That excess weight can shorten your life
“The medical community seems to be under a fog that we can constantly and forever reduce death rates, and that’s simply not true,” said Professor Olshansky, who published a study in 2012 showing that life spans for white women without a high school diploma had declined, a rare event in developed countries.
“You need to look at the health status of the living,” not the mortality statistics of the dead, he said, adding that obesity is afflicting younger generations in a way that will eventually make the numbers worse.
RTWT at The New York Times.
Do something about your obesity before it’s too late.
Steve Parker, M.D.
…according to an article at MedPageToday.
“One more rep then I’m outa here!”
The two experimental groups had about 60 participants each, so it was a relatively small study. (In general, the larger the study, the more reliable the findings.) Most participants were white women; mean age was 69. The experimental intervention ran for five months. An excerpt:
In one trial, the participants were randomized to a structured resistance training program in which three sets of 10 repetitions of eight upper and lower body exercises were done 3 days each week at 70% of one repetition maximum for 5 weeks, with or without calorie restriction of 600 calories per day.
In the second study, participants were randomized to an aerobic program which was conducted for 30 minutes at 65% to 70% heart rate reserve 4 days per week, with or without calorie restriction of 600 calories per day.
The beneficial bone effect was seen at the hip but not the lumbar spine.
Thin old bones—i.e., osteoporotic ones—are prone to fractures. Maintaining or improving bone mineral density probably prevents age-related fractures. In a five-month small study like this, I wouldn’t expect the researchers to find any fracture rate reduction; that takes years.
Most elders starting a weight-training program should work with a personal trainer.
Steve Parker, M.D.
Posted in Exercise, Osteoporosis, Overweight & Obesity
Tagged aerobic exercise, BMI, bone mineral density, elderly, exercise, resistance training, seniors, weight loss, weight training
See text for mention of pancreatic alpha and beta cells
A panel of university-based scientists convened by The Endocrine Society recently reviewed the available literature on health effects of endocrine-disrupting chemicals (aka EDCs). The executive summary is available free online. Some excerpts:
The full Scientific Statement represents a comprehensive review of the literature on seven topics for which there is strong mechanistic, experimental, animal, and epidemiological evidence for endocrine disruption, namely: obesity and diabetes, female reproduction, male reproduction, hormone-sensitive cancers in females, prostate cancer, thyroid, and neurodevelopment and neuroendocrine systems. EDCs such as bisphenol A, phthalates, pesticides, persistent organic pollutants such as polychlorinated biphenyls, polybrominated diethyl ethers, and dioxins were emphasized because these chemicals had the greatest depth and breadth of available information.
* * *
Both cellular and animal models demonstrate a role for EDCs in the etiology of obesity and T2D [type 2 diabetes]. For obesity, animal studies show that EDC-induced weight gain depends on the timing of exposure and the age of the animals. Exposures during the perinatal period [the weeks before and after birth] trigger obesity later in life. New results covering a whole range of EDC doses have underscored the importance of nonmonotonic dose-response relationships; some doses induced weight increase, whereas others did not. Furthermore, EDCs elicit obesity by acting directly on white adipose tissue, al- though brain, liver, and even the endocrine pancreas may be direct targets as well.
Regarding T2D, animal studies indicate that some EDCs directly target beta and alpha cells in the pancreas, adipocytes, and liver cells and provoke insulin resistance together with hyperinsulinemia. These changes can also be associated with altered levels of adiponectin and leptin— often in the absence of weight gain. This diabetogenic action is also a risk factor for cardiovascular diseases, and hyperinsulinemia can drive diet-induced obesity. Epide- miological studies in humans also point to an association between EDC exposures and obesity and/or T2D; however, because many epidemiological studies are cross-sectional, with diet as an important confounding factor in humans, it is not yet possible to infer causality.
Bix at Fanatic Cook blog says foods of animal origin are the major source of harmful persistent organic pollutants, some of which act as ECDs.
Keep your eyes and ears open for new research reports on this critically important topic.
Steve Parker, M.D.
I’m hearing ads on the radio that many in the U.S., including children, are suffering from hunger. Nutrition science journals in the last few years are covering “food insecurity,” which many would assume means not having enough food or fearing the lack of food.
These concerns seem at odds with the fact that two-thirds of us are overweight or obese. So how many of us at normal or below-average weights suffer from food insecurity or hunger?
James Bovard breaks it down for you in an excellent article. Read the whole thing. Some morsels (heh):
- seven times as many (low income) children are obese as are underweight
- 40% of food stamp (SNAP) users are obese, compared to 30% in the overall U.S. adult population
- if the food stamp program would prohibit purchase of sugary drinks, it would prevent 141,000 children from becoming fat and save a quarter million adults from type 2 diabetes
Fat hungry people would be less hungry if they’d cut way back on refined, nutrient-poor carbohydrates, replacing with protein and healthy fats.
Steve Parker, M.D.
It’s time to re-commit to the program
It’s common on any weight-loss program to be cruising along losing weight as promised, then suddenly the weight loss stops although you’re still far from goal weight. This is the mysterious and infamous stall.
Once you know the cause for the stall, the way to break it becomes obvious. The most common reasons are:
- you’re not really following the full program any more; you’ve drifted off the path, often unconsciously
- instead of eating just until you’re full or satisfied, you’re stuffing yourself
- you need to start or intensify an exercise program
- you’ve developed an interfering medical problem such as adrenal insufficiency (rare) or an underactive thyroid; see your doctor
- you’re taking interfering medication such as a steroid; see your doctor
- your strength training program is building new muscle that masks ongoing loss of fat (not a problem!).
If you still can’t figure out what’s causing your stall, do a nutritional analysis of one weeks’ worth of eating, with a focus on daily digestible carb (net carbs) and calorie totals. You can do this analysis online at places like FitDay (http://fitday.com/) or Calorie Count (http://caloriecount.about.com/).
What you do with your data depends on whether you’re losing weight through portion control (usually reflecting calorie restriction) or carb counting. Most people lose weight with one of these two methods.
If you’re a carb counter, you may find you’ve been sabotaged by “carb creep”: excessive dietary carbs have insidiously invaded you. You need to cut back. Even if you’re eating very-low-carb, it’s still possible to have excess body fat, even gain new fat, if you eat too many calories from protein and fat. It’s not easy, but it’s possible.
Those who have followed a calorie-restriction weight loss model for awhile may have become lax in their record-keeping. The stall is a result of simply eating too much. Call it “portion creep.” You need to re-commit to observing portion sizes.
A final possible cause for a weight loss stall is that you just don’t need as many calories as you once did. Think about this. Someone who weighs 300 lb (136 kg) is eating perhaps 3300 calories a day just to maintain a steady weight. He goes on a calorie-restricted diet (2800/day) and loses a pound (0.4 kg) a week. Eventually he’s down to 210 lb (95.5 kg) but stalled, aiming for 180 lb (82 kg). The 210-lb body (95.5 kg) doesn’t need 3300 calories a day to keep it alive and steady-state; it only needs 2800 and that’s what it’s getting. To restart the weight loss process, he has to reduce calories further, say down to 2300/day. This is not the “slowed down metabolism” we see with starvation or very-low-calorie diets. It’s simply the result of getting rid of 90 pounds of fat (41 kg) that he no longer needs to feed.
Steve Parker, M.D.
Are you tired of this stock photo yet?
MedPageToday has the details. A quote:
In a computer modeling study, very obese men lost just over 8 years of life compared with normal-weight men, and very obese women lost as many as 6 years, Steven Grover, PhD, of McGill University, and colleagues reported online in the Lancet Diabetes and Endocrinology.
They also found that very obese men and women (defined as a body mass index [BMI] of 35 and higher) lost about 19 years of healthy life, defined as living free of chronic disease such as diabetes and cardiovascular disease.
Note that “very obese” in this context has a specific definition: body mass index 35 or higher. Calculate yours.
The number of life years lost to obesity and disease were highest for those who were very obese in young adulthood and presumably stayed obese for years. In other words, becoming very obese at age 60 is not as dangerous as at 25.
I first got interested in weight loss in the 1990s when I had an office-based primary care medical practice. It was obvious that many of the medical problems I was treating were related to years of obesity. Believe me, you’re much better off preventing those problems via diet and exercise.
In the 1990’s, both Dr. Dean Ornish’s vegetarian diet and Dr. Robert Atkins low-carb diet were very popular, and you couldn’t find any two diets that were more polar opposites. And do you remember Susan Powter and her “Stop the Insanity” diet? My desire to lead my patients onto the right path resulted in the first edition of my Advanced Mediterranean Diet.
Click for The Lancet study abstract.
Steve Parker, M.D.