LAUGH YOUR STRESS AWAY

It seems like everyone I know complains about their stress level. Currently, it is the financial crisis that is stressing everyone out. But before that it was something else. The truth of the matter is there will always be stressors in our modern life. The question is: how are you dealing with them?

Stress management—as we all know—is the name of the game. We cannot afford to allow stress to overwhelm us. Stress is much more than just an annoyance—stress is deadly. That’s right. It causes a whole host of health problems. In fact, it is estimated that stress leads to a whopping 75%-90% of all doctor visits! Translated into costs associated with health care, it means thousands of dollars every years.

This sounds ridiculous that stress could do such harm but it really does. And here’s why: when you are stressed, your body believes there is a crisis and so your endocrine system releases stress hormones such as cortisol, GH and norepinephrine. For short periods, these hormones are fine but for longer periods—like perpetual stress—it can cause the following problems:

• Stomachaches, diarrhea and other digestive problems

• An increase in appetite, which may lead to weight gain

• Lowered immune function, making you vulnerable to every little bug going around

• Depression, which may lead to sleep problems, loss of sex drive and loss of appetite

• Increased heart rate, blood pressure and cholesterol levels, which can lead to a greater risk of heart disease and stroke

• Increased chronic health problems such as skin conditions, asthma, or autoimmune diseases such as lupus

• Possible increased risk of developing cancer (Studies done over the past 30 years that examined the relationship between psychological factors, including stress, and cancer risk have produced conflicting results. Although the results of some studies have indicated a link between various psychological factors and an increased risk of developing cancer, a direct cause-and-effect relationship has not been proven .)

Is it worth it? Do you really want to allow your stressful lifestyle to rob you of your health? Clearly, stress MUST be managed. But how?

There are many effective stress management tools available but laughter yoga is my favorite. It is a unique and simple system that helps to reduce both physical and emotional stress through laughter “exercises” and gentle yoga breathing. It enables the mind and body get relief at the same time. And yes, it has been scientifically proven.

Dr. Lee Berk—associate director for the Center for Neuroimmunology, assistant research professor in the Loma Linda University School of Medicine, and assistant clinical professor of health promotion and education in the School of Public Health—started researching the benefits of laughter back in the late 1970s. Once he found some positive results, he and his colleague Stanley Tan, MD, assistant professor of medicine at Loma Linda University, started to look further into the miracle drug of laughter.

So they extended a research invitation to William Fry, MD, then a psychiatrist at Stanford University, who had researched changes in blood pressure and heart rate related to laughter.

“Having the new tools in medicine to look at some of these stress hormones, we said [to Dr. Fry], ‘Fly down, bring your Laurel and Hardy tapes, let’s sit down, we’ll place an IV in your arm and we’ll draw continuous blood samples while you’re watching the tapes,’” Dr. Berk says.

Dr. Fry accepted the invitation.

“That was the initiation of everything,” Dr. Berk adds. “We looked at the data and we fell on the floor. It was mind-blowing.”

Since that time Drs. Berk and Tan have conducted controlled scientific experiments that have proven those early results that laughter does indeed lower stress hormones and give the immune system a boost among other things. Now these scientists who study laughter are known as gelotologists and they keep finding more exciting things about how laughter can help boost health.

So don’t let stress get the best of you, practice laughter yoga. Laugh, breathe, connect with others and reap the amazing benefits. Cultivate a joy that lasts despite the stressors you face. You’ll be glad you did. ha ha ha ha ha!

(NOTE: Start laughing more today by subscribing to this blog if you haven’t already. The subscription is absolutely free and you’ll also get 100 laughter yoga exercises to get you chuckling.)

Is Hypoglycemia Obesogenic? Is the GI Totally Worthless? Is Mild, But Chronic Stress Behind the Diabesity Pandemic? Is Leptin Obesogenic? And How Do You Calculate the Energy Requirements of Diabetics?

One of the mistakes researchers and dieters make time and again, using the scale as their only guide

Since I had a couple of interesting, but not earth-shatteringly exciting studies on obesity, body weight gain, the GI, leptin and a couple of other things lying around, I thought I’d compile a brief potpourri for you to get you on par with the helplessness with which researchers are still facing the diabesity pandemic. So don’t expect any of the one-size-fits-it-all solutions the scientists still appear to be looking for from any of the following items. What you may find, however, is some inspiration when you read between the lines or follow up on the suggested reads, I mention. And if that’s not the case, you can still browse previous articles on fat loss or simply go to the gym and try the fat loss example routine from the SuppVersity “Step By Step Guide for Your Own Workout Routine” or simply go to be early to preserve your circadian rhythm.

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  Going “Hypo” time and again will make you fat (McNay. 2012) — Usually you think of hyogylcemia as a sign of a lack of energy, yet despite the fact that this may well be the case this very lack in energy has recently been shown to exert obesogenic effects in a rodent model.
  
  
  
  
  
  
  
  

  

  Often a picture says more than 1000 words: Normal (left) and repeatedly hypoglycemic rodents after 8 months of weekly insulin injections (McNay. 2012)

  
  

  The weekly injections Ewan C McNay and his colleagues administered to their rodents and the subsequent episodes of hypoglycemia lead to profound weight gain in the absence of diabetes, hyperphagia, changes in hypothalamic NPY or POMC mRNA expression and  the other usual suspects that could explain this phenomenon. The one thing that’s left is therefore what the researchers call a “multi-faceted deficit in metabolic regulation” (McNay. 2012) – interestingly enough the 69.5% higher body weight at 12 months went hand in hand with the usual laziness (-25% activity) of people whose brains are starving in abundance (e.g. type II diabetics).
  

  
  

  What remains to be seen, though, is whether similar effects would occur in response to “regular” non-insulin induced hypoglycemia. In view of the easy with which crash dieters and people with roller-coaster blood glucose levels gain weight, it is yet not unlikely that it is actually the avoidance of (reactive) hypoglycemia and not so so much the prevention of hyperglycemia that makes low GI diets successful for weight maintenance (for weight loss the picture is more complicated, since this will require a energy deficit and that’s a game changer).

  
  

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  Dietary glycemic index and load are not associated with type II diabetes risk in 12,403 Europeans (Sluijs. 2012) — Apropos GI, scientists from the University Medical Center in Utrecht did not find statistical significant correlations dietary glycemic index and/or glycemic load and the risk to develop type II diabetes in in a subcohort of the European Prospective Investigation into Cancer and Nutrition Study (n = 12,403 participants).
  

  Even when they compared participants in the highest and lowest quantiles, the increase in risk was only 5% and 7% for GI and GL respectively. Since this is by no means the first study that suggests that the still propagated concept of the beneficial health effects “low GI diets” is faulty, I would suggest you rather watch the actual food items, than their respective glycemic indexes if you intend to ward off obesity and diabetes. Potatoes for example may have a high GI (including sweet potatoes, by the way), but their high potassium and overall mineral content, as well as the mere fact that you can hardly eat the same amount of total carbohydrates you can easily annihilate, when you are eating pasta still makes them one of the best sources of starchy carbs you have (learn more in the Potato Manifesto, Part I & II).

  
  

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  Figure 1: There were no statistically significant difference in terms of weight gain or loss, but the 2-week re-feed had a greater impact on blood glucose and insulin levels in the high GI group (Lagerpusch. 2012)

  
  

  There is use for the GI on a bulk or after a diet, but only if you are concerned about insulin sensitivity (Lagerpusch. 2012) — While the general value of the GI as a means to distinguish good from bad carbohydrate sources is certainly questionable, the recently published results from a study that was conducted at the Institute of Human Nutrition and Food Science, of the -Albrechts University in Kiel, Germany, does suggest that monitoring the GI of your diet and adding additional fiber to reduce the insulin response to your meals can come quite handy, in phases, where you are particularly prone to store body fat. On a bulk, for example, or even more so when you have been dieting and are trying to return to a normal caloric intake.
  

  
  

  According to the results Lagerpusch et al. present in the November issue of the British Journal of Nutrition even healthy young men who were subjected to a 3-week diet phase (-50% in caloric intake) and subsequent overfeeding (+50% in caloric intake) the subjects in the high GI study arm had a 135% higher increase in fasting insulin levels during the refeed than those in the low GI group. In view of the fact that the glucose clearance (measured in an oral glucose tolerance test) was identical, it is not only no wonder that the weight gain did not differ either (see figure 1), but also unlikely that we would see significant differences as far as the fat gains are concerned (the latter were unfortunately not measured in the study at hand). At the same time, longer hyper-caloric high GI diets are certainly a risk factor for both insulin resistance and obesity, so that you are probably still at lower risk with 65g instead of 27g of fibre per day and a mean GI of 40 vs. 74.

  
  

  If you are interested in the influence of different diets on weight gain and health during overfeeding, I suggest you check out the following two SuppVersity posts: “194 Bananas in Three Weeks” and “A Tale of Macro- and Micronutrient Modifications“.

  
  

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  Figure 2: Chronic mild stress leads to an overactivation of the HTPA and subsequen metabolic dysregulations (Takahashi. 2012)

  
  

  Further evidence that chronic mild stress is to blame for the obesity pandemic (Takahashi. 2012) — As researchers from the Tohoku University Graduate School of Medicine in Japan report in the latest issue of the  American Journal of Physiology – Endocrinology & Metabolism, the localized re-setting of the clock genes in the liver, yet not the hypothalamic suprachiasmatic nuculeus (SCN), of BALB/c mice in response to chronic mild stress exposure elevated and phase-shifted serum corticosterone levels (see figure 2).
  

  
  

  Takahashi et al. argue that the observed changes are indicative of an overactivation of the HPA axis, which induced disturbances in the rhythmic expressions of core clock genes, e.g. Clock, Npas2, Bmal1, Per1 and Cry1 in the liver and subsequently circadian patterns of glucose and lipid metabolism-related genes such as the proliferator activated receptor (PPAR) family which favor the storage and hamper the oxidation of fatty acids.

  
  

  If you want to learn more about clock genes and how you can modify them, (re-)read the SuppVersity Circadian Rhythm Series!

  
  

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  Scientists develop improved formula to calculate the resting energy expenditure of diabetics (Ikeda. 2012) — While I would hope that you don’t belong to the group who would have to use the new and improved formula scientists from the Department of Diabetes and Clinical Nutrition at the Kyoto University in Japan have now proposed, you may have clients or relatives who could benefit from its high predictive validity (78% +/- 103kcal vs. 50% for Harris-Benedict; 38% for Oxford, 42% for Liuand 63% for Ganpule):
  
  
  
  

  What you should keep in mind though, is that this equation was tested on Japanese individuals. Since we know from other studies that there are certain metabolic differences between people with different ethnic backgrounds I would remain a “healthy skeptic” as far as the outcomes of this equation are concerned – the same obviously goes for any other equation, e.g. the ones for athletes I provided in part III of the Female Athlete Triad series.

  
  

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  If you are interested in ways to modulate your leptin levels that may facilitate weight gain, I suggest you take a look at my second “Carbs Past 6PM Won’t Make You Fat” post.

  
  

  Leptin induced weight gain? 13% more body fat in 2 weeks, when it hits the wrong part of the brain (Harris. 2012) — With the mixed results from intervention trials, the enthusiasm around leptin has abated over the past months, the general consensus is yet still that leptin and leptin resistance loom large in the metabolic dysregulation that’s at the heart of the diabesity pandemic. Against that background, the results Ruth B.S: Harris presents in her latest paper in the American Journal of Physiology – Endocrinology & Metabolism are unquestionably surprising.
  

  
  

  When Harris injected twice the amount of leptin (0.6 µg leptin/day) that had previously been shown to decreased 24 food intake, body fat and lean tissue, when it was injected into the third ventricle of the hindbrain, into the fourth ventricle of her lab rats, the rodents gained an almost incredible amount of 13% body fat within only 2 weeks! And that in the absence of statistically significant change in daily food intake, suggests an “increase in efficiency of energy utilization” (Harris. 2012). Fortunately, further experiments showed that the pro-obesogenic effects of leptin in the 4th ventricle was antagonized when both the 3rd and the 4th ventricle were exposed to leptin. In this scenario the leptin exposure of the 4th ventricle did even protect the lean mass of the rodents from the negative effects the exclusive exposure of the 3rd ventricle had. Overall, the study is yet somewhat chaotic and a clearcut message aside from “look people things are even more complex than we already thought”, is probably not going to contribute to a solution of the obesity dilemma in the near future. 

  
  

There are, as usual more news on Facebook, some of them, such as the relation between hypothyroidism during pregnancy and the diabetes risk of the offspring later in life, are even related to the topic at hand. And if that’s nothing you are interested, you may want to read about …

• the non-existent effects of coffee consumption before bed on the sleep quality of habitual coffee drinkers (read more),


• the problem with inaccurate vitamin D tests and the absence of a reliable and scientifically sound definition of “vitamin D deficiency” (read more), or


• the strength promoting in-vitro effects of sodium bicarbonate, or in other words, a rather alkaline milieu on muscular force production (read more)

… and if neither of those can satisfy your thirst for more information from the realms of exercise and nutrition sciences, you can still wait for the next serving of facebook news or tomorrow’s SuppVersity article

References:

• Harris RB. Leptin-induced increase in body fat content of rats. Am J Physiol Endocrinol Metab. 2012 Dec 4.


• Ikeda K, et al. A new equation to estimate basal energy expenditure of patients with diabetes. Clinical Nutrition. 2012 [article in press] 


• Lagerpusch M, Enderle J, Later W, Eggeling B, Pape D, Müller MJ, Bosy-Westphal A. Impact of glycaemic index and dietary fibre on insulin sensitivity during the refeeding phase of a weight cycle in young healthy men. Br J Nutr. 2012 Nov 28:1-11.


• McNay EC, Teske JA, Kotz CM, Dunn-Meynell A, Levin BE, McCrimmon RJ, Sherwin RS. Long-term, intermittent, insulin-induced hypoglycemia produces obesity without hyperphagia or insulin resistance: a model for weight gain with insulin therapy. Am J Physiol Endocrinol Metab. 2012 Nov 20.


• Sluijs I, Beulens JW, van der Schouw YT, van der A DL, Buckland G, Kuijsten A, Schulze MB, Amiano P, Ardanaz E, Balkau B, Boeing H, Gavrila D, Grote VA, Key TJ, Li K, Nilsson P, Overvad K, Palli D, Panico S, Quirós JR, Rolandsson O, Roswall N, Sacerdote C, Sánchez MJ, Sieri S, Slimani N, Spijkerman AM, Tjønneland A, Tumino R, Sharp SJ, Langenberg C, Feskens EJ, Forouhi NG, Riboli E, Wareham NJ; on behalf of the InterAct consortium. Dietary Glycemic Index, Glycemic Load, and Digestible Carbohydrate Intake Are Not Associated with Risk of Type 2 Diabetes in Eight European Countries. J Nutr. 2012 Nov 28.


• Takahashi K, Yamada T, Tsukita S, Kaneko K, Shirai Y, Munakata Y, Ishigaki Y, Imai J, Uno K, Hasegawa Y, Sawada S, Oka Y, Katagiri H. Chronic mild stress alters circadian expressions of molecular clock genes in the liver. Am J Physiol Endocrinol Metab. 2012 Dec 4.

Stress and asthma

In this issue of JACI, Haczku and Panettieri review the evidence for the involvement of stress in asthma and find that it suggests that psychosocial stressors are important in asthma morbidity.

Chronic psychosocial stress has been correlated with asthma severity and exacerbations, as well as overall immunocompromise that leads to or worsens disease. The authors developed a mouse model of social stress in order to mimic socially disruptive stressors experienced by humans. They showed that mice exposed to allergen and persistent social stress had increased airway reactivity and lowered Th2 cell sensitivity to glucocorticoids. In their mouse model, Haczku and Panettieri noted that the social stress did not result in immunosuppression, but instead, activated innate and Th2 immune responses that resulted in sustained increases in circulating corticosterone. They suggest that this may lead to corticosteroid insensitivity and perpetuate airway inflammation.

Altered function, reduced expression and impaired translocation of the glucocorticoid receptor (GR) are among the possible mechanisms for steroid insensitivity proposed by Haczku and Panettieri. They suggest that GR may be down-regulated by agonistic ligands, or NF-κB transrepression of gene transcription. Their own studies reported increased expression of NF-κB concomitant with decreased GR nuclear translocation, DNA binding and GR expression.

Bias toward inflammatory cytokine stimulation by innate immune cells is another mechanism the authors discuss. Mice exposed to stress alone produced macrophage and dendritic cell secretion of IL-13 associated IgG1 and TARC as well as TNF-α and IL-6.

Finally, the authors talk about the role of structural cell responses to glucocorticoids, citing recent findings of reduced surfactant protein D (SP-D) in patients with chronic lung disease. Corticosteroids greatly increase the amounts of SP-D, which is known to have immunosuppressive effects, and they suggest that corticosteroid insensitivity of epithelial cells in chronic lung pathology is responsible for the impairment of this protective mechanism.

Haczku and Panettieri propose new approaches to circumvent corticosteroid non-response. They have shown that corticosteroid insensitive airway smooth muscle and whole lung tissue are still responsive to I κB and MAP kinase inhibitors, reducing cytokine secretion. This may be a possible pathway for therapeutic intervention in asthma patients who are steroid-insensitive.

We asked Dr. Haczku some questions about the implications of this review:

JACI: Since the evidence is pointing to a multiple-scale physiologic response, would this problem lend itself to a systems analysis approach to coordinate effective therapy?
Dr. Haczku: Susceptibility to the detrimental effects of chronic stress exposure on the neuro-endocrine, immune and hematopoietic systems as well as on various target organs maybe genetically regulated, organ- and cell type specific. A systems analysis approach therefore to disease assessment and effective therapy would be very beneficial.
JACI: Do you think kinase inhibitors would be primary or add-on therapy for patients with corticosteroid-resistant lung disease?
Dr. Haczku: Kinase inhibitors once developed would form a useful second line (add-on) therapy for patients with corticosteroid resistant chronic inflammatory diseases.

We want to hear from you. Please feel free to post your own questions or comments. All questions and comments will be forwarded to the authors for a response.