Tag Archives: overweight

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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Filed under Carbohydrate, Overweight and Obesity, Sugar

Ketogenic Diet Works for Children

ketogenic diet, children

Is there a trampoline out of view?

A ketogenic diet was safe and effective for weight loss in children and adolescents, according to a small study in the Journal of Pediatric Endocrinology and Metabolism.  Fifty-six children were placed on either a ketogenic diet or a calorie-restricted diet.  The investigators judged the low-carb ketogenic diet more effective.

I don’t treat children, so I don’t normally monitor the pediatric scientific literature.  Thanks to Diet Doctor Andreas Eenfeldt for bringlng this to my attention.  I’ve not read the full research report.

In 2010 I reported on research showing a low-carb, high-protein diet was safe and effective for severely obese adolescents.

Steve Parker, M.D.

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Filed under ketogenic diet, Weight Loss

David Mendosa Shares His Weight Management Expertise

Maybe his method works only for him, but I doubt it. David has diabetes, by the way. See his 2012 article at HealthCentral for details. Here’s a bit:

One cornerstone of this new way to lose weight and maintain weight loss is a twist on a standard dieting recommendation. But instead of weighing myself once a week, I weigh myself every morning.

Supposedly people get discouraged from daily weigh-ins because our weight seems to fluctuate up or down a couple of pounds every day for no good reason, or for at least for no reason that we can figure out. The fluctuations are certainly true in my experience. But, of course, the same fluctuations happen when we make our weigh-ins once a week, and that would be even more misleading.

Then, when the scales tell me that my weight is up that morning from the previous morning, I make an immediate course correction, which we know is easier in the long run than to wait until things get totally out of hand. My immediate course correction is simple. I skip dinner that day.

Note well, however, that skipping dinner could lead to major hypoglycemia if you’re taking certain diabetes drugs. Work with your personal healthcare provider on drug dose adjustments.

Steve Parker, M.D.

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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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What Causes Type 2 Diabetes?

“Beats me. I teach math!”

I have no simple answer for you, unfortunately.

You can lower your risk of type 2 diabetes significantly by avoiding overweight and obesity, by exercising regularly, and by choosing the right parents.  These provide clues as to the causes of diabetes.  The Mediterranean diet also prevents diabetes.

UpToDate.com offers a deceptively simple answer:

Type 2 diabetes mellitus is caused by a combination of varying degrees of insulin resistance and relative insulin deficiency. [Insulin is the pancreas hormone that lowers blood sugar.] Its occurrence most likely represents a complex interaction among many genes and environmental factors, which are different among different populations and individuals.

So, what causes the insulin resistance and relative insulin deficiency?

Understanding the pathogenesis [cause] of type 2 diabetes is complicated by several factors. Patients present with a combination of varying degrees of insulin resistance and relative insulin deficiency, and it is likely that both contribute to type 2 diabetes. Furthermore, each of the clinical features can arise through genetic or environmental influences, making it difficult to determine the exact cause in an individual patient. Moreover, hyperglycemia itself can impair pancreatic beta cell function and exacerbate insulin resistance, leading to a vicious cycle of hyperglycemia causing a worsening metabolic state.

The UpToDate article then drones on for a several thousand words discussing mouse studies, various genes, free fatty acids, adiponectin, leptin, amylin, insulin secretion, insulin resistance, impaired insulin processing, insulin action, body fat distribution, inflammation, various inflammatory markers, low birth weight, high birth rate, prematurity, etc.  More excerpts:

Increased free fatty acid levels, inflammatory cytokines from fat, and oxidative factors, have all been implicated in the pathogenesis of metabolic syndrome, type 2 diabetes, and their cardiovascular complications.

Insulin resistance may, at least in part, be related to substances secreted by adipocytes [fat cells] (“adipokines” including leptin adiponectin, tumor necrosis factor alpha, and resistin).

Type 2 diabetes most likely represents a complex interaction among many genes and environmental factors.

That’s the simplest answer I can give now.

Steve Parker, M.D.

Reference: “The Pathogensis of Type 2 Diabetes Mellitus”  by David K McCulloch, MD, and R Paul Robertson, MD, at UpToDate.com, updated June 2012, and accessed November 19, 2012.

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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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Is Fructose Unfairly Demonized as a Cause of Obesity?

Mainly because of its low cost, HFCS [high fructose corn syrup] consumption replaced approximately one-third of the total sugar consumption in the USA between 1970 and 2000, paralleling to some extent the increasing prevalence of obesity during this period. Consequently, HFCS has been a particular focus of possible blame for the obesity epidemic. However, HFCS consumption has remained very low in other parts of the world where obesity has also increased, and the most commonly used form of HFCS contains about 55% fructose, 42% glucose, and 3% other sugars, and hence is associated with similar total fructose and glucose intakes as with sugar. Furthermore, sucrose is hydrolyzed in the gut and absorbed into the blood as free glucose and fructose, so one would expect HFCS and sucrose to have the same metabolic consequences. In short, there is currently no evidence to support the hypothesis that HFCS makes a significant contribution to metabolic disease independently of the rise in total fructose consumption.

Given the substantial consumption of fructose in our diet, mainly from sweetened beverages, sweet snacks, and cereal products with added sugar, and the fact that fructose is an entirely dispensable nutrient, it appears sound to limit consumption of sugar as part of any weight loss program and in individuals at high risk of developing metabolic diseases. There is no evidence, however, that fructose is the sole, or even the main factor in the development of these diseases…

— Luc Tappy in BMC Biology, May 21, 2012 (the article is a review of fructose metabolism and potential adverse effects of high consumption)

PS: Luc Tappy believes that excessive calorie consumption is an important cause of overweight and obesity.

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