iyengar : "When I practice, I am a philosopher; When I teach, I am a scientist; when I demonstrate, I am an artist."(5)


Who were the subjects?

Inflammatory changes in "experts" as well as "novices" of yoga were compared and contrasted. For the purposes of this study, long term practitioners, described as "experts" were those who practiced at least 1-2 times per week (each session lasting 75-90 mins), for a total of at least 2 years, and at least 2 times per week for the past year. "Novices" were defined as those who either attended yoga classes, or had a home practice with videos, for a total of 6-12 sessions.


The subjects were controlled for immunological or endocrinological health conditions and were taking medication; and also those with medical conditions impacting such systems e.g. cancer, recent surgeries, diabetes etc. Additionally, smokers, those taking statin, beta blockers, psychoactive drugs, excessive alcohol users, those with convulsive disorders, as well as those with BMI above or equal to 30, were also excluded from the study.

Brief report on the results of the study.
Levels of cytokine IL-6 production were first measured from blood samples taken from both novice and expert groups following the administration of designated stressors on the subjects, but before the subjects underwent the yoga sessions. Results showed major differences between the 2 groups.
In novices’ blood samples, average IL-6 levels were 41% higher than the experts’. In addition, the chances of detecting C-reactive proteins in a novice’s blood stream were 4.75 times higher than detecting similar from an expert’s. C-reactive proteins are influenced by rising IL-6 levels, and released by fat cells during the occurrence of an inflammation.
Across the board, 60% of novices in the group were found to produce high levels of IL-6 cytokines whereas only 24% of experts in the group were found to be high producers. On the other hand, 40% of the experts were classified as low producers of IL-6 compared with 0% of novices who were low producers of IL-6.
Post yoga sessions, both novices’ and experts’ blood IL-6 levels were again measured, and compared with their individual baseline measurement taken before the yoga session. This time, no substantial comparative differences appeared from their individual baseline IL-6 measurements. 
Although at first sight, these results seem contradictory but in fact, they hold one very important implication : that a single short term session of yoga will not suffice to affect the status quo of IL-6 production within our bodies. However, a regular and long term practice of yoga will indeed make significant headways in creating beneficial changes to the inflammatory production of IL-6 in our bodies.
Conclusion.
Yoga, when practiced correctly, can bring significantly positive changes to our minds and bodies. Unfortunately, it is a common misconception that yoga is simply stretching to the outer limits of our flexibility, working up buckets of sweat, or twisting ourselves into positions that are purely idealization by popular media. In fact, simply jamming our bodies and joints by brute force into positions for which we are ill prepared, is contraindicative and highly injurious to our bodies.
Iyengar yoga is a sophisticated system, designed with a strong emphasis on alignment and the use of props, to sequentially prepare and lead the practitioner safely up to advanced postures that are within the practitioner's capabilities and anatomical limitations. Iyengar yoga does not approve of contorting our bodies to fit prescribed shapes at all costs. On the contrary, it is only when postures have been modified to fit our unique selves, our evolving development and our ever changing needs, that they will bring us the greatest gains!
As such, Iyengar yoga promotes better structural alignment; evens out muscular imbalances; increases flexibility, strength, endurance, stability and grace. Additionally, it instils a sense of proprioception in the practitioner, i.e. improving body awareness and neurological control over our muscles, joints etc., all of which are important yet often overlooked factors in the maintenance of health, especially as we age. Going even further, Iyengar yoga's ability to limit inflammation makes it an excellent alternative and complementary accessory in the treatment and prevention of many modern afflictions and aging. 
I am not against the use of pharmaceuticals and cosmetics. They are definitely a permanent fixture in today's context that is useful to have; and in many cases, they are a requisite for basic sustenance of modern life. That said, I feel there is generally an over reliance and excessive use of such materials presently. On top of that, way too little emphasis have been placed on preventative measures upfront. It has become the norm to think we can solve all our health and aging problems simply by popping pills or slathering "miracle creams" on our faces. Unfortunately, these merely serve to treat some symptoms, but fail to address the causation in most cases.
Moreover, in doing so, we overlook the fact that the human body is a highly intelligent, albeit complex, system that has a huge capacity to fine tune itself if only we would give it a chance, by creating the right conditions for it to flaunt its inherent talent. Science has now shown us one way towards creating a favourable condition under which our bodies  can flourish. Obviously, practicing Iyengar yoga alone won't prevent or cure all diseases, but incorporating it into our lives might put us in prime positions to receive bountiful health and radiant skin in the long run!
Sources:
  1. Kiecolt-Glaser, Janice K, Ph.D., Christian, Lisa, Ph.D., Preston, Heather, B.A., Houts, Carrie R., M.S., Malarkey, William B., M.D., Emery, Charles F., Ph.D., Glasser, Ronald, Ph.D. (2010). Stress, Inflammation, and Yoga Practice. The Ohio State University, Columbus, Ohio. Psychosom Med. 2010 February; 72(2): 113. doi: 10.1097/PSY.0b013e3181cb9377.
  2. Gabay, Cem. (2008). Interleukin-6 and Chronic Inflammation. University Hospital of Geneva and University of Geneva School of Medicine, Switzerland. Biomed Central Ltd. Arthritis Research and Therapy 2006. 8(Supp 2): S3 (doi:10.1186/ar1917).
  3. Bae, Ji-Young., Choi, Jung-Suk., Kang, Sang-Wook. (2009). Dietary compound ellagic acid alleviates skin wrinkle and inlfammation induced by UV-B irradiation. Hallym University, Chuncheon, Korea. 2010 John Wiley & Sons A/S. Experimental Dermatology. 19, Pp182-190.
  4. B.K.S. Iyengar. (2002) Light on the Yoga Sutras of Patanjali. 2002 Edition. Thorsons. Harper Collins Publishers. London, U.K. Pp 37.
  5. The Official Website, B.K.S. Iyengar. Ramamani Iyengar Memorial Yoga Institute. Pune, India. Retrieved 2011, 14 May from http://www.bksiyengar.com/default.asp

Monday, May 2, 2011

How Food, Sex & Drugs all share the same Neurochemical Pathways

What is your perception of a food addict? For most, it would conjure images of an ill disciplined glutton, perhaps even someone irresponsible and obese. What if the truth is that the individual does not have control over their decision to eat; that the compulsion to eat is driven by the biochemistry of their brain? Would that knowledge make us more empathetic in terms of eating disorders? Probably so. As someone who is passionate in learning about nutrition, I see it as my duty to understand the drivers of eating disorders, including compulsive eating and food addiction. Science has provided some answers to what I suspected - that compulsive eating is not simply a behavioral problem but in many cases, is indeed a behavior driven by problematic physiological mechanisms.
I chanced upon the article "Curb Compulsive Eating Naturally", published in a free magazine Life Extension (1), which expounds that the same neurochemical mechanism that pushes people to eat uncontrollably are the same ones which drive people to drug addiction. The article goes further to explore the power of saffron in combatting this problem. But for the sake of brevity, I shall focus on the mechanisms of the neurotransmitters dopamine and serotonin, pertaining specifically to compulsive eating and food addiction.
According to a study done in 2010 by Johnson PM and Kenny PJ (2), the similarity between drug and food addiction lies in the reaction of dopamine receptor D2. Dopamine is released by pleasurable experiences such as food, sex and drugs. Consumption of drugs blocks dopamine retrieval thereby flooding brain with the neurotransmitter, and overstimulating receptors. Over time, the brain adapts by decreasing activity. However, the need for constant stimulation will draw people to consume more drugs, creating a vicious cycle. In the same way, consumption of excessive or junk food drives food addicts into compulsive eating.
Although this is the first time parallels have been drawn between drug and food addiction, the relationship between food and release of dopamine is a well established one. In an earlier study in 2002 by scientists at Brookhaven National Laboratory (3), it has been determined that the mere sight and smell of food spikes levels of dopamine. Even more interesting is the fact that obese subjects had elevated levels of dopamine but decreased levels of dopamine receptors.
While researching for serotonin's role in regulating the psychiatric nature of compulsive eating, I came across a study by Kaye, Walter in 2008 (4) which showed how disruptions to 5 H-T functions upsets emotional and reward pathways which also mediates feeding, hence exposing individuals to the possibility of disturbed eating behaviors, known as emotional eating or worse, compulsive eating. Additionally, in 1992,  Blundell, J (5) had proven serotonin's central role in modulating feeding behavior lies in how nutritional information is being transcribed onto 5 H-T systems and also, in the distribution of 5 H-T neurons in the brain at locations known to be crucial for feeding. Based on these findings, the researchers showed how manipulation of serotonin could cause changes in feeding behavior.
This proves that our feeding behaviors can hardly be viewed in isolation from our psychiatric and physiological makeup. It is indeed heartening to learn that by targeting the neurochemistry of compulsive eating, which is the root of the problem, we might be in a better position to help food addicts, or at the very least, have more empathy for their predicament.
Sources:
1. Goepp, Julius. (2010). Curb Compulsive Eating Naturally. Life Ext. Sept-Oct 2010:29-35

2. Johnson PM, Kenny PJ. Scripps Research Institute (2010, March 29). Compulsive eating shares addictive biochemical mechanism with cocaine, heroin abuse, study shows. ScienceDaily. Retrieved September 23, 2010, from http://www.sciencedaily.com /releases/2010/03/100328170243.

3.  New Addiction Link Found. U.S. Dept of Energy Research News. (2002, June 3) Retrieved September 23, 2010 from http://www.eurekalert.org/features/doe/2002-06/dnl-nfl061302.php

4.  Kaye, W. (2008) Neurobiology of Anorexia and Bulimia Nervosa. Physiol Behav. 94(1): 121–135

5.  Blundell, J. (1992) Serotonin and the biology of feeding. The American Journal of Clinical Nutrition. 55 (1 Supp): 156S-157S

Sunday, April 24, 2011

A study on food components which target the regulation of inflammatory disorders induced by obesity [Revised version of original posting on April 10, 2011]




In a recent study which was published in “Mediators of Inflammation” (1), scientists reported that obesity is associated with a silent yet constantly ongoing inflammation of the body. Generally, we perceive inflammation to be characterized by some form of physical expression such as swelling, itching, the production of heat, pain, redness, or some manifestation which can be seen or felt. But inflammation in our bodies is, in fact, any reactionary response to offensive triggering factor/s; & such inflammation may not even be detectable by our senses! This latter form of inflammation, which best describes the type which besieges an obese individual, is unapparent to us because it occurs at a cellular level (more on that later).
Technically defined as having a BMI of 30 or above, obesity is known to induce the silent inflammation described above & consequently, may have serious & adverse effects on our healths. Obesity-induced inflammation which occurs in fat tissue, has been proven to lead to a host of diseases that plague us today including insulin resistance, type 2 diabetes, heart diseases & immune disorders. Fortunately, some food components have been discovered to have combative abilities against such inflammation. Let's look at the process of inflammation in greater detail, & how food components act to control it.
What causes inflammation in fatty tissue?
Before we delve further, it is important that you understand that these inflammatory responses take place at individual cellular levels within our fatty tissue. To give you a clearer idea - if you think of the spare tire around your belly {BG's comment: oh you know THAT spare tire}, that ream of fatty tissue is made up of hundreds, thousands or even {BG's comment: heaven forbid!} millions of individual fat cells. 
The onset of inflammation at the site of an individual fat cell happens as a result of interaction between 2 major players : Macrophages & MCP-1. Macrophages are a type of immune cells within our blood stream & MCP-1 is a substance found to be residing in the individual fat cell. The interaction between these 2 players, & hence inflammation, is described below.
First of all, MCP-1 induces macrophage infiltration from our blood stream into the individual fat cells. Post macrophage infiltration into the fat cell, MCP-1 is also responsible for activating these macrophages to release inflammatory mediators (substances that create inflammation). When released, inflammatory mediators will affect insulin signaling & at the same time, act to increase the production of fatty acids (in particular, harmful saturated fatty acids) within the fat cell. Elevated levels of saturated fatty acids will, in turn, influence our genes to express pro-inflammatory factors that encourage even further inflammatory responses. In this manner, macrophages & MCP-1 interact at the sites of individual fat cells to create a vicious cycle of inflammation within our bodies.
Therefore, it is not surprising to learn that macrophage infiltration is found to be prominent in fat tissue and correlates positively with BMI, fat tissue size as well as total amount of overall body fat in an individual. The presence of MCP-1 is also known to be significantly higher in the obese individual. 
How do food components act to control inflammation?
Food components act by targeting various master regulators of inflammatory gene expression, thereby inhibiting the release of various inflammatory mediators. 
Master regulators of inflammatory gene expression include firstly, NF-kB & JNK, both of which are important transcription factors i.e. proteins involved in the flow of genetic information; and secondly, PPARy, which is a protein that acts as a receptor for other molecules to bind on to. Food components control mediators of inflammation either by acting to directly influence NF-kB & JNK (PPARy-independent) or indirectly via PPARy (PPARy-dependent).
Therefore, in a PPARy-independent situation, food components act on NF-kB & JNK to suppress mediators of inflammation by direct interference of the flow of genetic information, which in turn results in interruption of the genetic signaling pathways necessary for the inflammatory gene expression.
On the other hand, in a PPARy-dependent scenario, food components work hand in hand with PPARy to exert an anti inflammatory effect. PPARy acts as the lock in a "Lock and Key system" which certain food components can latch onto. This locking action then sets off a chain of molecular mechanisms in the cell, which interferes with the signaling pathways of inflammatory gene expression resulting in suppressed production of inflammatory mediators.
Phew! Now that the hard part is over, here is the good news! So which food components regulate inflammation? As explained, food components can work either dependent or independent of PPARy.
PPARy-dependent food components:

Compound
Origin
Actions
Abietic Acid
Pine - in rosin fraction of species such as grand fir, lodgepole pine.
Suppress proinflammatory mediators; increase adiponection (hormone which regulates fat metabolism); act with PPARy to mitigate inflammation.
Auraptene
Citrus Fruits - mainly in peel.
regulate flow of information in genes targeted by PPARy; increase adiponectin secretion; decrease proinflammatory mediators; promote glucose uptake.
Capsaicin
Hot Pepper
induce thermogenisis & fat oxidation; decreases secretion of inflammatory mediators, increases expression of adiponectin; suppresses macrophage migration and activation, improves insulin resistance.
Dehydroabietic Acid
Pine Rosin
PPARy agonist - binds to & acts like PPARy.
Isohumulone
Hummulus Lupulus
PPARy agonist.
Isoprenoid
Herbs
anti-tumor proliferation, anti-diabetes, controls cholesterol.
Resveratrol
Red Wine (dont u love this)
PPARy agonist.
6-Shogaol
Ginger
Acts with PPARy to increase production of adiponectin.
PPARy-independent food components:

Compound
Origin
Actions
Anthocyanin
Red/Purplish Fruit such as grapes, blueberries; apples; beans.
Anti-oxidant; inhibition of inflammatory mediators.
Diosgenin
Fenugreek; wild yam.
Suppress inflammatory mediators induced by interaction between fat cells & macrophages.
6-Gingerol
Ginger
increase adiponectin, a hormone which regulates fat metabolism.
Luteolin
Medicinal plants; some vegetables & fruits.
Anti-oxidant; anti-inflammatory; anti-allergy; inhibit JNK activity in macrophages.
Naringenin
Citrus fruits
Inhibit inflammation caused by interaction between fat cells & macrophages.
Naringenin Chalcone
Tomato peel
same effect as Naringenin, only more significant.
Polyunsaturated Fatty  Acids
Fish Oil
Anti-obesity; anti-inflammatory factors. However, requires cofactors such as folic acid, vitamins, minerals, L-arginine (a protein) for anti-inflammatory actions.
Conclusion:
By learning how compounds derived from food sources regulate inflammation in fat cells, we may have seeded various new & natural avenues to managing inflammatory related diseases caused by obesity, such as diabetes & cardiovascular diseases.
In the same vein, another recent study published in the Journal of Obesity, "Anti-Inflammatory Nutrition as a Pharmalogical Approach to treat Obesity" (2), the researchers have also concluded that a food based anti-inflammatory approach, which targets & suppresses inflammation in our bodies, could be used in conjunction with conventional drugs to enhance the treatment of obesity.
In view of the rising socio-economic costs of waging an uphill fight against epidemic obesity & related diseases, these studies bring renewed hopes for a more holistic, cheaper & hopefully, more effective solution for containing the spiraling situation
Sources: 
(1)Shizuka Hirai, Nobuyuki Takahashi, Tsuyoshi Goto, Shan Lin, Taku Uemura, Rina Yu, Teruo Kawada (March, 2010). Functional Food Targeting the Regulation of Obesity-Induced Inflammatory Responses and Pathologies. Mediators of Inflammation. Hidawi Publishing Corporation. Vol 2010; Article 367838.
(2) Barry Sears, Camillo Ricordi (May, 2010). Anti-Inflammatory Nutrition as a Pharmalogical Approach to Treat Obesity. Journal 0f Obesity. Hidawi Publishing Corporation. Vol 2011; Article 431985.