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Showing posts with label obesity. Show all posts
Showing posts with label obesity. Show all posts

Wednesday, January 26, 2011

Fatty Liver Disease: Another Reason to Avoid Obesity

An article in the January 2011 issue of the Harvard Health Letter reveals that the epidemic of obesity has increased the occurrence of fatty liver disease. Previously, most cases of fatty liver disease were related to excess alcohol consumption, but now, many cases are related to excess body fat, which can lead to Type II diabetes. Fatty liver disease affects 70-90% of those who are obese and/or have diabetes.

Abdominal obesity can lead to metabolic syndrome (elevated blood pressure and levels of triglycerides and blood sugar, and low HDL (good cholesterol). Overfilled fat cells become resistant to insulin (which lowers blood sugar by storing it in the cells) resulting in excess fatty acids in the blood. Fat then accumulates in liver cells, which can lead to inflammation and liver tissue damage.  This can in turn bring about liver fibrosis (buildup of fibrous tissue) or cirrhosis (buildup of scar tissue). Cirrhosis increases the risk of liver cancer.

Fatty liver disease increases the risk of heart attack and stroke because a fatty liver produces inflammatory factors that can promote the deposition of plaque in the arteries, leading to arterial narrowing.

The only effective treatment for fatty liver disease is to lose weight.

Bottom Line
If you want to avoid or reverse fatty liver disease, avoid gaining unnecessary body fat or lose existing excess body fat through a program of good nutrition and exercise. Both caloric restriction and exercise are essential parts of any weight-loss program.

Friday, January 14, 2011

New Insights into Obesity

The December 2010 issue of the Nutrition Action Health Letter, published by the Center for Science in the Public Interest, featured an interview with Eric Ravussin, head of the Nutrition Obesity Research Center of the highly regarded Pennington Biomedical Research Center in Baton Rouge, LA. The discussion centered on new clues as to why we gain weight, and revealed the following:
  • Leptin, a hormone discovered in 1994, is produced by fat cells and  tells the brain when the cells are full.
  • When people diet and lose weight, leptin levels drop sharply, causing food cravings and weight regain.
  • Loss of 10-20% of body weight slows the metabolism and rate of caloric burn.
  • Injecting leptin can bring the metabolism back up.
  • However, most overweight people are resistant to leptin, just as Type II diabetics are resistant to insulin.
  • Using drugs to shut down hunger mechanisms doesn’t work well because the human body has developed several redundant systems to stimulate eating as protection against starvation.
  • People have natural ranges of body fat depending on their genes that control energy intake and expenditure.
  • Nutrition in the womb and infancy can affect propensity for overweight and obesity by switching different genes on and off.
  • Brown adipose tissue, which burns calories to produce body heat, previously thought to exist only in infants, was recently discovered in adults.
  • By maintaining homes at a steady comfortable temperature throughout the year, we don’t burn calories via brown fat to keep warm in winter, and we miss the appetite-suppressing effect of heat in the summer.
  • A common cold virus (adenovirus-36) makes experimental animals gain a lot of weight. Antibodies to this virus, an indication of exposure, are much more common in obese than in normal-weight people.
  • Gut bacteria can be a factor. Transplanting feces from a fat animal to a lean one results in weight gain for the latter, while transplanting from the lean to the fat animal makes the fatter one leaner. Similar transplants in humans have reduced insulin-resistance of people with metabolic syndrome, a set of symptoms indicative of heart-disease risk characterized by excess fat around the waist, low HDL, and elevated blood pressure, blood triglycerides, and fasting blood glucose.
Ravussin feels that we should tax soft drinks and other unhealthy foods while subsidizing healthy foods, create areas where kids can safely play, and make physical education mandatory so that everyone, not only the athletically-gifted, engages in physical activity,

Thursday, December 30, 2010

Eating Nuts Provides Several Health Benefits

An article in the January 2011 Harvard Health Letter listed several health benefits of eating nuts. Although the calories in nuts come mainly from fat, the type of fat is largely of the unsaturated healthful variety. The article cited a study done at the Beth Israel Deaconess Medical Center showing that walnuts eaten at breakfast made subjects feel more full before lunch, potentially reducing caloric consumption. Other health benefits include favorable effects on blood cholesterol, blood pressure, and inflammatory factors. Studies on large populations have linked high nut consumption with lower heart disease rates. Nuts also contain little or no carbohydrate so they do not cause spikes in blood sugar and may even blunt blood sugar spikes caused by carbohydrates eaten along with the nuts. Peanuts, almonds, and pistacios have the highest protein content, while brazil nuts, cashews, hazelnuts, and walnuts have intermediate protein content, and pecans and macadamias have the lowest protein content. Walnuts have the additional benefit of being high in omega-3 fatty acids, which are widely considered the most healthful kind.

Tuesday, December 21, 2010

Are There Hidden Causes of the Overweight Epidemic?

In the December 20, 2010 issue of Newsweek magazine, Sharon Begley, the magazine’s science columnist, wrote that there are some little-known factors that may contribute to the continued increase in the prevalence of overweight and obesity. Her main argument is that it must be more than a matter of exercising more and eating better because, among animals that have contact with human beings, such as pets, lab animals and rodent pests, 23 of the 24 species studied since 1940 have shown significant increases in the percentages of overweight and obese animals, a statistic that could have occurred by chance only once in 8 million. Yet changes in diet and exercise don’t appear to be the reason, as these factors haven’t changed much for these animals over the years.

Begley cites some possible reasons other than diet and exercise for the weight gain of animals and, by extension, us:
  • The type of bacteria in our gut - more efficient bacteria wring more calories out of our food than do less efficient bacteria. In this case, efficiency is not our friend.
  • Lack of sleep, which increases the appetite-stimulating hormone ghrelin, and decreases the hormone leptin that suppresses our appetite when we’ve eaten enough.
  • Environmental chemicals such as BPA that stimulate fat-cell production.
  • Home heating, which lessens the need for the body’s calorie-consuming heat production.
  • Home air conditioning, which lessens the appetite-suppressing effect of environmental heat.
  • Infection with adenovirus-36, which causes obesity in  lab animals and is correlated with obesity in humans.
In addition, I feel that there may be another contributor to obesity:
  • The lack of internal parasites due to modern sanitary practices. If parasites eat some of our food, less of it can be packed on as fat. If they partake of our bodies, then energy must be consumed for repair. This assumes the kind of parasites that are relatively harmless other than consuming some of our food or body tissue.
Bottom Line
There is no doubt that our health benefits from exercising regularly and eating a healthy diet without excess calories. However, we must continue to look for other contributing factors in order to effectively deal with and counteract the continued rise in overweight and obesity that threatens to undermine the gains we’ve made in improving our health and increasing our lifespan.

Thursday, November 18, 2010

Estimating the Caloric Cost of Running or Walking

A recently published article by Loftin et al. in the Journal of Strength and Conditioning Research (vol. 24, no. 10, pp. 2794-2798, 2010) measured the caloric consumption per mile of 19 normal-weight walkers, 11 overweight walkers, and 20 marathon runners. The subjects were about evenly divided among males and females.

Results
  • Caloric consumption was more related to lean body mass than to total body mass
  • Men burned more calories per mile than women
  • Men and women did not differ in calories consumed per mile per unit body mass
  • In terms of calories per mile per unit body mass, marathon runners burned significantly more than normal-weight walkers who burned significantly more than overweight walkers
The following equation was developed from the experimental data to predict an individual’s caloric consumption per mile:

Men weighed in kilograms:
Calories per mile = (0.789 x kg body mass) + 43.5

Men weighed in pounds:
Calories per mile = (0.3586 x lb body mass) + 43.5

Women weighed in kilograms:
Calories per mile = (0.789 x kg body mass) + 35.8

Women weighed in pounds:
Calories per mile = (0.3586 x lb body mass) + 35.8

Bottom Line
The equation can be useful for those interested in estimating the caloric cost of their walking or running workout.

Monday, August 30, 2010

Heart Attack Deaths in the U.S. Have Dropped Sharply

In the Harvard Health Letter, vol 35, no. 10, August 2010, and article appeared entitled, "Is the heart attack going out of style?". It stated that, based on Medicare data, the U.S. heart-attack hospitalization rate declined by 23% from 2002 to 2007. Also, a study based on 3 million members of a northern California health plan showed a 24% drop in heart attack hospitalizations between 1999 and 2008. While an increasing number of people are diagnosed with heart disease, fewer are dying from it - heart attack deaths have been declining in the U.S. for the past 40 years.

The article conjectures that, "Maybe decades of efforts to eat right and exercise more, stop smoking, lower LDL cholesterol levels, and control blood pressure are working." This appears only partially true. Yes, fewer Americans smoke, and Lipitor, a medication for reducing LDL and total cholesterol, is the most prescribed drug in the U.S. Many people are also taking blood pressure medication. Yet, there is little evidence that people are "eating right" as fast-food consumption and obesity continue to increase. Also, various national campaigns, such as the American College of Sports Medicine's Healthy People 2000, have failed dismally to get people to exercise more. Thus, it appears that the reduction in heart attacks is less due to anything that requires will power than to modern medicine. Another possible factor is reduced stress, as the economy was doing well over the study period. It remains to be seen what the recession and high unemployment rate will do to the heart attack rate. Hopefully, and emphasis on family and personal fulfillment and relationships will help keep stress to a minimum, even in the face of economic difficulties.

The reduction in heart attacks is encouraging, yet it would be even better if people became healthier through lifestyle changes such as exercise and good nutrition.

Friday, April 30, 2010

Is Fructose Unhealthy?

There has recently been some concern from various sources that fructose might be unhealthy. The focus on fructose has likely been prompted by the widely increased use of high-fructose corn syrup to sweeten various foods and drinks such as sodas, iced tea, yogurt, and snacks. Yet fructose can also be found in relatively high amounts in fruits, especially apples, pears, grapes (including raisins), and pineapples, and even in vegetables such as tomatoes, cabbage and squash. Table sugar (sucrose) is a 50/50 amalgam of fructose and glucose, while high-fructose corn syrup is 55% free fructose and 45% free glucose, industrially manufactured from corn starch,

There is some fairly solid evidence supporting the negative health effects of fructose on mice, but the evidence concerning humans is much less conclusive. In human studies, fructose intake has been positively correlated with obesity (1, 2), especially fatty deposits around the waist, which is thought to be the most dangerous to health and, of course, detrimental to the 6-pack look. Fructose also increases blood triglycerides, a recognized risk factor for heart disease (3). All cells in the body can metabolize glucose, but only the liver can metabolize fructose, and high fructose consumption appears to load the liver with fatty deposits (4, 5). Also, fructose tends to suppress insulin and leptin, both of which are hormones that decrease appetite, while increasing ghrelin, which raises appetite (6, 7), thus possibly contributing to excess weight gain. However, there is little evidence that the fructose in high-fructose corn syrup is more damaging than the fructose in table sugar (typically sucrose from sugar cane).

Bottom Line
While more studies must be done to solidify the evidence on the effects of fructose on human health, it appears wise to avoid excessive intake of fructose. This can be accomplished by:
  • Completely avoiding foods and drinks containing high-fructose corn syrup
  • Limiting consumption of table sugar and any product with a high sugar content
  • Limiting fruit juice consumption, especially juice from apples and grapes
References:
1. Lustig RH (2006). "Childhood obesity: behavioral aberration or biochemical drive? Reinterpreting the First Law of Thermodynamics". Nature clinical practice. Endocrinology & metabolism 2 (8): 447–58. doi:10.1038/ncpendmet0220. PMID 16932334.

2. Isganaitis E, Lustig RH (2005). "Fast food, central nervous system insulin resistance, and obesity". Arterioscler. Thromb. Vasc. Biol. 25 (12): 2451–62. doi:10.1161/01.ATV.0000186208.06964.91. PMID 16166564.

3. Bantle JP, Raatz SK, Thomas W, Georgopoulos A (2000). "Effects of dietary fructose on plasma lipids in healthy subjects". Am. J. Clin. Nutr. 72 (5): 1128–34. PMID 11063439.

4. Forristal, Linda (Fall 2001). "The Murky World of High-Fructose Corn Syrup". Weston A. Price Foundation. http://www.westonaprice.org/motherlinda/hfcs.html.

5. Ouyang X, Cirillo P, Sautin Y, et al. (June 2008). "Fructose consumption as a risk factor for non-alcoholic fatty liver disease". J. Hepatol. 48 (6): 993–9. doi:10.1016/j.jhep.2008.02.011. PMID 18395287.


6. Teff, KL; Elliott SS, Tschöp M, Kieffer TJ, Rader D, Heiman M, Townsend RR, Keim NL, D'Alessio D, Havel PJ (June 2004). "Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women". J Clin Endocrinol Metab. 89 (6): 2963–72. doi:10.1210/jc.2003-031855. PMID 15181085.

7. Swan, Norman; Lustig, Robert H. "ABC Radio National, The Health Report, The Obesity Epidemic". http://www.abc.net.au/rn/healthreport/stories/2007/1969924.htm. Retrieved 2007-07-15.