ARTICLE SUMMARY #6
Drapeau, V., Therrien, F., Richard, D., & Tremblay, A. (2003). Is visceral obesity a physiological adaptation to stress? Panminerva Medica, 45(3), 189-95.
· Visceral obesity is associated with a disruption of the functioning of the HPA axis
- HPA Axis stands for “hypothalamic-pituitary-adrenal axis” and is basically acts as a liaison communicating the interactions between the hypothalamus, pituitary gland and adrenal glands. It plays a huge part of the system that controls the body’s reaction to stress
· Abdominal fat storage has been associated with when the HPA-Axis is set off by stress
· HPA axis activation increases cortisol production which has been shown increase appetite, consumption of food and anti-thermogenic effects (this is the opposite of a thermogenic effect which produces weight loss)
· “Since abdominal adipose tissue has more cells per mass units, higher blood flow and more glucocorticoid receptors, glucocorticoids affect abdominal fat to a greater extent than subcutaneous adipose tissue” (I quoted this because I couldn’t word it any more clearly myself)
· Cushing's syndrome is evidence that links overproduction of cortisol (hypercortisolemia) and accumulation of central fat.
- Visually, people with Cushing’s Syndrome are centrally obese. They carry all of their weight in abdominal area and face (“moon face”). They tend to have more slender limbs and a very small bum. There are lots of pictures on the internet if you are interested.
· “Hervey's hypothesis”suggests that fat cells take up and metabolizes cortisol and has a regulatory effect that adapts the body into accumulating visceral fat in response to stress.
- Evidence shows obesity is associated with an increased cortisol clearance. Hormonal and enzymatic changes have been implicated in this preferential body fat accumulation in response to stress.
· Genetics can emphasize this belly fat storage
· Article discusses that this could be a vicious cycle. People gain weight because stress and excess weight causes stress - they clearly state that “Even if the available literature does not permit to establish clearly which comes first, it suggests that visceral obesity could represent a non optimal physiological adaptation to stress”
· Article suggests that treatment of visceral obesity should focus on stress management to help break the stress/fat circle.
_____________________________________________________________________________ARTICLE 5 SUMMARY
Abe, T., Kawakami, Y., Sugita, M., & Fukunaga, T. (1997). Relationship between training frequency and subcutaneous and visceral fat in women. Medicine & Science in Sports & Exercise, 29(12), 1549-1553.
· Twenty-six healthy women with sedentary lifestyles ( defined as less than 30min a day, 1 day a week) were randomly assigned to three groups:
1. Control group – changed nothing
2. Group that performed aerobic exercise 1-2 sessions/week and restricted calorie program
(-200 cal from current intake)
3. Group that performed aerobic exercise 3-4/week and maintaining current caloric intake
· Training programs lasted 13 weeks. Aerobic activity consisted of stationary cycling with intensity set at 50-60% of maximal heart rate
· Weight was measured using hydrostatic weighing technique
· Visceral vs. Subcutaneous fat was measured using B-mode ultrasonography
· Results
- Average energy cost of each training session ranged from 150 to 220 calories
- Approx weekly caloric deficits were 1960 cal/week
- Reduction in total body weight, body fat % and total fat mass following training was significant for both Groups 2 & 3.
- Group 3 showed no training induced differences in Visceral fat
- Subcutaneus fat was significantly reduced in Groups 3 but not Group 2.
- Group 2 exercised less and had less change in subcutaneous fat, there was a significant loss in visceral fat.
- Group 3 exercised more with less diet restriction and lost more subcutaneous fat than visceral fat but both losses were significant.
· Findings
- Decrease in subcutaneous fat (but not visceral) is proportional to the amount of aerobic exercise training whereas Visceral fat appears to be related more to a caloric deficit.
ARTICLE #4 SUMMARY
Abdominal fat and what to do about it. (2006). Harvard Women's Health Watch, 14(4), 1-3.
NOTE: This was very much so an "overview" article and I don't think I will make guidelines from it until I get to review the original research it referenced (which is included in the reference list of this blog to be reviewed)
Intro
· As women age, their proportion of to body weight tends to increase (especially during menopause)
· Visceral fat has been linked to metabolic disturbances, increased risk of cardiovascular disease, higher LDL (bad) cholesterol and Type 2 diabetes
· In women, visceral fat has been linked to breast cancer, colorectal cancer and the need for gallbladder surgery
· Fat accumulated in pear-shaped women (weight carried in lower half) is subcutaneous fat while those with apple shaped bodies (weight carried in middle) is largely visceral.
Common causes of abdominal fat in women:
· Heredity (genetics) can influence your shape. A number of genes have been identified that determine how many fat cells an individual has and where their fat gets stored
· Hormones are also a big player
o lowered estrogen can lead to increased abdominal fat after menopause
o menopause can also lead to an increase of cortisol, the stress hormone that promotes the accumulation of abdominal fat
· There is much evidence that waist circumference is a better predictor of health problems than BMI
Our fat is not lazy
· Abdominal fat is biologically active and should be thought of as an endocrine organ/gland that produces hormones than just a storage area
· Fat releases leptin (hormone that lowers appetite) after meals
· Fat releases adiponectin (chemical that affects your body’s response to insulin)
· Excess body fat disrupts the normal balance and functioning of these hormones
· One reason visceral fat is so harmful is because of its location near the portal vein (vein that carries blood from the intestinal area to the liver)
What can we do about visceral fat?
· What works
o At least 30 min of physical activity a day - Duke University Medical Center study shows - non-exercisers experienced nearly 9% gain in visceral fat after 6 months compared to those who walked/jogged the equivalent of 12 miles per week who put on no visceral fat
o Strength training – study where experimental group received 1 hour of strength training 2x a week reduced total body fat by nearly 4%
· What doesn’t work
o Spot exercising – sit-ups, etc tighten ab muscles but will nto get at visceral fat
o Drastically reducing calorie intake – puts body into starvation mode
o DHEA – hormone that declines with age. A two year randomized trial published in the New England Journal of Medicine showed that the hormone had ZERO effect on aging markers (including body composition) in men and women aged 60+
· Drug treatments
o Meridia – drug’s greatest effects are on visceral fat
o Acomplia – not yet FDA approved – new class of drug that blocks brain receptor that increases appetite and has been shown to modestly reduce storage of fat on the waist
ARTICLE #3 SUMMARY
Sofer, S., Eliraz, A., Kaplan, S., Voet, H., Fink, G., Kima, T., & Madar, Z. (2011). Greater weight loss and hormonal changes after 6 months diet with carbohydrates eaten mostly at dinner. Obesity (Silver Spring, Md.), 19(10), 2006-14
· Study investigated the effect of a low-calorie diet with carbs eaten mostly at dinner on anthropometric (weight and measurement of the body) , hunger/satiety, biochemical and inflammatory parameters. They also measured hormonal secretions.
· This was randomized clinical trial with random blind group assignment and inclusion of a control group. However, the participants were not chosen at random but included only healthy obese male and female police officers (BMI over 30 but do not have hypertension, diabetes, etc). The analysis used was appropriate (T-test, Anova, and they controlled for bias with analysis of covariance, etc). Hormone levels were taken and hunger questionnaires were completed every 4 hours before meals on days 7, 90 and 180 of the diets)
· The study built upon previous research that showed the patterns of the following bodily secretions:
ü Leptin is the “satiety hormone” that regulates hunger, satiety and food intake. Our bodies increase its secretion between 1600hrs (4pm) and 0100 (1am) – meaning its levels are highest by dinner time and highest while we are usually asleep.
ü Adiponectin is a protein that regulates energy and lipid / carb metabolism (which reduces serum glucose/lipids – improving insulin sensitivity and having an anti inflammatory effect). This protein in obese individuals is found to be low throughout the day.
· Researchers are testing to see if an innovative dietary regimen could work with the obese persons body and be beneficial in aiding obesity. Similar studies examining the Muslim Ramadan diet were discussed (when they fast all day and eat a carbohydrate rich evening meal). They hypothesized that holding out carbs until dinner will alter the secretion of these hormones into a new schedule that is higher during the day when the majority of calories are consumed (making people feel less hungry and more satisfied).
· THE DIET: Standard low calorie diet – 20% protein, 30-35% fat, 45-50% carbohydrates = 1,300 – 1,500 calories daily. (I cannot post the example of their daily food intake from the study because of copyright law)
· The control group and experimental group ate the EXACT same foods, the only difference being the time of day in which carbs were eaten. Control group contained their carbs throughout the day with every meal and the experimental ate theirs at dinner.
· BODY MEASUREMENT RESULTS:
ü Significantly greater weight loss was found in the experimental group (11.6 vs 9.06kg) – (P=0.024)
ü Trends of greater BMI reduction were found (3.99 vs. 3.16 BMI points), abdominal circumference reduction (11.7 vs. 9.39 cm) and absolute body fat percent (6.98 vs. 5.13%) were found in the experimental group. After controlling for baseline measurements, these results were not scientifically significant (P=>0.05) but still noteworthy.
· HUNGER/SATIETY QUESTIONNAIRE RESULTS
ü HUNGER: Control group felt significantly hungrier at noon on day 90 and 180 compared to first week on diet (5.9%); experimental group felt less hungry compared to the first week (27.7%) on diet. The most significant difference (P=0.03) between the groups with hunger was found in the evening of day 180 (28% increase in hunger vs. 6.6% decrease in hunger).
ü URGE TO EAT: Experimental diet participants had a 67% reduction in the urge to eat vs. 19% of the control diet group when comparing to the first week of the diet.
ü PREOCCUPATION WITH THOUGHTS OF FOOD: Experimental group had no increase preoccupation with thoughts of food vs. 33% of the control group having increased preoccupation with thoughts of food on day 180 compared to the first week on diet.
· BIOCHEMICAL RESULTS
ü Day 180 on the experimental diet showed significantly lower average daily insulin concentrations when compared to baseline and control group (68%, P=<0.05)
ü Experimental diet led to significant decrease (20%, P=0.01) in fasting glucose vs. 8.3% decrease in the control group
ü HOMA (method used to quantify insulin resistance and beta-cell function) 30.9% decrease found in experimental group vs. 19.7% increase in the control group. These results were significant at P=0.015.
ü Both diets led to significant reduction in morning fasting triglyceride concentrations compared to baseline when measured on days 90 and 180 (P=0.0001).
ü Experimental diet led to 8.1% significant decrease in total cholesterol concentrations (P=0.01)
ü HDL-cholesterol (good cholesterol) increase in experimental diet was significantly greater compared to the control diet increase after 180 days (P=0.022)
· SERUM INFLAMMATORY LEVELS
ü Experimental diet had greater CRP reduction (protein found in the blood that rises in response to inflammation) although not scientifically significant once adjusting for baseline levels
ü Experimental diet had significantly lower TNF-a concentrations (small cell-signaling protein molecules that stimulate an increase or decrease in plasma concentrations in response to inflammation). Experimental diet led to a 9.2% decrease in TNFa levels va. The control group had a 16.1% increase compared to baseline.
· SERUM HORMONAL LEVELS
ü Both diets led to an average 12-hours leptin concentrations on day 90 and 180 (P=<0.05)
ü Experimental diet led to significant increase (43.5%, P=<0.05) in average 12-h adiponectin (regulates glucose levels and fatty acid breakdown) concentrations vs. the control diets insignificant 13.9% after 180 days.
ARTICLE #2 SUMMARY
Ismail, I., Keating, S. E., Baker, M. K., & Johnson, N. A. (2012). A systematic review and meta-analysis of the effect of aerobic vs. resistance exercise training on visceral fat. Obesity Reviews : An Official Journal of the International Association for the Study of Obesity, 13(1), 68-91.
Ismail, I., Keating, S. E., Baker, M. K., & Johnson, N. A. (2012). A systematic review and meta-analysis of the effect of aerobic vs. resistance exercise training on visceral fat. Obesity Reviews : An Official Journal of the International Association for the Study of Obesity, 13(1), 68-91.
· Performed a meta-analysis (not a great one in my opinion) of studies that compared aerobic and resistance exercise effects on visceral fat. Out of 12,196 studies located, they only compared only 9 (nine). Their findings were not significant (P = 0.07) but their data suggests that aerobic exercise is central to exercise programs aimed at reducing Visceral fat (WELL DUH).
ARTICLE #1 SUMMARY
Bray, A. (2009). Dietary patterns may modify central adiposity American Dietetic Association, 109(8), 1356-66.
· Higher Red meat and fruit intake were associated with a smaller increase in waist size but with less than 25% dietary intake from fructose.
· Higher snack intake is associated with increase in waist circumference
· In Women, high-fat dairy consumption (e.g. butter, higher fat milk, etc) and vegetable intake are inversely related to change in waist circumference ( as intake of these foods increase, waist size decreases).
· Potatoes are positively related to increased waist circumference
· In women, higher consumption of processed meat and poultry found to be associated with larger incr3ease in waist circumference
· Recognized issue with these types of studies, underreporting of consumption in self report surveys can affect degree of correlational data (strength of associations)
· Difference in belly fat gain/loss in men and women
ü Change in waist size for men is more visceral fat (the kind that can be dangerous and we want to lose)
ü Change in waist size for women is more likely subcutaneous fat
· Belly fat, age & hormones
ü Both men & women – Growth Hormone decreases with age and is known to decrease visceral fat . Cortisol is a stress hormone (and increases blood sugar) and is associated with an increase in subcutaneous fat.
ü Men – Testosterone decreases with age and isa related to the storage of visceral fat
ü Women – decrease in estradiol with age (as ovaries slow in functioning) which leads to an decrease in circulating testosterone .
· Suggested that home-prepared meals with food variety (fruits, veggies, whole grains, dairy) may be beneficial and result in a more healthful weight and less increase in waist circumference (requires further study) - (makes sense)
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