Ministry to Partner SLAD on Diabetes Awareness

Prof Onyebuchi  Chukwu


Sandra Alumona

The Federal Ministry of Health is set to organise a convention in partnership  with Saving Life for African Diabetes Foundation (SLAD), a  Non Governmental Organisation (NGO)   put together by Nollywood stars and musicians to create awareness on diabetes.
The  convention titled, “Nollywood Health Convention 2013,” with the theme;  Ignorance is not an Excuse, will kick off on November 23, at the Golden Tulip Hotel, Festac, Lagos.
A Nollywood movie producer and the President of SLAD, Mr. Obi Madubogwu, who disclosed this, noted that the convention would attract dignitaries from both governmental and non-governmental organisations.
Madubogwu also disclosed that award would be given to Nigerians that has contributed so much in the development of the society at the convention.
According to him, after the convention, there will be a free medical administration and lectures on the causes and prevention of diabetes on November 24, at the National Stadium Surulere, Lagos State.

Gram Negative Bacteria and Obesity – 180 Degree Health

By Andrew Kim 

Introduction

As the research evolves, the matter of diet and nutrition is being forced to be recognized as not only the most poorly understood of all the sciences but also one of the most complex, outranking all the others.

Weight loss is a recurrent theme on this site and this should be expected, as obesity is the most common “disease” in the United States.1 But herein lies a wrinkle that adds to the complexity of this matter: What constitutes a healthy weight is not an objective, uniformly agreed upon standard.

Suffice it to say here, we know that having excess body fat is strongly linked to cardiovascular disease, kidney disease, diabetes, and hypertension.  It also aggravates arthritis, gout, gallbladder disease, and blood lipid disorders.  And, it appears to aggravate certain cancers.2 

The interplay among the fat tissue, organs, muscles, and immune system is, to me, highly complex – even after drawing out all the ways in which they do in great detail.  However, up until doing researching for this post, I hadn’t fully appreciated the dimension added to this interplay by the intestinal flora and biome.

In light of the extreme claims made on behalf of (expensive) probiotic and prebiotic supplements, such as in the video below…

…my inaugural post for this site will present, in my estimation, the most important experiments that have added clarity about the connection among intestinal flora, metabolism, and weight loss.  What will be clear is that:

  1. There are observed differences between the intestinal flora of lean and the intestinal flora of obese individuals.
  2.   The interaction between the host and the intestinal flora is intricate and entails changes in the host gene expression involved in nutrient – particularly carbohydrate – processing and appetite regulation, which are not fully understood.
  3.   High-fat diets promote the passage of a bacterial poison called endotoxin into the body, potentially leading to endotoxemia (arbitrarily defined as when endotoxin levels rise by 2- to 3-fold above normal levels).
  4.  Weight loss is probably the great equalizer in that weight loss, in and of itself, reverts the intestinal flora and biome of obese individuals to that of lean individuals.

OBESITY AND THE INTESTINAL FLORA

Obesity changes the gut flora, and these changes have been directly correlated with a host of metabolic imbalances and diseases in animals.  This fact should not be a surprise anymore, as the intestinal flora is now known to play an indispensable role in the nutrient metabolism – particularly carbohydrate metabolism – of its host.  It was shown, for instance, that in the rectum, over 100 genes are regulated differentially by intestinal flora; and in the jejunum, over 200 genes.3

But test tube studies like the one described above are obviously limited in what we can take away from them.  Luckily, many of the assumptions and hypotheses about the intestinal flora are testable in living organisms.

In one now classic experiment, despite eating 30 percent less food than germ-free mice, normal mice were 40 percent fatter than germ-free mice.  In a follow up experiment, upon inoculating germ-free mice with the flora from normal mice, the germ-free mice became about 60 percent fatter and developed insulin resistance after 2 weeks, despite eating less food than normal.4 Leptin levels increased, too, and though the authors merely correlated the increase in leptin to the increase in fatness, it was probably also driving the insulin resistance that had developed.

Since living in a germ-free environment isn’t possible and since wiping out the flora in our intestines entirely would lead to serious deficiencies and malnutrition, we could, next, investigate dietary interventions that alter the microbial biome in a way that matches that of healthy and lean individuals.

Generally, mice fed on high-fat diets have a significant increase in endotoxin levels – indicating either a greater ratio of gram-negative bacteria to gram-positive bacteria in the intestines, as only gram-negative bacteria have coats that bear endotoxin.  Endotoxin is quite toxic to the human body5 and large exposures to it can be quickly life threatening and fatal.

In short, endotoxin creates a state of shock in the human body – known as septic shock.  Lucky for us, to get to this point, very large bacterial invasions into the body are needed by way of breaks in the skin – including the “skin” of the intestines.

However, at relatively lower, chronic doses, endotoxin:

  • Favors wide spread blood clotting
  • Leads to fatty liver conditions
  • Promotes oxidative stress and metabolic disorders (including glucose intolerance and insulin resistance)
  • Initiates an immune response (however, I’m open to the possibility that this effect, though the mechanisms are less clear to me, may actually serve the host favorably in the big picture)5

Further, mice fed on high-fat diets, compared to high-carbohydrate diets, have reduced concentrations of Bifidobacterium species – a major type of gram-positive bacteria normally present in the intestines of mammals.  A lower concentration of Bifidobacterium species creates a vacuum in which more virulent, endotoxin-bearing gram-negative bacteria could seed and proliferate. (Because of the presence of endotoxin in their coats, gram-negative bacteria are not only more virulent than gram-positive bacteria, but they are also more resistant to antibiotics, as antibiotics have difficulty penetrating this outer coat.)  In fact, Bifidobacterium species reduce the intestinal endotoxin load, and at the same time, strengthens the intestinal barrier.6

I mention this fact to point out how a simple dietary change could, by altering the intestinal biome, bring about marked changes in a person’s metabolism and health – regardless of the amount of calories consumed.

Further, the introduction of Bifidobacterium species has been shown to reduce the intestinal endotoxin load, improve the barrier functioning of the intestinal wall, and protect against obesity and endotoxemia brought about by a high-fat diet.7

Although the majority of studies showing an increase an endotoxin levels caused by high-fat diets were performed in rodents, I think, considering the major way in which endotoxin moves into the body, it’s reasonable to assume that the same result would be seen in humans.

Endotoxin is continuously generated and released into the intestines by bacteria upon their destruction or death.  From there, endotoxin is transported into the capillaries, which surround the intestines, via newly made lipoproteins called chylomicrons, whose formation is stimulated by the presence of dietary fat.  So following a high-fat meal, a rise, albeit a usually modest rise, of endotoxin would be seen in the blood.

Before I leave this train of thought and move cautiously along to my recommendations, we need to consider one additional seminal experiment, which was carried out in humans.  In said experiment, weight loss – via a low-fat diet or a calorie restricted low-carbohydrate diet – resulted in a shift in the intestinal microbial ecology in obese subjects, more closely matching that of lean controls.4 In other words, weight loss, in and of itself, altered the intestinal microbial biome favorably.

RECOMMENDATIONS

I’ve always been skeptical about the use of probiotics and prebiotics, and up until doing research for this post saw little evidence to justify their use for any condition – the evidence was so thin.

However, evidence from clinical trials in humans is emerging on the use of prebiotics and probiotics – particularly for the reduction in heart disease risk.

But whether an altered intestinal biome through the use of probiotics or prebiotics could accelerate fat lass and eradicate obesity in humans is unclear to me at this point and I seriously have my doubts about the effectiveness of orally administered probiotic and prebiotic supplements and foods.

From my own experiments and observations, I have been an advocate for, foremost, maximizing and expanding the capacity of oxidative energy generation to promote weight loss and health at the same time – cliché as this is. (At least until fecal probiotic transplants are properly tested for safely reducing body fat and become easily available to us all).  Fundamentally, this entails the following:

  • Increasing oxygen delivery to cells.
  • Supplying adequate amounts of B vitamins, as many of the coenzymes and carrier molecules that operate (as cardinal adsorbents) in the mitochondrial respiratory chain are made from thiamine, riboflavin, niacin, etc.  Ubiquinone, also known as CoQ10, is also important, and the more cholesterol we produce, the more ubiquinone will be made in the amounts needed by cells. Sucrose, namely its fructose half, is a potent stimulator of cholesterol synthesis.8
  • Maintaining the optimal rate of secretion, blood levels, and conversion of thyroid hormone, as thyroid hormone is the main regulator of a person’s metabolic rate and stimulates all reactions in the mitochondria involved in oxidative metabolism.

Regarding the first point, suffice it to say here, putting a brake on the excessive release and oxidation of fatty acids enhances the delivery of oxygen to cells and prevents tissue hypoxia.  Ditching high-fat low-carbohydrate diets serve this purpose.  In addition, “fast-moving” blood is essential, so platelet aggregation and fibrin production must be kept under control.

Because absorbed endotoxin stimulates fibrin production (and interferes with oxidative metabolism), its entry into the body must be minimized (or its removal from the body must be cranked up).

Vitamins K1 and K2, for instance, by enhancing the activity of an intestinal enzyme, minimizes the errant passage of endotoxin (and other harmful substances) into the body.  Vitamin K can be gotten from green vegetables and smaller amounts from fermented dairy and soy products.

Salicylates block the production of a certain prostaglandin that causes platelets to clump and blood vessels to constrict.  Aspirin and other non-steroidal antiinflammatory drugs (NSAIDs) are end products of salicylates, which occur abundantly in plants – especially in fruits.  Gotten from plants – namely fruits – salicylates are delivered to the body at a safer rate and concentration than drugs.  Salicylates also happen to prevent some of the inflammatory responses initiated by endotoxin.

Stress should be kept as low as possible.  Space does not permit me to go further into what I mean here except to say that cravings – namely for salt, sugar, and more food – should not be ignored or suppressed.  This act of defiance imposes undue stress on the body, further enhancing fibrin production.  Listen closely to your body, not diet gurus or Jenny Craig, please.

Of obvious note yet still worth bringing to your attention, one should avoid smoking and excessive alcohol consumption to promote efficient oxidative metabolism because smoking increases the exposure to carbon monoxide, a metabolic poison, and alcohol increases the permeability of the intestinal barrier.

And finally, although the research and evidence for this last recommendation is relatively scant, I would try to eat smaller meals spaced equally throughout the day, instead of large, infrequent meals.  Compared to large meals, I think small meals place less burden on the liver, keep blood sugar levels more steady, reduce endotoxin levels, and decrease the likelihood of storing the food you eat as fat, rather than to generate energy.

Andrew KimAndrew Kim is a graduate of the University of Maryland with degrees in Microbiology and Japanese. His blog has garnered much attention since its release earlier this year. Read more of Kim’s work at www.andrewkimblog.com

 REFERENCES

  1. Overweight and Obesity. Centers for Disease Control and Prevention (2013). at http://www.cdc.gov/obesity/data/adult.html
  2. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults–The Evidence Report. National Institutes of Health. Obesity research 6 Suppl 2, 51S–209S (1998).
  3. Mutch, D. M. et al. Impact of commensal microbiota on murine gastrointestinal tract gene ontologies. Physiological genomics 19, 22–31 (2004).
  4. Ley, R. E. et al. Obesity alters gut microbial ecology. Proceedings of the National Academy of Sciences of the United States of America 102, 11070–5 (2005).
  5. Rang, H. P., Dale, M. M., Ritter, J. M., Flower, R. J. Henderson, G. Rang Dale’s Pharmacology. 792 (2011).
  6. Griffiths, E. A. et al. In vivo effects of bifidobacteria and lactoferrin on gut endotoxin concentration and mucosal immunity in Balb/c mice. Digestive diseases and sciences 49, 579–89 (2004).
  7. Cani, P. D. et al. Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia. Diabetologia 50, 2374–83 (2007).
  8. Silbernagel, G. et al. Cholesterol synthesis is associated with hepatic lipid content and dependent on fructose/glucose intake in healthy humans. Experimental diabetes research 2012, 361863 (2012).

Chronic stress may lead to diabetes

Dr S V Madhu, the lead researcher, said increased secretion of the stress hormone—cortisol—leads to redistribution of fat, central obesity and insulin resistance. He added, “Higher stress levels also causes activation of oxidative and inflammatory pathways resulting eventually in development of type II diabetes.”

Dr Madhu, who heads the medicine and the endocrinology and metabolism division at UCMS, said this is the first study that has used different stress scales to characterize chronic psychological stress and evaluate its role in development of diabetes.

Doctors said, among the stress scales, the ability to cope with stress was found to be the strongest independent predictor of diabetes with an odds ratio of 0.77 that translates to a 33 percent lower risk of diabetes. “This is a positive finding. It shows that de-stressing mechanisms such as yoga, listening to music, sports or travelling can reduce the risk factor,” said another senior doctor.

Simply put, diabetes is a condition in which the body has trouble turning food into energy. All bodies break down digested food into a sugar called glucose, their main source of fuel. In a healthy person, the hormone insulin helps glucose enter the cells. But in a diabetic, the pancreas fails to produce enough insulin, or the body does not properly use it. Cells starve while glucose builds up in the blood.

There are two predominant types of diabetes. In Type 1, the immune system destroys the cells in the pancreas that make insulin. In Type 2, which accounts for an estimated 90-95% of all cases, either the body’s cells are not sufficiently receptive to insulin or the pancreas makes too little of the hormone, or both.

With more than 63 million diabetic patients, India is second only to China in the number of people living with the ailment. However, awareness about the disease remains low, says Dr B M Makkar from Research Society for the Study of Diabetes in India, RSSDI.

“Studies show almost 85 percent of type II diabetics are overweight. However, only six to ten percent are aware that being overweight put them at a higher risk for diabetes,” Dr Kakkar added.

New Drug May Someday Battle Obesity and Diabetes – WebMD

New Drug May Someday Battle Obesity and Diabetes

Researchers find slim evidence to support many

By Dennis Thompson

HealthDay Reporter

WEDNESDAY, Oct. 30 (HealthDay News) — A new diabetes drug may one day perform double duty for patients, controlling both their blood sugar levels and helping them lose weight, researchers report.

In mouse trials, doctors found the drug prompted weight loss, in addition to managing blood sugar levels.

“That [weight loss] is not what this drug was designed to do, but it’s a very attractive additional benefit,” said study co-author Richard DiMarchi, a research chemist at Indiana University in whose lab the drug was created.

The injectable medication is based on a single molecule that combines the properties of two hormones that send chemical signals to the pancreas, said DiMarchi.

“They signal to the pancreas that you are taking a meal,” DiMarchi said. “The pancreas then responds by secreting insulin and to synthesize additional amounts of insulin for subsequent use.”

People with type 2 diabetes have lower levels of these pancreas-signaling hormones, which are known as incretins, explained Dr. John Anderson, president of medicine and science at the American Diabetes Association.

“The incretin defect in type 2 diabetes is well known, and it’s only within the last few years we have had agents to treat it,” Anderson said.

Human and primate trials revealed that the new drug controls blood sugar with fewer side effects than other diabetes medications. Those side effects can include nausea, vomiting and stomach pain.

“In this study, the degree of gastrointestinal discomfort is much more modest than is experienced in conventional drugs,” DiMarchi said. “We get beneficial glycemic control with this combination drug, and it seems to be with less adverse drug effect.”

The medication combines the action of the hormones GLP-1 and GIP. Current diabetes medications of this sort target GLP-1 receptors in the body; studies involving GIP have produced mixed results.

GLP is known to suppress appetite, and DiMarchi said the weight loss observed in mice might be occurring because the second hormone, GIP, is somehow “turbo-charging” that appetite suppression.

In the mouse trials, a drug based on GLP-1 alone decreased body weight by an average 15 percent. But the new drug combining GLP-1 and GIP decreased body weight by nearly 21 percent, as well as controlling blood glucose and decreasing appetite.

A six-week human trial involving 53 patients with type 2 diabetes found that the medication effectively controlled their blood sugar levels. However, the researchers did not note any change in weight during the relatively short study period.

The higher potency of the combined molecule suggests it could be administered at lower doses than other incretin-based medications, reducing side effects and making the drug easier to take.

“Currently approved drugs are quite effective,” DiMarchi said, “but they are insufficient in normalizing glucose, and they certainly don’t cause much loss of body weight.”

The Magi and The Sleeping Star Offers A New Type of Diabetes Management

The Magi and The Sleeping Star is a Kickstarter campaign with a cause. In this fantasy adventure game by Game Equals Life, your hero will battle against ancient kings and robots, as well as a very real-word problem, type 1 diabetes.

Developer Adam Grantham is a game designer who has lived with type 1 diabetes for over 19 years. He’s always wanted to make a game that will help people better understand the disease, which is how he thought up the idea for The Magi and The Sleeping Star. If the game is funded, not only will it help people to learn about diabetes, but kids who have been newly diagnosed will finally have a hero to look up to.

“The Magi and The Sleeping Star is unlike any health game before,” explains Grantham on the Kickstarter page. “Rather than coming from the realms of medical research and academia, it comes straight from the game industry. I knew from the beginning that if the game wasn’t fun, it wasn’t going to be teaching anyone anything. So we designed a core game that was strong enough to stand alone as an exciting, evocative adventure.”

He goes on to discuss one of the game’s core mechanics, blood sugar balance. In order to be able to access all of your hero’s abilities, players will need to manage blood sugar levels. According to Grantham, the game isn’t about diabetes, instead it’s about a hero’s journey and that hero just happens to have the disease.

If you want to help bring The Magi and The Sleeping Star to life, check out the game’s Kickstarter campaign.

Leah B. Jackson is an Associate Editor at IGN. Feel free to follow her/send tips on Twitter and MyIGN.

Childhood obesity drops in Chicago kindergarteners

As thousands of Chicago Public School kids sit anxiously waiting for trick or treat time, the city offers some good news and some bad news.

First the good news: New figures released today by the Chicago Department of Public Health suggest that childhood obesity among CPS kindergarteners has dropped by five percentage points, from 24 percent in 2003 to 19.1 percent in 2012.

Yay, right?

Well, don’t break out the king size Snickers yet. That figure still puts their obesity levels well above the national average (12 percent) for kids their age, and even the average (14 percent) for low-income kids.

Additionally, the latest figures don’t show any statistically significant improvements among older students who are measured at 6th and 9th grade.  Instead, those levels seem to be hitting a plateau, which mirrors overall obesity figures in the U.S. during the last decade.

Despite these qualifiers, the news was greeted with some optimism by local folks who have been working on this issue for years.

“I think the new numbers are promising,” said Adam Becker, who heads the Consortium to Lower Obesity in Chicago Children. “For decades we’ve seen major increases in the rates and so to see the rates going down, even in small increments at a time, is an indication that we are moving in the right direction.”

The improvement among CPS kindergarteners follows modest progress in 21 states across the country among very young children, and improvements in other big cities including New York and Los Angeles. But Chicago still posts higher childhood obesity numbers than those big cities for reasons researchers are not quite able to explain.

“I think we are starting to see what we all hope will be an ongoing national decline in obesity levels for all kids,” Becker said. “And this should just encourage us to step it up.” 

Most researchers agree that tripling of childhood obesity in the U.S. over the last 35 years was a result of several converging factors.

To combat them, the city has recently taken a multifaceted approach that has included adding more fruits and vegetables to school lunches and ditching the daily nachos. Other initiatives have involved offering grocers incentives to open in underserved neighborhoods, supporting fresh produce cart vendors, restoring recess to schools and finally gathering and calculating these CPS obesity figures to begin with.

“Obviously I’m really excited about seeing these numbers headed in the right direction,” said Health Commissioner Bechara Choucair. “But we’ve still got a lot of work to do.” 

10 celebrities living with diabetes

diabetes main pictureRecently, actor Tom Hanks revealed that he was diagnosed with type 2 diabetes, a lifelong condition, which occurs when the body does not produce enough insulin. The 57-year-old has already been dealing with high blood pressure since the age of 36, reports contactmusic.com. Though the condition can be controlled through an effective diet, Hanks chooses to do otherwise. ‘Well it’s controllable through diet. My doctor said, ‘If you can weigh what you weighed in high school, you’ll essentially be completely healthy and not have Type 2 diabetes.’ And I said, ‘Well, I’m going to have Type 2 diabetes then’, he added.  Tom Hanks is not the only celebrity suffering from diabetes. Here are some other celebrities who’ve tackled the menace:

Sonam Kapoor

Anil Kapoor’s daughter has struggled with diabetes from her teenage years. She has followed a strict diet regime with daily insulin to stay healthy. Her hectic schedule did take a toll on her but she soon learned to manage the condition, and hasn’t let it stop her from becoming one of the most sought-after actresses in B-town. (Read: Sonam Kapoor’s weight loss secrets)

Halle Berry

The Bond girl was diagnosed was diabetes when she was 23 after she fainted on a TV set. She was taken aback by the disease because none of her family members suffered from it. Since then, she has been taking daily insulin injections for the rest of her life and overhauled her diet. She now follows a diet that is low in fat, sugar, processed carbs and avoids all junk food or sweets. (Read: How celeb trainer Ramona Braganza got Jessica Alba and Halle Berry to shed their post pregnancy weight)

Salma Hayek

The curvy actress suffered from gestational diabetes (diabetes during pregnancy), which she claimed runs in her family. She told American Baby magazine, ‘I had gestational diabetes, which I didn’t realize at first. It occurs in women who have high blood sugar levels during pregnancy. I didn’t know whether I was feeling bad because I was pregnant or whether something was seriously wrong. I was nauseated for nine months, which can be one of the symptoms.’ (Read: Gestational Diabetes: Causes, prevention and treatment)

Wasim Akram

The King of Swing was diagnosed with diabetes when he was 30. It was shocking for the ace swing bowler who always associated diabetes with a sedentary lifestyle. Nonetheless, he modified his diet and exercise regime to counter the illness and also took insulin doses. The disease didn’t stop him from making his mark in the cricketing world, and becoming one of the greatest bowlers cricket has ever seen. (Read: Cut risk of diabetes by 30 per cent with just 30 minutes of physical activity)

Kamal Haasan

The talented actor suffers from type 1 diabetes and is part of 5% of  Indian diabetic population that suffers from this variety of diabetes. The actor hasn’t let the disease dampen his zest for life and has even become an advocate for diabetes awareness, promoting the website www.sugarbp.org.

Gaurav Kapur

The former Channel V VJ and IPL Extra Innings host was diagnosed with type 1 diabetes when he was 22. The witty actor took the diagnosis in his stride and lives a healthy lifestyle to counter the disease. He practices yoga and jogs regularly to keep fit and also follows a strict diet while abstaining from alcohol to keep his blood sugar under control.

Drew Carrey

Famous as an overweight comedian and sitcom star, Carey dropped 80 pounds after being diagnosed with type 2 diabetes. He claims that after losing weight he now no longer requires diabetic medicine every day.

George Lucas

The Star Wars creator learned his condition when he was graduating from college and when he was drafted for the Vietnam War; his physical exam revealed he suffered from type 2 diabetes, which exempted him from the draft.

Billie Jean King

Perhaps the greatest women tennis player of all time, she was diagnosed with the condition in 2006. She lost 35 pounds to fight the disease and went on to become a spokesperson for diabetes awareness.

As we can diabetes knows no class but it’s a manageable condition. All you need to do is be aware to tackle the menace.

For more articles on diseases and conditions, check out our diseases conditions section and for videos, check out our YouTube Channel.

New Obesity Panacea Feature: Participants Needed

WP Greet Box iconHello there! If you enjoy the content on Obesity Panacea, consider subscribing for future posts via email or RSS feed. Also, don’t forget to like us on Facebook!

Every so often here on Obesity Panacea I have posted details about studies looking for participants (thanks to everyone who has decided to participate!).

I’ve recently had requests from a few colleagues asking if I would be willing to post details about their studies, and I’ve decided to make it a semi-regular feature on the blog. Once each month, I will put up a post with short descriptions of studies requiring human subjects.

I have two basic requirements. To be included, a study must:

  1. Have received institutional ethics approval.
  2. Be related in some way to physical activity, sedentary behaviour, diet, or obesity.

If I feel a study is inappropriate for some reason, then I won’t post it. But otherwise I’m happy to promote studies in any geographic location, and on any specific population. Research can’t happen without participants, and I’m happy to help people find out about studies that might be of interest to them.

Today we have two studies, both looking for participants in the Ottawa region. Although I am ineligible for Study 1 (sadly, I am neither female nor perimenopausal), I just finished participating in Study 2 and it was a pretty interesting study.  If you are interested in learning more about either study, please contact the researchers directly.  And if you would like to have your own study featured here on Obesity Panacea, email me the study details at saunders (dot) travis (at) gmail (dot) com.

Study 1: Menopause and Body Composition

Joseph StudyLocation: Ottawa

Participant Population: Females aged 40-60 years

Study Outcomes: The effects of exercise on body composition changes at different menopausal statuses

Contact: Joseph Abdulnour at 613-562-5800 ext. 7361 or by email at jabdu037@uottawa.ca.

Study 2: Body Morphology and Sweating Response

Matt poster

Location: Ottawa

Participant Population: Males aged 18-40 years

Study Outcomes: The impact of body morphology (e.g. size) on sweating response to exercise

Contact: Matthew Cramer at 613-562-5800 x2655 or by email et mcram028@uottawa.ca.

Travis’ Note: I just finished participating in this study myself, and it mainly involved watching movies while cycling at a light-moderate intensity.  And you get a VO2max test, so not a bad deal if you’d like to quantify your fitness.

 

 

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City doctors find high stress levels linked to diabetes

Could high stress levels, identified as a risk factor for cardiovascular diseases and hypertension, also be associated with metabolic disorders like diabetes? A Delhi based study funded by the Indian Council of Medical Research (ICMR), and carried out by Delhi government’s Guru Teg Bahadur (GTB) Hospital and its associated University College of Medical Sciences (UCMS), has found “significant” clinical evidence to link high stress levels to diabetes, in patients newly diagnosed with Type 2 diabetes, according to doctors.

The study which is currently under publication, found that individuals who had low glucose tolerance levels diagnosed through glucose tolerance tests (GTT) indicating diabetes, had correspondingly high stress levels and low coping levels for stress, on the basis of questionnaires developed to validate stress. Other scientific indicators were used to identify levels of stress in diabetics.

Dr S V Madhu, head of the department of endocrinology and secretary of the Research Society for Study of Diabetes in India, who was the principal investigator, said, “Stress hormone levels, measured as the human body’s hormonal response to stress was also found to be higher in people diagnosed with diabetes. Hormones associated with stress like cortisol and catecholamines were found to be altered or disturbed in people who had low GTT levels.” He added that established chemical changes in the brain, which are associated with stress were also found to be activated in patients with diabetes. “Certain pathways in the brain, like oxidative stress pathways were found to be disturbed in patients with diabetes, indicating stress,” Dr Madhu explained.

The study identified 1,000 people who were put through diagnostics including glucose tolerance and insulin sensitivity tests, and identified 500 as newly detected with diabetes. There stress levels were compared with another 500 who were found to have normal glucose tolerance levels. “To the best of our knowledge, this is the first time that we have been able to establish direct evidence demonstrating that stress plays a clinically significant role in the expression of human diabetes, in India. Again as far as we know, this is the first time that different stress scales have been used to characterise chronic psychological stress to evaluate its role in development of Type 2 diabetes,” Dr Madhu explained.

… contd.




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Is DDT a time-bomb behind the obesity epidemic? | Grist

ddt_adMichael Skinner didn’t start the experiment with the hypothesis that he’d find a connection between the insecticide DDT and obesity.

“We didn’t expect to find that,” he said. “In fact, the frequency of obesity really came as a surprise.”

Skinner, a scientist at Washington State University, wanted to take a close look at the way DDT affected inheritance. So his team injected DDT into pregnant rats and watched first their children, and then their grandchildren (or is it grandrats?). It was only in the third generation, the great-grand-rat, that they saw it: Fully half of these rats were obese. The implication is that the same thing could be happening with humans.

Michael Skinner
Michael Skinner.

“Is there a correlation between the fact that we were all exposed to DDT in the 1950s for 10 years, and the fact that we are now seeing high levels of obesity?” Skinner asked. His work suggests that there could be.

Of course, the more immediate cause of obesity is too many calories. But there may be more going on here than too much food. Humans are getting fat, so are our pets, so are wild animals. There’s a trend toward obesity in nearly every species scientists have studied.

Of course it’s too early to lay the blame on DDT. This study simply raised the possibility. But the findings are plausible.

“I do believe that the observed obesity is real,” emailed Andrea Gore, a professor of pharmacology and toxicology at the University of Texas Austin. Other experiments have already shown that endocrine-disrupting chemicals can cause obesity generations after exposure, Gore said.

Skinner had already seen that he could trigger the inheritance of disease with various chemicals. There’s a narrow window during the gestation, where an exposure to lots of things can cause heritable epigenetic changes.

“The majority of things we’ve tested came up positive,” he said.

So the obvious question: Is this a problem specific to DDT, or would we have seen similar results if Skinner’s team had decided to inject the rats with vitamin C? In other words, is this about the chemical, or just the timing of the exposure?

If the DDT had caused kidney disease, Skinner said, he would have been reassured. A lot of things seem to have epigenetic effects that lead to kidney disease. But obesity is unusual — that suggests a problem with DDT itself, Skinner said.

Skinner started this experiment after the World Health Organization lifted the ban on DDT to help fight malaria. That was a good decision based on the available information, Skinner said, but no one had looked to see if DDT had an effect on subsequent generations. “On the one hand, there are 2 million deaths per year in Africa from malaria. On the other hand, we’re looking at the possibility of metabolic disease in every generation to come,” Skinner said.

The word “possibility” there is key. This wasn’t a risk assessment study, and we don’t know if we’d see something similar in humans from environmental exposure to DDT, as opposed to direct injection. But this study should give pause to the people arguing to reintroduce DDT to places even without a malaria problem, Skinner said. It’s now being used in France, among other places. And once you spray DDT, it’s out there for a long time.

“If you go to any river in the U.S., and push your finger down into the mud one or two inches, the primary contaminant you will find there is DDT,” Skinner said. The stuff just takes a really long time to break down, and Skinner’s research suggests that its effects could last much longer.