Category Archives: Overweight and Obesity

February 19, 2014 · 5:04 PM

Ketogenic Diet Overview

"Waiter, I didn't order sushi!"

“Waiter, I didn’t order sushi!”

Below is my contribution to Low-Carbing Among Friends—Vol. 4, which is an excellent source of low-carb recipes. Get the whole series so you’ll never suffer from diet boredom!

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We’re starting to see a resurgence of interest in ketogenic diets for weight loss and management, at least in the United States. Also called “very-low-carb diets,” ketogenic diets have been around for over a hundred years. A few writers in the vanguard recently are Jimmy Moore, Dr. Peter Attia, and Dr. Georgia Ede. Before them, Dr. Robert Atkins was a modern pioneer with his famous Atkins Diet and its Induction Phase.

What is a Ketogenic Diet?

There are many different programs but they tend to share certain characteristics. They restrict digestible carbohydrate consumption to 50 or fewer grams a day, sometimes under 20 grams. This totally eliminates or drastically reduces some foods, such as grains, beans, starchy vegetables (corn, potatoes, peas, etc), milk, and sugar. Nor can you have products made from these, such as bread, cookies, pies, cakes, potato and corn chips, and candy. You eat meat, eggs, fish, chicken, certain cheeses, nuts, low-carb vegetables (e.g., salad greens, broccoli, green beans, cauliflower), and oils. Total calorie consumption is not restricted; you count carb grams rather than calories. This is a radical change in eating for most people.

Raspberries and blackberries are low-carb fruits

Raspberries and blackberries are low-carb fruits

You’re may be wondering what “ketogenic” means. First, understand that your body gets nearly all its energy either from fats, or from carbohydrates like glucose and glycogen. In people eating normally, 60% of their energy at rest comes from fats. In a ketogenic diet, the carbohydrate content of the diet is so low that the body has to break down even more of its fat to supply energy needed by most tissues. Fat breakdown generates ketone bodies in the bloodstream. Hence, “ketogenic diet.” Some of the recent writers are using the phrase “nutritional ketosis” to summarize this metabolic state.

Ketogenic Versus Traditional Calorie-Restricted Dieting

Are there advantages to ketogenic diets for weight loss and management? Numerous recent studies have demonstrated superior weight-loss results with very-low-carb diets as compared to traditional calorie-restricted diets. Weight loss is often faster and more consistently in the range of one or two pounds (0.5 to 0.9 kg) a week. Very-low-carb dieters have less trouble with hunger. If you do get hungry, there’s always something you can eat. From a practical, day-to-day viewpoint, these diets can be easier to follow, with a bit less regimentation than calorie-restricted plans.

Ketogenic diets typically lower blood sugar levels, which is important for anyone with diabetes, prediabetes, and metabolic syndrome. We see higher levels of HDL cholesterol (the good kind), lower triglyceride levels, and a shift in LDL cholesterol to the “large fluffy” kind, all of which may reduce the risk of heart disease. Getting even further into the science weeds, very-low-carb diets reduce insulin levels in people who often have elevated levels (hyperinsulinemia), which may help reduce chronic diseases like type 2 diabetes, high blood pressure, some cancers, and coronary heart disease.  Clearly, ketogenic diets work well for a significant portion of the overweight population, but not for everybody.

Sounds great so far! So why aren’t very-low-carb diets used more often? Many dieters can’t live with the restrictions. Your body may rebel against the switch from a carbohydrate-based energy metabolism to one based on fats. Most of us live in a society or subculture in which carbohydrates are everywhere and they’re cheap; temptation is never-ending.

What Could Go Wrong on a Ketogenic Diet?

Very-low-carb ketogenic diets have been associated with headaches, bad breath, easy bruising, nausea, fatigue, aching, muscle cramps, constipation, and dizziness, among other symptoms.

“Induction flu” may occur around days two through five, consisting of achiness, easy fatigue, and low energy. Atkins dieters came up with the term. It usually clears up after a few days. Some people think of induction flu as a withdrawal syndrome from sugar or refined carbohydrate. My conception is that it’s simply an adjustment period for your body to switch from a carbohydrate-based energy system to one based on fat. Your body cells need time to rev up certain enzymes systems while mothballing other enzymes. To prevent or minimize induction flu, Drs. Stephen Phinney, Jeff Volek, and Eric Westman routinely recommend eating 1/2  tsp (2.5 ml) of table salt daily.

Very-low-carb ketogenic diets may have the potential to cause osteoporosis (thin, brittle bones), kidney stones, low blood pressure, constipation, gout, high uric acid in the blood, excessive loss of sodium and potassium in the urine, worsening of kidney disease, deficiency of calcium and vitamins A, B, C, and D, among other adverse effects. From a practical viewpoint, these are rarely seen, and many experts say they don’t occur in a well-designed ketogenic diet eaten by an essentially healthy person. I favor ketogenic diets designed by physicians or dietitians. In view of these potential adverse effects, however, it’s a good idea to run your ketogenic diet of choice by your personal physician before you get started. This is especially important if you have diabetes, chronic kidney or liver disease, or a history of gout, low blood pressure, or kidney stones.

Athletic individuals who perform vigorous exercise should expect a deterioration in performance levels during the first four weeks or so of any ketogenic very-low-carb diet. Again, the body needs that time to adjust to burning mostly fat for fuel rather than carbohydrate.

Competitive weightlifters or other anaerobic athletes (e.g., sprinters) may be hampered by the low muscle glycogen stores that accompany ketogenic diets. They may need more carbohydrates, perhaps 150 grams a day.

What’s Next After Losing Weight on a Ketogenic Diet?

Caprese salad: mozzarella cheese, tomatoes, basil, extra virgin olive oil

Caprese salad: mozzarella cheese, tomatoes, basil, extra virgin olive oil

A majority of folks eventually increase their carbohydrate consumption above 50 grams a day, which usually takes them out of nutritional ketosis. If they return to the typical 200-300 grams a day that most people eat, they’ll probably gain the lost weight back. Many have found, however, that they can go up to 70-100 grams and maintain at a happy weight. A well-designed program should give careful instructions on the transition out of ketosis and avoidance of regain.

To see a ketogenic diet I designed for my patients, click here.

Steve Parker, M.D.

PS: Another ketogenic diet blogger I’ve been following lately is ItsTheWooo (The Scribble Pad), a nurse who lost major weight on the diet. And don’t overlook Amber and Z. Wilcox-O’Hearn at The Ketogenic Diet for Health.

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January 14, 2014 · 1:23 PM

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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January 6, 2014 · 1:51 AM

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. 2008; Melzer 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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December 7, 2013 · 6:41 AM

Sugary Drinks Linked to Overweight in Preschoolers

…according to an article at MedPageToday. A sample:

DeBoer and colleagues evaluated the effect of sugary drinks on body mass index in 9,600 children evaluated at ages 9 months, 2 years, 4 years, and 5 years, who were enrolled in the Early Childhood Longitudinal Survey — Birth Cohort, a representative survey of the U.S. population of children born in 2001.

Parents answered survey questions about beverage intake at ages 2, 4, and 5. Sugar-sweetened beverages were defined as soda, sports drinks, and fruit drinks that were not 100% fruit juice. They also looked at when the drinks were consumed — such as at meals or with snacks — and if the child was a regular or infrequent/nondrinker.

diabetic diet, low-carb mediterranean diet

Why not teach your kids to cook?

Toddlers drinking at least one sugary drink daily were much more likely to have mothers who were overweight or obese. The sugared-up kids also watched more TV and drank less milk.

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November 26, 2013 · 3:52 AM

Do Heated Buildings Cause Obesity? Does Cold Exposure Prevent It?

diabetic mediterranean diet paleobetic diet, advanced mediterranean diet

Are heated buildings making us fat?

Dr. Stephan Guyenet thinks they might. It’s not so much central heat as it is failing to expose our bodies adequately to temperatures around 60° F (15.6° C) or lower on a regular basis. Here’s a human experiment Dr. G wrote about:

The second study went further, using a longer cold exposure protocol to investigate changes in fat mass among people with low brown fat activity at baseline (4).  Researchers exposed volunteers to 63 F (17 C) air for two hours a day over a six-week period; again I assume they were lightly clothed.  As in the previous study, they observed an increase in brown fat activity with cold training, and they found that calorie expenditure was higher when subjects were in the ‘cold’ air.  After six weeks of training, body fat mass had declined by about 5 percent.  This is despite the fact that all subjects were lean to begin with!

Read the rest.

I thought this study tied in with that one showing an inverse relationship between altitude and obesity. Environmental temperature rises roughly 3° F with every 1,000 feet (305 meters). But the altitude study controlled for (accounted for) temperature, meaning that the temperature had nothing to do with the association.

Somebody’s probably already tried to link environmental temperatures—whether inside the house or out—to obesity rates. Let me know if you find it.

—Steve

Addendum (after a little searching):

A few minutes at Pubmed.gov revealed this 2013 abstract:

Objective: Raised ambient temperatures may result in a negative energy balance characterized by decreased food intake and raised energy expenditure. This study tested whether indoor temperatures above the thermoneutral zone for clothed humans (approx. 23 o C) were associated with a reduced body mass index (BMI). Design and Methods: Participants were 100,152 adults (≥ 16 years) drawn from 13 consecutive annual waves of the nationally representative Health Survey for England (1995 – 2007). Results: BMI levels of those residing in air temperatures above 23 o C were lower than those living in an ambient temperature of under 19 o C (b = -.233, SE =.053, p <.001), in analyses that adjusted for participant age, gender, social class, health and the month/year of assessment. Robustness tests showed that high indoor temperatures were associated with reduced BMI levels in winter and non-winter months and early (1995 – 2000) and later (2001 – 2007) survey waves. Including additional demographic, environmental, and health behavior variables did not diminish the link between high indoor temperatures and reduced BMI. Conclusions: Elevated ambient indoor temperatures are associated with low BMI levels. Further research is needed to establish the potential causal nature of this relationship.

And consider this abstract, probably from the altitude study I mentioned:

http://www.ncbi.nlm.nih.gov/pubmed/23357956

“There was an approximately parabolic relationship between mean annual temperature and obesity, with maximum prevalence in counties with average temperatures near 18 °C [64.4° F].”

I don’t have the full article, but “parabolic” in this context probably means the obesity incidence was highest at 64.4° F, with lower obesity incidence both above and below 64.4°.

Of course, living in a particular environment doesn’t equate to exposing yourself to outdoor temperatures. But it makes sense that someone living in a cold environment will have more cold exposure than someone in a hot climate.

Perhaps 64.4° F is a sweet spot for efficient body temp regulation and energy partitioning. Living at temps significantly above or below that may cost you energy-wise: you expend extra calories maintaining a normal body temperature, tending to result in lower obesity incidence.

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November 2, 2013 · 5:04 PM

Canadian Study Finds Abdominal Obesity Health Markers Much Improved With Mediterranean Diet and High-Intensity Interval Training

…according to the Heart and Stroke Foundation. Some quotes:

The study found an average reduction in waist circumference of eight centimeters, a reduction in systolic blood pressure of 6 mm Hg and an aerobic fitness improvement of 15 per cent over the first nine months of the study.

Improvements in waist circumference, blood pressure and fitness can lead to numerous other health benefits including a reduced risk of developing high blood pressure, as well as improving osteoarthritis symptoms, quality of life, physical functioning, and cognition.

The high-intensity interval training was done two or three times a week over 20-30 minutes each session. Click for an example of HIIT on a stationary bike. More basic info on HIIT.

The classic Mediterranean diet has too many carbohydrates for many diabetics, although it’s better for them than the Standard American Diet. That’s why I devised the Low-Carb Mediterranean Diet.

Steve Parker, M.D.

Steve Parker MD, low-carb diet, diabetic diet

Olives, olive oil, and vinegar: classic Mediterranean foods

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April 13, 2013 · 2:00 AM

Periodic Tests, Treatments, and Goals for PWDs (Persons With Diabetes)

If you don't like your physician, find a new one

If you don’t like your physician, find a new one

So, you’ve got diabetes. You’re trying to deal with it or you wouldn’t be here. You’ve got a heck of a lot of medical information to master.

Unless you have a good diabetes specialist physician on your team, you may not be getting optimal care. Below are some guidelines you may find helpful. The goal is to prevent diabetes complications. Many primary care physicians will not be up-to-date on the guidelines. Don’t hesitate to discuss them with your doctor. Nobody cares as much about your health as you do.

Annual Tests

The American Diabetes Association (ADA) recommends the following items be done yearly (except as noted) in non-pregnant adults with diabetes. (Incidentally, I don’t necessarily agree with all ADA guidelines.) The complete ADA guidelines are available on the Internet.

  • Lipid profile (every two years if results are fine and stable)
  • Comprehensive foot exam
  • Screening test for distal symmetric polyneuropathy: pinprick, vibration, monofilament pressure sense
  • Serum creatinine and estimate of glomerular filtration rate (MDRD equation)
  • Test for albumin in the urine, such as measurement of albumin-to-creatinine ratio in a random spot urine specimen
  • Comprehensive eye exam by an ophthalmologist or optometrist (if exam is normal, every two or three years is acceptable)
  • Hemoglobin A1c at least twice a year, but every three months if therapy has changed or glucose control is not at goal
  • Flu shots

Other Vaccinations, Weight Loss, Diabetic Diet, Prediabetes, Alcohol, Exercise, Etc.

Additionally, the 2013 ADA guidelines recommend:

  • Pneumococcal vaccination. “A one time re-vaccination is recommended for individuals >64 years of age previously immunized when they were <65 years of age if the vaccine was administered >5 years ago.” Also repeat the vaccination after five years for patients with nephrotic syndrome, chronic kidney disease, other immunocompromised states (poor ability to fight infection), or transplantation.
  • Hepatitis B vaccination to unvaccinated adults who are 19 through 59 years of age.
  • Weight loss for all overweight diabetics. “For weight loss, either low-carbohydrate, low-fat calorie-restricted, or Mediterranean diets may be effective in the short-term (up to two years).” For those on low-carb diets, monitor lipids, kidney function, and protein consumption, and adjust diabetic drugs as needed. The optimal macronutrient composition of weight loss diets has not been established. (Macronutrients are carbohydrates, proteins, and fats.)
  • “The mix of carbohydrate, protein, and fat may be adjusted to meet the metabolic goals and individual preferences of the person with diabetes.” “It must be clearly recognized that regardless of the macronutrient mix, total caloric intake must be appropriate to weight management goal.”
  • “A variety of dietary meal patterns are likely effective in managing diabetes including Mediterranean-style, plant-based (vegan or vegetarian), low-fat and lower-carbohydrate eating patterns.”
  • “Monitoring carbohydrate, whether by carbohydrate counting, choices, or experience-based estimation, remains a key strategy in achieving glycemic control.”
  • Limit alcohol to one (women) or two (men) drinks a day.
  • Limit saturated fat to less than seven percent of calories.
  • During the initial diabetic exam, screen for peripheral arterial disease (poor circulation). Strongly consider calculation of the ankle-brachial index for those over 50 years of age; consider it for younger patients if they have risk factors for poor circulation.
  • Those at risk for diabetes, including prediabetics, should aim for moderate weight loss (about seven percent of body weight) if overweight. Either low-carbohydrate, low-fat calorie-restricted, or Mediterranean diets may be effective in the short-term (up to 2 years). Also important is exercise: at least 150 minutes per week of moderate-intensity aerobic activity. “Individuals at risk for type 2 diabetes should be encouraged to achieve the U.S. Department of Agriculture (USDA) recommendation for dietary fiber (14 g fiber/1,000 kcal) and foods containing whole grains (one-half of grain intake).” Limit intake of sugar-sweetened beverages.
  • “Adults with diabetes should be advised to perform at least 150 min/week of moderate-intensity aerobic physical activity (50–70% of maximum heart rate), spread over at least 3 days/week with no more than two consecutive days without exercise. In the absence of contraindications, adults with type 2 diabetes should be encouraged to perform resistance training at least twice per week.”
  • Screening for coronary artery disease before an exercise program is depends on the physician judgment on a case-by-case basis. Routine screening is not recommended.
Steve Parker MD, low-carb diet, diabetic diet

Olive, olive oil, and vinegar: classic Mediterranean foods

Obviously, some of my dietary recommendations conflict with ADA guidelines. The experts assembled by the ADA to compose guidelines were well-intentioned, intelligent, and hard-working. The guidelines are supported by 528 scientific journal references. I greatly appreciate the expert panel’s work. We’ve simply reached some different conclusions. By the same token, I’m sure the expert panel didn’t have unanimous agreement on all the final recommendations. I invite you to review the dietary guidelines yourself, discuss with your personal physician, then decide where you stand.

General Blood Glucose Treatment Goals

The ADA in 2013 suggests these therapeutic goals for non-pregnant adults:

  • Fasting blood glucoses: 70 to 130 mg/dl (3.9 to 7.2 mmol/l)
  • Peak glucoses one to two hours after start of meals: under 180 mg/dl (10 mmol/l)
  • Hemoglobin A1C: under 7%
  • Blood pressure: under 140/80 mmHg
  • LDL cholesterol: under 100 mg/dl (2.6 mmol/l). (In established cardiovascular disease: <70 mg/dl or 1.8 mmol/l may be a better goal.)
  • HDL cholesterol: over 40 mg/dl (1.0 mmol/l) for men and over 50 mg/dl (1.3 mmol/l) for women
  • Triglycerides: under 150 mg/dl (1.7 mmol/l)

The American Association of Clinical Endocrinologists (AACE) in 2011 proposed somewhat “tighter” blood sugar goals for non-pregnant adults:

  • Fasting blood glucoses: under 110 mg/dl (6.11 mmol/l)
  • Peak glucoses 2 hours after start of meals: under 140 mg/dl (7.78 mmol/l)
  • Hemoglobin A1C: 6.5% or less

The ADA reminds clinicians, and I’m sure the AACE guys agree, that diabetes control goals should be individualized, based on age and life expectancy of the patient, duration of diabetes, other diseases that are present, individual patient preferences, and whether the patient is able to easily recognize and deal with hypoglycemia. I agree completely.

Steve Parker, M.D.

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February 12, 2013 · 7:32 AM

Once Again, Low-Carbohydrate Ketogenic Diet Beats Low-Calorie For Overweight Diabetes

Kuwait City and Towers

Kuwait City and Towers

A low-carbohydrate ketogenic diet is safe, effective, and superior to a low-calorie diet in type 2 diabetics, according to a report last year in Nutrition.

Kuwaiti researchers gave 102 adult overweight diabetic men and women their choice of diet: 78 chose ketogenic, 24 went low-calorie.  Average age was 37, average weight 211 lb (96 kg).  The study lasted six months.  The ketogenic diet was very much Atkins-style, starting out at 20 grams of carbohydrate daily.  Once good weight-loss progress was made, and if carb cravings were an issue, dieters could increase their carbs in small increments weekly.

This is all they said about the low-calorie diet: “Participants in the low-calorie diet group were given appropriate guidelines and a sample low-calorie diet menu of 2200 calories is presented in Table 1” (it’s typical and reasonable).

What Did They Find?

The low-carb ketogenic dieters lost 12% of body weight, compared to 7% lost by the low-calorie dieters.  Furthermore, the ketogenic dieters showed significant lowering of total cholesterol, LDL cholesterol (bad cholesterol), and triglycerides.  HDL cholesterol (good cholesterol) rose.  The low-calorie dieters seem to have had a significant drop in LDL cholesterol, but no changes in the other lipids.

Fasting blood sugar levels dropped significantly in both groups, but more in the ketogenic dieters.  Both groups started with fasting blood sugars around 162 mg/dl (9 mmol/l) and fell to 108 mg/dl (6 mmol/l) in the ketogenic group and to 126 mg/dl (7 mmol/l) in the low-calorie group.

Glycosylated hemoglobin (hemoglobin A1c) levels fell in both groups, more so in the ketogenic dieters.  The drop was statistically significant in the ketogenic group, but the authors were unclear about that in the low-calorie dieters.  It appears hemoglobin A1c fell from 7.8% to 6.3% with the ketogenic diet (the units given for glycosylated hemoglobin were stated as mg/dl).  In the low-calorie dieters, hemoglobin A1c fell from 8.2 to 7.7%.

What’s Odd About This Study?

The title of the research report indicates a study of diabetics, but only about 25% of study participants had diabetes (total subjects = 363).  (The figures I share above are for the diabetics only.)

Glycosylated hemoglobin, a test of overall diabetes control, is reported in Fig. 1 in terms of mg/dl.  That’s nearly always reported as a percentage, not mg/dl.  Misprint?

None of the participants dropped out of the study.  That’s incredible, almost unbelievable.

The low-calorie diet was poorly described.  Were 140-lb women and 250-lb men all put on the same calorie count?

Food diaries were kept, but the authors report nothing about compliance and actual food intake.

Clearly, some of these diabetics were on insulin and other diabetic drugs.  The authors note necessary reductions in drug dosages for the ketogenic group but don’t say much about the other dieters.  They imply that the drug reductions in the low-calorie group were minimal or nonexistent.

Grand Mosque of Kuwait

Grand Mosque of Kuwait

So What?

Calorie-restricted diets are effective in overweight type 2 diabetics, but ketogenic diets are even better.

The effectiveness and safety of ketogenic diets for overweight type 2 diabetics has been demonstrated in multiple other populations, so this study is not surprising.  We’ve seen these lipid improvements before, too.

The favorable lipid changes on low-carb ketogenic diets would tend to reduce future heart and vascular disease.

I know little about Kuwaiti culture and genetics.  Their contributions to the results here, as compared with other populations, is unclear to me.  Type 2 diabetes is spreading quickly through the Persian Gulf, so this research may have wide applicability there.

Steve Parker, M.D.

Reference:  Hussain, Talib, et al.  Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes.  Nutrition, 2012; 28(10): 1016-21. doi: 10.1016/j.nut.2012.01.016

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October 17, 2012 · 6:05 AM

The Two Secrets to Prevention of Weight Regain

Researchers are constantly searching for safe, effective weight loss pills.  More helpful would be a pill that prevents weight regain.  Weight loss is relatively easier.

Regain of lost body fat is the most problematic area in the field of weight management.  Whoever solves this problem for good will win a Nobel Prize in Medicine.  Why do most diets ultimately fail over the long run?  Because people go back to their old habits.  Here are the two secrets to prevention of weight regain:

  1. Restrained eating
  2. Regular physical activity

“Successful losers” apply self-restraint on an almost daily basis, avoiding food they know will lead to weight regain.  They limit how much they eat.  They consciously choose not to return to their old eating habits, despite urges to the contrary.

The other glaring difference is that, compared to regainers, the successful losers are physically active.  Oftentimes, they exercised while losing weight, and almost always continue to exercise in the maintenance phase of their program.  This is true in at least eight out of 10 cases.  It’s clear that regular exercise isn’t always needed, but it dramatically increases your chances of long-term success.

Steve Parker, M.D.

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October 12, 2012 · 1:26 AM

Does Decreased Activity Explain Recent Overweight Trend?

Less active

Much of the globe has seen a significant decline in populaton-wide physical activity over the last few decades, according to Nike-sponsored research reported in Obesity Reviews.

Countries involved with the study are the U.S., U.K., Brazil, China, and India.  How did they measure activity levels?

Using detailed historical data on time allocation, occupational distributions, energy expenditures data by activity, and time-varying measures of metabolic equivalents of task (MET) for activities when available, we measure historical and current MET by four major PA domains (occupation, home production, travel and active leisure) and sedentary time among adults (>18 years).

The authors note the work of Church, et al, who found decreased work-related activity in the U.S. over the last half of the 20th century.

Inexplicably, they don’t mention the work of Westerterp and colleagues who found no decrease in energy expenditure in North American and European populations since the 1980s.

 

 

More active

My gut feeling is that advanced populations around the globe probably are burning fewer calories by physical activity over the last 50 years, if not longer, thanks to technologic advances.  We in the U.S. are also eating more calories lately.  Since the 1970s, average daily consumption by women is up by 150 calories, and up 300 by men.  Considering both these trends together, how could we not be fat?

Steve Parker, M.D. 

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