Category Archives: metabolic syndrome

Carbohydrate Restriction for Diabetes I and II

Abstract

“The inability of current recommendations to control the epidemic of diabetes, the specific failure of the prevailing low-fat diets to improve obesity, cardiovascular risk or general health and the persistent reports of some serious side effects of commonly prescribed diabetic medications, in combination with the continued success of low-carbohydrate diets in the treatment of diabetes and metabolic syndrome without significant side effects, point to the need for a reappraisal of dietary guidelines.”

Here are the opening paragraphs.

“The benefits of carbohydrate restriction in diabetes are immediate and well-documented. Concerns about the efficacy and safety are long-term and conjectural rather than data-driven. Dietary carbohydrate restriction reliably reduces high blood glucose, does not require weight loss (although is still best for weight loss) and leads to the reduction or elimination of medication and has never shown side effects comparable to those seen in many drugs.

Here we present 12 points of evidence supporting the use of low-carbohydrate diets as the first approach to treating type 2 diabetes and as the most effective adjunct to pharmacology in type 1. They represent the best-documented, least controversial results. The insistence on long-term random-controlled trials as the only kind of data that will be accepted is without precedent in science. The seriousness of diabetes requires that we evaluate all of the evidence that is available. The 12 points are sufficiently compelling that we feel that the burden of proof rests with those who are opposed.

“At the end of our clinic day, we go home thinking, ‘The clinical improvements are so large and obvious, why don’t other doctors understand?’ Carbohydrate restriction is easily grasped by patients: because carbohydrates in the diet raise the blood glucose, and as diabetes is defined by high blood glucose, it makes sense to lower the carbohydrate in the diet. By reducing the carbohydrate in the diet, we have been able to taper patients off as much as 150 units of insulin per day in eight days, with marked improvement in glycemic control – even normalization of glycemic parameters.”

— Eric Westman, MD, MHS [1].

Here is the link to the whole article.

Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base

Peace and good health.

Bob Hansen MD

The bacteria in your gut are essential to your health Part II, obesity, metabolic syndrome and dysbiosis

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I have discussed the evidence linking the mix of bacteria in your gut (gut flora) to health and disease in Part I. The Bacteria in your Gut are essential to your health Part I | Practical Evolutionary Health

Today I will discuss the evidence related specifically to obesity and metabolic syndrome (the constellation of obesity, insulin resistance, high blood pressure, and abnormal blood lipids). My discussion will follow closely the evidence and theory presented in research and review papers authored by Dr. Cani and colleagues. The first one is titled:

“Gut microbiota controls adipose tissue expansion, gut barrier and glucose metabolism: novel insights into molecular targets and interventions using prebiotics.”

You can find the full text of this article here .

I have had the pleasure of corresponding with Dr. Cani by e-mail regarding her many publications investigating the relationship between gut flora, obesity, and metabolic syndrome.

“Recently, we and others have identified several mechanisms linking the gut microbiota with the development of obesity and associated disorders (e.g. insulin resistance, type 2 diabetes, hepatic steatosis).”

Explanation: The gut microbiota are the bacteria, viruses and other “bugs” that reside in our intestines. Insulin resistance can occur in various parts of the body, wherever insulin has an effect including fat cells, liver, muscle, brain. When higher amounts of insulin are required to achieve an effect this is called insulin resistance. In Type 2 diabetes, the pancreas is still able to make insulin but insulin is less effective in controlling blood sugar. In Type I diabetes the pancreas no longer produces insulin. Hepatic Steatosis means fatty liver disease. The liver accumulates fat and this can lead to cirrhosis, liver failure and death. Alcohol consumption can cause this but when alcohol is not involved this is called Non-Alcoholic-Fatty-Liver Disease (NAFLD). Our nation presently has an epidemic of not just obesity but also NAFLD. Evidence points to excess carbohydrate consumption and excess consumption of vegetable oils (linoleic acid) as contributing factors in NAFLD. Carbohydrate restriction and consumption of saturated fat, particularly medium chain fats (as found in coconut) can protect against NAFLD. But the gut flora also play a role. The mechanisms involved are many.

“Among these, we described the concept of metabolic endotoxaemia (increase in plasma lipopolysaccharide levels) as one of the triggering factors leading to the development of metabolic inflammation and insulin resistance.”

Endotoxemia occurs when a toxin from certain kinds of bacteria circulates in the blood. This endotoxin enters our blood through our intestines under conditions in which the protective barrier of the intestines is compromised. The compromise of the intestinal barrier is variously referred to as ” leaky gut” or “increased intestinal permeability”. Wheat gluten-gliadin causes increased intestinal permeability (especially in celiac disease) as can other plant lectins. In this discussion, the gut bacteria also contribute in the setting of “dysbiosis” (the beneficial effects of helpful bacteria are overwhelmed by the harm-causing bacteria when a healthy balance is not present)

Lipopolysaccharide (LPS) comes from the outer wall membrane of certain bacteria. Blood plasma is the liquid part of blood in which the blood cells circulate. So an “increase in plasma lipopolysaccharide” simply means that there is more LPS circulating in the blood. That is a bad thing. Depending on how much is circulating this alone can cause organ failure and death and is a major part of the physiologic changes involved in septic shock. But lower levels of LPS circulating in the blood can cause chronic low grade inflammation and insulin resistance. Obesity is associated with chronic inflammation and increased LPS circulating in the blood and being distributed to various organs where it wreaks havoc.

“Growing evidence suggests that gut microbes contribute to the onset of low-grade inflammation characterizing these metabolic disorders via mechanisms associated with gut barrier dysfunctions.”

“We have demonstrated that enteroendocrine cells (producing glucagon-like peptide-1, peptide YY and glucagon-like peptide-2) and the endocannabinoid system control gut permeability and metabolic endotoxaemia.”

That is a mouth-full. Over thirty different kinds of hormone producing cells have been found in the human intestine. These cells are called enteroendocrine cells. The hormones produced by these cells have many effects. You can find a great review of these cells and their effects here .

In Dr. Cani’s review article she describes how some of these hormones produced in the gut can increase intestinal permeability and allow more of the toxic, inflammation producing LPS to enter the bloodstream. But these hormonal effects are just part of the picture. Another part relates to endocannabinoids.

The Endocannabinoid system in humans is complex and relates to hunger, satiety, energy metabolism, and yes gut permeability. Endocannabinoid refers to our internal (endo) production of cannabis like substances. Pot smoking people get the munchies because of the appetite stimulating effects of marijuana. But endocannabinoids have many other physiologic effects including the modulation of pain, mood, immune function and memory.

Dr. Cani describes in great detail the evidence supporting the roles that the gut flora play in influencing intestinal permeability mediated through the effects of various hormones and endocannabinoids. In animal and human studies changing the gut flora produces changes in these hormones and endocannabinoids which in turn can increase or decrease intestinal permeability and increase or decrease circulating LPS.

It turns out that specific Prebiotics can produce growth of beneficial gut bacteria and through the series of steps outlined above, reduce inflammation in the body, improve blood sugar, improve insulin sensitivity, and decrease fat,

Oh, and similar to the endocannabinoid system, there is an “apelinergic system” in our bodies that also plays a role. If you want to read more about these systems you should read the original article and the other links below to related articles.

I have discussed in the past that fecal transplants have been used to treat the specific dysbiosis that occurs with C Difficile colitis. But fecal transplants have many potential beneficial uses.

The Fatlose 2 trial is presently studying the effects of fecal transplants on insulin resistance and related problems in human volunteers. I will let you know when the results are published, Studies conducted in rodents have demonstrated significant weight loss and improved insulin sensitivity when obese rodents receive fecal transplants from lean rodents.

In summary: dysbiosis represents an unhealthy mix of bacteria in the gut

dysbiosis causes increased intestinal permeability (leaky gut)
increased intestinal permeability leads to increased circulating LPS, which is bad
elevated levels of circulating LPS create a chronic state of inflammation which contributes to obesity and metabolic syndrome
the mechanisms that link dysbiosis to intestinal permeability include hormonal disruption (enteroendocrine cells) and the endocannabinoid system. Other mechanisms are also likely in play.
prebiotics and probiotics can mitigate dysbiosis, reduce intestinal permeability, reduce inflammation, and offer potential therapy for obesity and metabolic syndrome
fecal transplantation offers a potential for treatment for obesity and metabolic syndrome, research is underway

Our ancestors lived and evolved for a few million years prior to the relatively brief ten thousand years of agriculture and one hundred years of industrialization. The overuse of antibiotics in medicine and animal husbandry have contributed to dysbiosis. Other factors include stress, disruption of circadian rhythm, sleep deprivation. Cesarean delivery and avoidance of breast feeding conspire to dysbiosis. Processed foods feed unfriendly bacteria in our guts at the expense of beneficial bugs. Agricultural foods have introduced dietary lectins which also increase intestinal permeability and thereby contribute to chronic inflammation. The further we stray from our evolutionary niche, the more problems we experience.

This discussion just touches the surface of gut flora, dysbiosis, health and disease. We have yet to explore the gut-brain axis. Our gut and microflora communicate with and effect the function of our brain and other organs as well.

We will continue to explore health and disease from an evolutionary perspective.

Below are links to articles related to our discussion.

Peace, health and happiness.

BOB

Gut microbiota controls adipose tissue expans… [Benef Microbes. 2014] – PubMed – NCBI

Glucose metabolism: Focus on gut microbiota, … [Diabetes Metab. 2014] – PubMed – NCBI

Probiotics, prebiotics, and the host microb… [Ann N Y Acad Sci. 2013] – PubMed – NCBI

Crosstalk between the gut microbiota a… [Clin Microbiol Infect. 2012] – PubMed – NCBI

Gut microbiota and its possible relationship … [Mayo Clin Proc. 2008] – PubMed – NCBI

Enteroendocrine Cells: Neglected Players in Gastrointestinal Disorders?

Lose weight, control blood sugar, reduce inflammation

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The Duke University Lifestyle Medicine Clinic prescribes a nutritional program based upon a very simple concept, limit carbohydrate intake and multiple problems improve. This approach is so powerful in controlling blood sugar that diabetic patients must reduce their medication before adopting the nutritional program in order to avoid very low blood sugars.

Compared to a low-fat diet weight loss approach, it is better or equal on every measurement studied. Here is what happens on the carbohydrate restricted program when compared to a low fat diet (American Heart Association diet). The carbohydrate restricted diet results in

Greater reduction in weight and body fat
Greater reduction in fasting blood sugar
Reduction in the amount of saturated fat circulating in the blood despite a higher intake than a low fat diet
Greater reduction in insulin with improved insulin sensitivity
Reduction in small LDL (low fat diets increase small LDL which is considered to be associated with more heart attacks and strokes)
Increase in HDL (low fat diets decrease HDL, decreased HDL is associated with increased risk of heart attack and stroke)
Greater reduction in Triglycerides
Reduction in the ApoB/ApoA-1 ratio (low fat diets do the opposite, and the opposite is considered to increase risk of heart attack and stroke).
Reduction in multiple markers of inflammation
Spontaneous reduction in caloric consumption without counting or restricting calories (people automatically eat less as a result of restricting carbohydrates, low-fat diets require counting and restricting calories in order to lose weight)
Increased consumption of non-starchy vegetables

All of these beneficial effects are accepted by the medical community as reducing cardiovascular risk .

The improved metabolic outcome can occur even without weight loss simply by substituting fat for carbohydrate.

“The key principle is that carbohydrate, directly or indirectly through the effect of insulin, controls the disposition of excess dietary nutrients. Dietary carbohydrate modulates lipolysis, lipoprotein assembly and processing and affects the relation between dietary intake of saturated fat intake and circulating levels.” see here

Yet despite these proven effects, the proponents of low-fat diets refer to the carbohydrate restriction approach as a “fad diet”. In his excellent discussion of this term, Richard Feinman points out that historically, a carbohydrate restriction approach is actually the longest standing and proven approach to the treatment of obesity compared to a low-fat diet which is a relative newcomer. He describes how a low-fat diet more closely meets the dictionary’s definition of a “fad”.

Multiple Studies have compared carbohydrate restriction to low fat diet approaches and the results are consistent. In addition to the advantages cited above, carbohydrate restricted approaches when compared to low-fat diets reveal that symptoms of “negative affect and hunger improved to a greater degree” compared with those following a low fat diet”. (see here)

When one analyzes the carbohydrate restricted diet (CRD) approach employed by many centers, including the Duke Interventional Medicine Clinic, one finds great similarity to a paleolithic diet.

They both eliminate or dramatically reduce

sugar-sweetened foods and beverages,
grains, flour foods and cereal foods
legumes (paleo completely, CRD to a large extent)
processed-refined vegetable oils
dairy (paleo completely, CRD to a large extent)

Fruits under a CRD are limited to small amounts of berries initially and this is liberalized over time as weight loss is achieved and metabolic parameters are improved. This is consistent with a paleolithic approach that recognizes that fruits and vegetables grown today have been bred to provide much higher sugar and starch content compared to the pre-agricultural fruits and vegetables that early hominids consumed for hundreds of thousands of years.

A carbohydrate restricted nutritional approach to treat obesity, diabetes, or metabolic syndrome appears to be a valid and arguably superior remedy to a growing problem in the developed world. Yet despite this strong and convincing scientific data, dietary fat-phobia has impaired the utilization of this proven therapeutic modality.

Peace,

Bob Hansen M.D.

Sugar II

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In my first post about sugar I discussed increased cardiovascular risk associated with consumption of added sugar, sweetened foods and beverages. This post will discuss other risks including childhood obesity and adult obesity, diabetes and Metabolic syndrome.

The marketing efforts directed at young children by soda producers and fast food restaurants is astounding. You can view a video produced by a concerned mother here.

Some highlights of the video include:

1:14 How her daughter’s obsession with one particular person made her realize what was happening.
2:20 Can you guess how much money the food industry spends marketing to kids?
3:15 There’s even a term for the way they make children more annoying.
3:55 Find out just how many thousands of ads kids see if they watch a regular amount of television.
4:30 Here’s why just turning off the TV isn’t a solution.
4:50 Learn which school supplies are now sponsored by junk food.
5:54 Find out how companies like Coca-Cola and Pepsi are straight-up conning school communities to buy their products.
6:47 Here’s what she finds most upsetting.
8:10 And here’s how they get even more information about kids.
9:30 She talks about the life and death consequences that hang in the balance with this issue.
10:24 We’re seeing the most depressing innovations in health care now thanks to the food industry.
12:00 You’ll never believe where McDonald’s wanted to advertise.
13:01 Find out who’s fighting these food behemoths and saving generations to come.

So what’s all the fuss? Where is the data to support a connection between sweetened beverages, sweetened foods and obesity, diabetes and metabolic syndrome?

Let’s start with a study by Gitanjali Singh and associates from Harvard School of Public Health reported here, the Epidemiology and Prevention/Nutrition, Physical Activity and Metabolism 2013 Scientific Sessions. I read about this on Medscape published on-line. You must establish a user name and password to access these reviews, written for physicians and health professionals.

They reported that drinking large amounts of sugar sweetened beverages (SSBs) was associated with an increased body-mass index (BMI). Increased BMI is associated with deaths from diabetes, cardiovascular disease and cancer, so the authors calculated deaths associated with consumption SSBs from diabetes, CVD and cancer.

The researchers found that in 2010

“132,000 deaths from diabetes, 44,000 deaths from CVD, and 6000 deaths from cancer in the world could be attributed to drinking sugar-sweetened soft drinks, fruit juice, or sports beverages.”

“As part of the Global Burden of Disease study, the researchers obtained data from 114 national dietary surveys, representing more than 60% of the world’s population.

Based on data from large prospective cohort studies, they determined how changes in consumption of sugary drinks affected BMI, and next, how elevated BMI affected CVD, diabetes, and 7 obesity-related cancers (breast, uterine, esophageal, gallbladder, colorectal, kidney, and pancreatic cancer). Using data from the World Health Organization, they calculated the number of deaths from BMI-related CVD, diabetes, and cancer for men and for women aged 20 to 44, 45 to 64, and 65 years and older.”

Mexico had the highest number of deaths and Japan the lowest number of deaths attributed to the risk factor of sweetened beverage consumption. The USA had an estimated 25,000 deaths per year associated with drinking sugar sweetened beverages.

Medscape quoted Rachel K. Johnson, Ph.D. an AHA spokesperson.

“The evidence base that sugar-sweetened beverages are associated with excess weight gain is well established; what these investigators have done is to take it a step further by saying the excess weight gain that is attributable to sugary drinks actually increases the risk of death from diabetes, CVD, and cancer,”

The obesity literature is in agreement that consuming beverages with calories does not result in a decrease in an equivalent amount of calories from solid food consumption. In fact studies of humans demonstrate that sugar sweetened beverages increase the total amount of calories consumed by an amount equal to the calories in the beverage. This is added calories that do not produce satiety. This is why my Manifesto recommends drinking only water, coffee, tea, and no sweetened beverages.

Here is a discussion about sugar added beverages vs sweetened solid foods.

Consumption of Added Sugars from Liquid but Not Solid Sources Predicts Impaired Glucose Homeostasis and Insulin Resistance among Youth at Risk of Obesity.

“a higher consumption (10 g/d) of added sugars from liquid sources was associated with 0.04 mmol/L higher fasting glucose, 2.3 pmol/L higher fasting insulin, 0.1 unit higher homeostasis model assessment of insulin resistance (HOMA-IR), and 0.4 unit lower Matsuda-insulin sensitivity index (Matsuda-ISI) in all participants (P < 0.01).”

Translation, just 10 grams (1/3 ounce) of added sugar from beverages increased fasting blood sugar, increased fasting insulin, worsened Insulin resistance. Insulin resistance is the precursor to diabetes. This is a chronic inflammatory state.

How much sugar is in a can of coke? Look here. How Much Sugar in Sodas and Beverages? 39 grams in a 12 oz bottle of coke, 79 grams in a 7-Eleven 32 oz Big gulp, 128 grams in a 7-Eleven 44 oz Super Gulp. 77 grams in a 20 oz bottle of Mountain Dew, But it only takes 10 grams a day to cause harm.

” liquid added sugars were a risk factor for the development of impaired glucose homeostasis and insulin resistance over 2 y among youth at risk of obesity.”

But let’s look at another study.

A meta-analysis published in 2010 reported that consumption of just one or two sugar-sweetened beverages per day is associated with a 26% greater risk of developing type 2 diabetes and a 20% increased risk of developing metabolic syndrome. Abstract

They concluded:

“In addition to weight gain, higher consumption of SSBs (sugar sweetened beverages) is associated with development of metabolic syndrome and type 2 diabetes. These data provide empirical evidence that intake of SSBs should be limited to reduce obesity-related risk of chronic metabolic diseases”

Malik VS, Popkin BM, Bray GA, et al. Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: A meta-analysis. Diabetes Care 2010: 33:2477–2483.

At the time of this study publication, cities and states were introducing legislation for “soda taxes” on sugar-sweetened beverages. There were also attempts to make sodas and sugar drinks ineligible for food stamp purchases. See the discussion here.

That same year the American Journal of Clinical Nutrition published a study Carbohydrate quantity and quality and risk of type 2 diabetes in the European Prospective Investigation into Cancer and Nutrition–Netherlands (EPIC-NL) study

We investigated the associations of dietary glycemic load (GL), glycemic index (GI), carbohydrate, and fiber intake with the incidence of type 2 diabetes.

They followed 37,846 participants for a mean follow up period of 10 years.

They concluded:

“Diets high in GL, GI, and starch and low in fiber were associated with an increased diabetes risk. Both carbohydrate quantity and quality seem to be important factors in diabetes prevention. “

There is plenty of low quality carbohydrate in the sodas featured above. And there is no fiber to slow the absorption of the sugar. You might as well start an IV and deliver 128 grams of super-gulp sugar directly into the blood.

In 2010 a Health Policy Report concerning the consumption of sweetened beverages was published in the New England Journal of Medicine.

The Public Health and Economic Benefits of Taxing Sugar-Sweetened Beverages – NEJMhpr0905723

They open up by stating:

The consumption of sugar-sweetened beverages

has been linked to risks for obesity, diabetes,

and heart disease.

A meta-analysis showed positive associations between intake of sugar-sweetened beverages and body weight-associations that were stronger in longitudinal studies than in cross-sectional studies and in studies that were not funded by the beverage industry than in those that were.

They go on to discuss how a meta-analysis funded by the beverage industry was interpreted as showing no evidence of an association between consumption of sugar-sweetened beverages and body weight,

“but it erroneously gave large weight to several small negative studies: when a more realistic weighting was used, the meta-analysis summary supported a positive association”

The authors site several studies linking sugar sweetened beverages to obesity in children and adults. Please click on the link above and go to page two for charts demonstrating the historical trend in sugared beverage consumption.

Since that publication multiple studies, discussions and policy statements have appeared in the medical literature. If you perform a PubMed search with “tax AND sugar” you will get 8 pages of citations. Here are some of them.

Evidence that a tax on sugar sweetened beverages reduces the obesity rate: a meta-analysis.

This one concluded that:

Six articles from the USA showed that a higher price could also lead to a decrease in BMI, and decrease the prevalence of overweight and obesity.

More studies from the search “sugar AND tax”.

Overall and income specific effect on prevalence of overweight and obesity of 20% sugar sweetened drink tax in UK: econometric and comparative risk assessment modelling study.

A substantial tax on sugar sweetened drinks could help reduce obesity.

Building a strategy for obesity prevention one piece at a time: the case of sugar-sweetened beverage taxation.

The potential impact on obesity of a 10% tax on sugar-sweetened beverages in Ireland, an effect assessment modelling study.

The sugar-sweetened beverage wars: public health and the role of the beverage industry.

A typology of beverage taxation: multiple approaches for obesity prevention and obesity prevention-related revenue generation.

Taxing sugar-sweetened beverages: the fight against obesity.

Sugar tax and obesity.

Intended and unintended consequences of a proposed national tax on sugar-sweetened beverages to combat the U.S. obesity problem.

Despite all of this discussion there has not been a “sugar tax” on sweetened beverages and here are several reasons.

Taxes on sugar-sweetened beverages: results from a 2011 national public opinion survey.

“Consumption of sugar-sweetened beverages including non-diet sodas, sport drinks, and energy drinks has been linked with obesity. Recent state and local efforts to tax these beverages have been unsuccessful. Enactment will be unlikely without public support, yet little research is available to assess how to effectively make the case for such taxes.

The objectives were to assess public opinion about arguments used commonly in tax debates regarding sugar-sweetened beverages and to assess differences in public opinion by respondents’ political party affiliation.

Findings indicated greater public agreement with anti- than pro-tax arguments. The most popular anti-tax argument was that a tax on sugar-sweetened beverages is arbitrary because it does not affect consumption of other unhealthy foods (60%). A majority also agreed that such taxes were a quick way for politicians to fill budget holes (58%); an unacceptable intrusion of government into people’s lives (53.8%); opposed by most Americans (53%); and harmful to the poor (51%). No pro-tax arguments were endorsed by a majority of the public. Respondents reported highest agreement with the argument that sugar-sweetened beverages were the single largest contributor to obesity (49%) and would raise revenue for obesity prevention (41%).”

So the relationship between sugar sweetened beverages and diabetes, obesity and metabolic syndrome seems well established but as a public policy issue there has been no traction on taxation remedies. And as the video above demonstrates, Coke and Pepsi have more than a foot in the door in our school systems and our homes (TV adds).

You can make a difference. vote here Tell the Soda Industry to Use Their Influence to Combat Childhood Obesity

A future post will discuss artificial sweeteners (diet beverages) which unfortunately also have a dismal track record.

Until next time,

Peace

Bob Hansen MD

Abstract

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