Tag Archives: overweight

How to Overcome a Weight-Loss Stall

 

Strength Training Helps Get Excess Blood Sugar Out of Circulation, But Exercise Is Often Disappointing As A Weight-Loss Method

Strength training helps get excess blood sugar out of circulation, but exercise is often disappointing as a weight-loss method

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 or Calorie Count.

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.

Are you eating too many of these?

Are you eating too many of these?

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.

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Do Artificial Sweeteners Cause Diabetes and Overweight?

Would aspartame or stevia be healthier than those sugar cubes?

Would aspartame or stevia be healthier than those sugar cubes?

We don’t know with certainty yet. But a recent study suggests that non-caloric artificial sweeteners do indeed cause overweight and type 2 diabetes in at least some folks. The study at hand is very small, so I wouldn’t bet the farm on it. I’m not even changing any of my recommendations at this point.

exercise for weight loss and management, dumbbells

Too many diet sodas?

The proposed mechanism for adverse metallic effects is that the sweeteners alter the mix of germs that live in our intestines. That alteration in turn causes  the overweight and obesity. See MedPageToday for the complicated details. The first part of the article is about mice; humans are at the end.

Some quotes:

“Our results from short- and long-term human non-caloric sweetener consumer cohorts suggest that human individuals feature a personalized response to non-caloric sweeteners, possibly stemming from differences in their microbiota composition and function,” the researchers wrote.

The researchers further suggested that these individualized nutritional responses may be driven by personalized functional differences in the micro biome [intestinal germs or bacteria].

***

Diabetes researcher Robert Rizza, MD, of the Mayo Clinic in Rochester, Minn., who was not involved with the research, called the findings “fascinating.”

He noted that earlier research suggests people who eat large amounts of artificial sweeteners have higher incidences of obesity and diabetes. The new research, he said, suggests there may be a causal link.

“This was a very thorough and carefully done study, and I think the message to people who use artificial sweeteners is they need to use them in moderation,” he said. “Drinking 17 diet sodas a day is probably a bad idea, but one or two may be OK.”

I won’t argue with that last sentence!

Finally, be aware the several clinical studies show no linkage between human consumption of non-caloric artificial sweeteners and overweight, obesity, and T2 diabetes.

Steve Parker, M.D.

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Filed under Causes of Diabetes, Overweight and Obesity, Sugar Substitutes

Are We Fat Because We’re Eating Away From Home More?

So easy to over-eat!

So easy to over-eat!

The U.S. trend of increasing overweight and obesity started about 1970. I wonder if eating away from home is related to the trend. I found a USDA report with pertinent data from 1977 to 1995. It also has interesting info on snacking and total calories consumed. Some quotes:

“We define home and away-from-home foods based on where the foods are obtained, not where they are eaten. Food at home consists of foods purchased at a retail store, such as a grocery store, a convenience store, or a supermarket. Food away from home consists of foods obtained at various places other than retail stores (mainly food-service establishments).”

***

“Over the past two decades, the number of meals consumed has remained fairly stable at 2.6 to 2.7 per day. However, snacking has increased, from less than once a day in 1987–88 to 1.6 times per day in 1995. The increased popularity in dining out is evident as the proportion of meals away from home increased from 16 percent in 1977–78 to 29 percent in 1995, and the proportion of snacks away from home rose from 17 percent in 1977–78 to 22 percent in 1995. Overall, eating occasions (meals and snacks) away from home increased by more than two-thirds over the past two decades, from 16 percent of all eating occasions in 1977–78 to 27 percent in 1995.”

***

“Average caloric intake declined from 1,876 calories per person per day in 1977–78 to 1,807 calories per person per day in 1987–88, then rose steadily to 2,043 calories per person per day in 1995.”

***

“These numbers suggest that, when eating out, people either eat more or eat higher-calorie foods or both.”

Parker here. I’m well aware that these data points don’t prove that increased eating-out, increased snacking,  and increased total calorie consumption have caused our overweight and obesity problem. But they sure make you wonder, don’t they? None of these factors was on a recent list of potential causes of obesity.

If accurate, the increased calories alone could be the cause. Fast-food and other restaurants do all they possibly can to satisfy your cravings and earn your repeat business.

If you struggle with overweight, why not cut down on snacking and eating meals away from home?

Steve Parker, M.D.

Bonus:

Here’s a pie chart I found with more current and detailed information from the U.S. government (h/t Yoni Freedhoff):

feb13_feature_guthrie_fig03

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Dining Out and Obesity: Related?

No need to dine out if you have one of the four "Low-Carbing Among Friends" cookbooks

No need to dine out if you have one of the four “Low-Carbing Among Friends” cookbooks

The U.S. trend of increasing overweight and obesity started about 1970. I wonder if eating away from home is related to the trend. I found a USDA report with pertinent data from 1977 to 1995. It also has interesting info on snacking and total calories consumed. Some quotes:

“We define home and away-from-home foods based on where the foods are obtained, not where they are eaten. Food at home consists of foods purchased at a retail store, such as a grocery store, a convenience store, or a supermarket. Food away from home consists of foods obtained at various places other than retail stores (mainly food-service establishments).”

***

“Over the past two decades, the number of meals consumed has remained fairly stable at 2.6 to 2.7 per day. However, snacking has increased, from less than once a day in 1987-88 to 1.6 times per day in 1995. The increased popularity in dining out is evident as the proportion of meals away from home increased from 16 percent in 1977-78 to 29 percent in 1995, and the proportion of snacks away from home rose from 17 percent in 1977-78 to 22 percent in 1995. Overall, eating occasions (meals and snacks) away from home increased by more than two-thirds over the past two decades, from 16 percent of all eating occasions in 1977-78 to 27 percent in 1995.”

***

“Average caloric intake declined from 1,876 calories per person per day in 1977-78 to 1,807 calories per person per day in 1987-88, then rose steadily to 2,043 calories per person per day in 1995.”

***

“These numbers suggest that, when eating out, people either eat more or eat higher-calorie foods or both.”

Parker here. I’m well aware that these data points don’t prove that increased eating-out, increased snacking,  and increased total calorie consumption have caused our overweight and obesity problem. But they sure make you wonder, don’t they? None of these factors was on a recent list of potential causes of obesity.

If accurate, the increased calories alone could be the cause. Fast-food and other restaurants do all they possibly can to satisfy your cravings and earn your repeat business.

If you struggle with overweight, why not cut down on snacking and eating meals away from home?

Steve Parker, M.D.

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Do Low-Carb Diets Help Overweight Kids?

DietDoctor Andreas Eenfeldt has located three studies that answer in the affirmative. Click through to his blog.

Steve Parker, M.D.

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What Causes Obesity?

"It's been three months. That HCG should kick in right about now."

“It’s been three months. That HCG should kick in right about now.”

Isn’t it just ’cause we eat too much and exercise too little due to lack of discipline and willpower?

Science writer David Berreby has an article at Aeon suggesting it’s way more complicated than that. Even if we do eat too much, why do we? Some quotes:

And so we appear to have a public consensus that excess body weight (defined as a Body Mass Index of 25 or above) and obesity (BMI of 30 or above) are consequences of individual choice. It is undoubtedly true that societies are spending vast amounts of time and money on this idea. It is also true that the masters of the universe in business and government seem attracted to it, perhaps because stern self-discipline is how many of them attained their status. What we don’t know is whether the theory is actually correct.

***

As Richard L Atkinson, Emeritus Professor of Medicine and Nutritional Sciences at the University of Wisconsin and editor of the International Journal of Obesity, put it in 2005: ‘The previous belief of many lay people and health professionals that obesity is simply the result of a lack of willpower and an inability to discipline eating habits is no longer defensible.’

Like liver, skeletal muscle, and brain, our body fat is a tissue that is carefully regulated by genes, hormones, enzymes, etc., which I’ll lump together as “metabolism.” Regulatory metabolic processes for liver, muscle, and brain will be different from each other and from fat tissue. Some processes aid fat storage, others lead to fat breakdown and weight loss.

Mr. Berreby discusses various trendy factors that may directly alter fat tissue metabolic processes, leading to overweight and obesity. Here’s his list:

  • lack of sleep
  • viruses (e.g., Ad-36)
  • stress
  • bacteria (e.g., Methanobrevibacter smithii in the large intestine)
  • industrial chemical contaminants (e.g., BPA, heavy metals, detergents, sunscreen, fire retardants, cosmetics)
  • electrification (e.g., too much light exposure, especially at night)
  • heat and air conditioning
  • undernutrition (“starvation”) during pregnancy: the children hatched are more likely to be overweight or obese as adults
  • intergenerational influence (epigenetic)

Read all about it.

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Do Chemical Contaminants Cause Diabetes or Obesity?

"Today we're going to learn about odds ratios and relative risk."

“Today we’re going to learn about odds ratios and relative risk.”

Last year I watched part of a documentary called “Plastic Planet” on Current TV (Now Al Jazeera TV). It was alarming. Apparently chemicals are leaking out of plastics into the environment (or into foods contained by plastic), making us diabetic, fat, impairing our fertility, and God knows what else. The narrator talked like it was a sure thing. I had work to do at the hospital, so I didn’t see the whole thing. A couple chemicals I remember being mentioned are bisphenol A (BPA) and phthalates. I freaked my wife out when I mentioned it to her—she went and bought some storage containers for leftover food the next day. I always take my lunch to work in plastic containers and often cover microwaved food with Glad Press’n Seal plastic wrap.

A few days later I saw a report of sperm counts being half of what they were just half a century ago. (It’s debatable.) Environmental contaminants were mentioned as a potential cause.

So I spent a couple hours trying to figure out if chemical contamination really is causing obesity and type 2 diabetes. In the U.S., childhood obesity has tripled since 1980, to a current rate of 17%. Even preschool obesity (age 2-5) doubled from 5 to 10% over that span. In industrial societies, even our pets, lab animals (rodents and primates), and feral rats are getting fatter! The ongoing epidemics of obesity and type 2 diabetes, and our lack of progress in preventing and reversing them, testify that we may not have them figured out and should keep looking at root causes to see if we’re missing anything.

Straightaway, I’ll tell you it’s not easy looking into this issue. The experts are divided. The studies are often contradictory or inconsistent. One way to determine the cause of a condition or illness is to apply Bradford Hill criteria (see bottom of page for those). We could reach a conclusion faster if we did controlled exposure experiments on humans, but we don’t. We look at epidemiological studies and animal studies that don’t necessarily apply to humans.

Regarding type 1 diabetes and chemical contamination, we have very little data. I’ll not mention type 1 again.

What Does the Science Tell Us?

For this post I read a couple pertinent scientific reviews published in 2012, not restricting myself to plastics as a source of chemical contaminants.

The first was REVIEW OF THE SCIENCE LINKING CHEMICAL EXPOSURES TO THE HUMAN RISK OF OBESITY AND DIABETES from non-profit CHEM Trust, written by a couple M.D., Ph.D.s. I’ll share some quotes and my comments. My clarifying comments within a quote are in [brackets].

“It should be noted that diabetes itself has not been caused in animals exposed to these chemicals [a long list] in laboratory studies, but metabolic disruption closely related to the pathogenesis of Type 2 diabetes has been reported for many chemicals.”

“In 2002, Paula Baillie-Hamilton proposed a hypothesis linking exposure to chemicals with obesity, and this is now gaining credence. Exposure to low concentrations of some chemicals leads to weight gain in adult animals, while exposure to high concentrations causes weight loss.”

“The obesogen hypothesis essentially proposes that exposure to chemicals foreign to the body disrupts adipogenesis [fat tissue growth] and the homeostasis and metabolism of lipids (i.e., their normal regulation), ultimately resulting in obesity. Obesogens can be functionally defined as chemicals that alter homeostatic metabolic set-points, disrupt appetite controls, perturb lipid homeostasis to promote adipocyte hypertrophy [fat cells swelling with fat], stimulate adipogenic pathways that enhance adipocyte hyperplasia [increased numbers of fat cells] or otherwise alter adipocyte differentiation during development. These proposed pathways include inappropriate modulation of nuclear receptor function; therefore, the chemicals can be termed EDCs [endocrine disrupting chemicals].”

Don't assume mouse physiology is the same as human's

Don’t assume mouse physiology is the same as human’s

Literature like this talks about POPs: persistent organic pollutants, sometimes called organohalides. The POPs and other chemical contaminants that are currently suspicious for causing obesity and type 2 diabetes include arsenic, pesticides, phthalates, metals (e.g., cadmium, mercury, organotins), brominated flame retardants, DDE (dichloro-diphenyldichloroethylene), PCBs (polychlorinated biphenyls), trans-nonachlor, dioxins.

Another term you’ll see in this literature is EDCs: endocrine disrupting chemicals. These chemicals mess with hormonal pathways. EDCs that mimic estrogen are linked to obesity and related metabolic dysfunction. Some of the chemicals in the list above are EDCs.

The fear—and some evidence—is that contaminants, whether or not EDCs, are particularly harmful to embryos, fetuses, and infants. For instance, it’s pretty well established that mothers who smoked while pregnant predispose their offspring to obesity in adulthood. (Epigenetics, anyone?) Furthermore, at the right time in the life cycle, it may only take small amounts of contaminants to alter gene expression for the remainder of life. For instance, the number of fat cells we have is mostly determined some time in childhood (or earlier?). As we get fat, those cells simply swell with fat. When we lose weight, those cells shrink, but the total cell number is unchanged. What if contaminant exposure in childhood increases fat cell number irrevocably? Does that predispose to obesity later in life?

The authors note that chemical contaminants are more strongly linked to diabetes than obesity. They do a lot of hemming and hawing, using “maybe,” “might,” “could,” etc. They don’t have a lot of firm conclusions other than “Hey, people, we better wake up and look into this further, and based on the precautionary principle, we better cut back on environmental chemical contamination stat!” [Not a direct quote.] It’s clear they are very concerned about chemical contaminants as a public health issue.

Here’s the second article I read: Role of Environmental Chemicals in Diabetes and Obesity: A National Toxicology Program Workshop Review. About 50 experts were empaneled. Some quotes and my comments:

“Overall, the review of the existing literature identified linkages between several of the environmental exposures and type 2 diabetes. There was also support for the “developmental obesogen” hypothesis, which suggests that chemical exposures may increase the risk of obesity by altering the differentiation of adipocytes [maturation and development of fat cells] or the development of neural circuits that regulate feeding behavior. The effects may be most apparent when the developmental [early life] exposure is combined with consumption of a high-calorie, high-carbohydrate, or high-fat diet later in life.”

“The strongest conclusion from the workshop was that nicotine likely acts as a developmental obesogen in humans. This conclusion was based on the very consistent pattern of overweight/obesity observed in epidemiology studies of children of mothers who smoked during pregnancy (Figure 1) and was supported by findings from laboratory animals exposed to nicotine during prenatal [before birth] development.”

I found some data that don’t support that conclusion, however. Here’s a graph of U.S. smoking rates over the years since 1944. Note that the smoking rate has fallen by almost half since 1983, while obesity rates, including those of children, are going the opposite direction. If in utero cigarette smoke exposure were a major cause of U.S. childhood obesity, we’d be seeing less, not more, childhood obesity. I suppose we could still see a fall-off in adult obesity rates over the next 20 years, reflecting lower smoking rates.  But I doubt that will happen.

The CDC suggests a slight drop in childhood obesity in recent years (2010 data).

“The group concluded that there is evidence for a positive association of diabetes with certain organochlorine POPs [persistent organic pollutants]. Initial data mining indicated the strongest associations of diabetes with trans-nonachlor, DDT (dichloro-diphenyltrichloroethane)/DDE (dichloro-diphenyldichloroethylene)/DDD (dichloro-chlorophenylethane), and dioxins/dioxin-like chemicals, including polychlorinated biphenyl (PCBs). In no case was the body of data considered sufficient to establish causality [emphasis added].”

“Overall, this breakout group concluded that the existing data, primarily based on animal and in vitro studies [no live animals involved], are suggestive of an effect of BPA on glucose homeostasis, insulin release, cellular signaling in pancreatic β cells, and adipogenesis. The existing human data on BPA and diabetes (Lang et al. 2008Melzer et al. 2010) available at the time of the workshop were considered too limited to draw meaningful conclusions. Similarly, data were insufficient to evaluate BPA as a potential risk factor for childhood obesity.”

“It was not possible to reach clear conclusions about BPA and obesity from the existing animal data. Although several studies report body weight gain after developmental exposure, the overall pattern across studies is inconsistent.”

“The pesticide breakout group concluded the epidemiological, animal, and mechanistic data support the biological plausibility that exposure to multiple classes of pesticides may affect risk factors for diabetes and obesity, although many significant data gaps remain.”

“Recently, the focus of investigations has shifted toward studies designed to understand the consequences of developmental exposure to lower doses of organophosphates [insecticides], and the long-term effects of these exposures on metabolic dysfunction, diabetes, and obesity later in life. [All or nearly all the studies cited here were rodent studies, not human.] The general findings are that early-life exposure to otherwise subtoxic levels of organophosphates results in pre-diabetes, abnormalities of lipid metabolism, and promotion of obesity in response to increased dietary fat.”

In case it’s not obvious, remember that “association is not the same as causation.” For example, in the Northern hemisphere, higher swimsuit purchases are associated with summer. Swimsuit sales and summer are linked (associated), but one doesn’t cause the other. Swimsuit purchases are caused by the desire to go swimming, and that’s linked to warm weather.

In at least one of these two review articles, I looked carefully at the odds ratios of various chemicals linked to adverse outcomes. One way this is done is too measure the blood or tissue levels of a contaminant in a population, then compare the adverse outcome rates in animals with the highest and lowest levels of contamination. For instance, if those with the highest contamination have twice the incidence of diabetes as the least contaminated, the odds ratio is 2. You could also call it the relative risk. Many of the potentially harmful chemicals we’re considering have a relative risk ratio of 1.5 to 3. Contrast those numbers with the relative risk of death from lung cancer in smokers versus nonsmokers: the relative risk is 10. Smokers are 10 times more likely to die of lung cancer. That’s a much stronger association and a main reason we decided smoking causes lung cancer. Odds ratios under two are not very strong evidence when considering causality; we’d like to have more pieces of the puzzle.

These guys flat-out said arsenic is not a cause of diabetes in the U.S.

Overall, the authors of the second article I read were clearly less alarmed than those of the first. Could the less-alarmed panelists have been paid off by the chemical industry to produce a less scary report, so as not to jeopardize their profits? I don’t have the resources to investigate that possibility. The workshop was organized (and paid for, I assume) by the U.S. government, but that’s no guarantee of pure motivation by any means.

You need a break. Enjoy.

You need a break. Enjoy.

My Conclusions

For sure, if I were a momma rat contemplating pregnancy, I’d avoid all those chemicals like the plague!

It’s premature to say that these chemical contaminants are significant causes of obesity and type 2 diabetes in humans. That’s certainly possible, however. We’ll have to depend on unbiased scientists to do more definitive research for answers, which certainly seems a worthwhile endeavor. Something tells me the chemical producers won’t be paying for it. Universities or governments will have to do it.

You should keep your eyes and ears open for new evidence.

There’s more evidence for chemical contaminants as a potential cause of type 2 diabetes than for obesity. Fetal and childhood exposure may be more harmful than later in life.

If I were 89-years-old, I wouldn’t worry about these chemicals causing obesity or diabetes. For those quite a bit younger, taking action to avoid these environmental contaminants is optional. As for me, I’m drinking less water out of plastic bottles and more tap water out of glass or metal containers. Yet I’m not sure which water has fewer contaminants.

Humans, particularly those anticipating pregnancy and child-rearing, might be well advised to minimize exposure to the aforementioned chemicals. For now, I’ll leave you to your own devices to figure out how to do that. Good luck.

Why not read the two review articles I did and form your own opinion?

Unless the chemical industry is involved in fraud, bribery, obfuscation, or other malfeasance, the Plastic Planet documentary gets ahead of the science. I’m less afraid of my plastic containers now.

Steve Parker, M.D.

Additional Resources:

Sarah Howard at Diabetes and the Environment (focus on type 1 but much on type 2 also).

Jenny Ruhl, who thinks chemical contaminants are a significant cause of type 2 diabetes (search her site).

From Wikipedia:

The Bradford Hill criteria, otherwise known as Hill’s criteria for causation, are a group of minimal conditions necessary to provide adequate evidence of a causal relationship between an incidence and a consequence, established by the English epidemiologist Sir Austin Bradford Hill (1897–1991) in 1965.

The list of the criteria is as follows:

  1. Strength: A small association does not mean that there is not a causal effect, though the larger the association, the more likely that it is causal.
  2. Consistency: Consistent findings observed by different persons in different places with different samples strengthens the likelihood of an effect.
  3. Specificity: Causation is likely if a very specific population at a specific site and disease with no other likely explanation. The more specific an association between a factor and an effect is, the bigger the probability of a causal relationship.
  4. Temporality: The effect has to occur after the cause (and if there is an expected delay between the cause and expected effect, then the effect must occur after that delay).
  5. Biological gradient: Greater exposure should generally lead to greater incidence of the effect. However, in some cases, the mere presence of the factor can trigger the effect. In other cases, an inverse proportion is observed: greater exposure leads to lower incidence.
  6. Plausibility: A plausible mechanism between cause and effect is helpful (but Hill noted that knowledge of the mechanism is limited by current knowledge).
  7. Coherence: Coherence between epidemiological and laboratory findings increases the likelihood of an effect. However, Hill noted that “… lack of such [laboratory] evidence cannot nullify the epidemiological effect on associations”.
  8. Experiment: “Occasionally it is possible to appeal to experimental evidence”.
  9. Analogy: The effect of similar factors may be considered.

Science-Based Medicine blog has more on Hill’s criteria.

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