Tag Archives: prediabetes

Is Insulin Making You Hungry All the Time?

So easy to over-eat!

So easy to over-eat! Is it the insulin release?

No, insulin probably isn’t the cause of constant hunger, according to Dr. Stephan Guyenet. Dr. G gives 11 points of evidence in support of his conclusion. Read them for yourself. Here are a few:

  • multiple brain-based mechanisms (including non-insulin hormones and neurotransmitters) probably have more influence on hunger than do the pure effect of insulin
  • weight loss reduces insulin levels, yet it gets harder to lose excess weight the more you lose
  • at least one clinical study (in 1996) in young healthy people found that foods with higher insulin responses were linked to greater satiety, not greater hunger
  • billions of people around the world eat high-carb diets yet remain thin

An oft-cited explanation for the success of low-carbohydrate diets involves insulin, specifically the lower insulin levels and reduced insulin resistance seen in low-carb dieters. They often report less trouble with hunger than other dieters.

Here’s the theory. When we eat carbohydrates, the pancreas releases insulin into the bloodstream to keep blood sugar levels from rising too high as we digest the carbohydrates. Insulin drives the bloodstream sugar (glucose) into cells to be used as energy or stored as fat or glycogen. High doses of refined sugars and starches over-stimulate the production of insulin, so blood sugar falls too much, over-shootinging the mark, leading to hypoglycemia, an undeniably strong appetite stimulant. So you go back for more carbohydrate to relieve the hunger induced by low blood sugar. That leads to overeating and weight gain.

Read Dr. Guyenet’s post for reasons why he thinks this explanation of constant or recurring bothersome hunger is wrong or too simplistic. I agree with him.

The insulin-hypoglycemia-hunger theory may indeed be at play in a few folks. Twenty years ago, it was popular to call this “reactive hypoglycemia.” For unclear reasons, I don’t see it that often now. It was always hard to document that hypoglycemia unless it appeared on a glucose tolerance test.

Regardless of the underlying explanation, low-carb diets undoubtedly are very effective in many folks. And low-carbing is what I always recommend to my patients with carbohydrate intolerance: diabetics and prediabetics.

Steve Parker, M.D.

front cover

front cover

Which Diet for a 41-Year-Old Asian Indian With Prediabetes?

The CulinaryRx blogger at MedPageToday asked two physicians what diet modifications they’d recommend for a 41-year-old Asian-Indian man with prediabetes. (To read the article you may need to do a free sign-up.)

The moderator asked his experts twice whether carbohydrate restriction is important, and never got a straight answer. These experts must not think it’s important since they push legumes, lentils, fruits, and whole grains. Dr. Nadeau said he believes there is no specific diet for folks with diabetes. I almost fell off my chair when I read one comment recommending cookies and sweets, because they’re traditional. They also recommend low glycemic load, nuts, higher protein consumption, vegetables, and “good oils” like olive oil (ghee not even  mentioned).

Read this blog post for prior comments that include advice from possible clinicians.

I’m confident that Dr. Ronesh Sinha in Silicon Valley, California, would disagree with the advice of MedPageToday’s experts. Dr. Sinha would likely recommend limiting digestible carbohydrates to 50–150 grams/day as the most important dietary step.

I’m still looking for clinical studies of various diets for South Asians with prediabetes and diabetes.

Steve Parker, M.D.

Paleobetic Diet Book Now Available

Paleobetic Diet-FrontCover_300dpi_RGB_5.5x8.5

 

 

 

I started this blog four years ago as an exploration of the Paleolithic diet as a therapeutic option in diabetes and prediabetes. Scientific studies from Ryberg (2013), Mellberg (2014), Boers (2014), and Masharani (2015) have convinced me that the paleo diet indeed has true potential to improve these conditions.

A couple years ago I published a bare-bones preliminary version of the Paleobetic Diet. Here’s an outline. I just finished a comprehensive fleshed-out version in book format.

The central idea is to control blood sugars and eliminate or reduce diabetes drugs by working with Nature, not against her. This is the first-ever Paleolithic-style diet created specifically for people with diabetes and prediabetes.

Also known as the caveman, Stone Age, paleo, or ancestral diet, the Paleolithic diet provides the foods our bodies were originally designed to thrive on. You’ll not find the foods that cause modern diseases of civilization, such as concentrated refined sugars and grains, industrial seed oils, and over-processed Franken-foods. Our ancestors just five generations ago wouldn’t recognize many of the everyday foods that are harming us now. On the Paleolithic diet, you’ll enjoy a great variety of food, including nuts and seeds, vegetables, fruit, meat, seafood, and eggs.

In the book you’ll find one week of meal plans to get you started, plus additional special recipes. Meals are quick and easy to prepare with common ingredients. You’ll find detailed nutritional analysis of each meal, including carbohydrate grams.

All measurements are given in both U.S. customary and metric units. Blood glucose values are provided as both mmol/l and mg/dl. Also included is information and advice on exercise, weight loss, all 12 classes of diabetes drugs, management of hypoglycemia, and recommended drug dose adjustments. All recipes are gluten-free.

 

Availability and Formats

You’ll find Paleobetic Diet at all major online bookstores. For example, Amazon (290-page paperback book in U.S.), Kindle ebook, and multiple ebook formats at Smashwords.

If you have diabetes or prediabetes, please give this program careful consideration. Help me spread the word if you know someone else who might benefit. Thank you.

Steve Parker, M.D.

Family Physician Robert Oh Attacked His Prediabetes With Low-Carb Paleo Diet

Robb Wolf’s version of the paleo diet plus stopping his statin drug was just the ticket for Robert Oh, M.D., to cure his prediabetes, or at least put it into remission. Dr. Oh couldn’t blame genetics, physical inactivity, or obesity for his prediabetes. He was very active with CrossFit and had a healthy BMI of 23 at the time of his diagnosis. everydayHEALTH has the story. A quote by Dr. Oh:

Since I was already doing everything in terms of fitness, I began to experiment with my nutrition. Being a CrossFit fanatic, I heard about the low-carb Paleo diet, which is popular in the CrossFit community. Based on gut instinct alone, I took the 30-day challenge described in Robb Wolf’s book The Paleo Solution. Even though I started at 150 lbs. on my 5’7” frame, at the end of 30 days, I had lost eight pounds of body fat and felt great. Most importantly, my hemoglobin A1C, a marker of glucose control, dropped back to normal.

We’ve known for a few years that statin drugs are linked to type 2 diabetes in some way. Is it possible that Dr. Oh’s prediabetes cure stems simply from his discontinuation of the statin? Yes. I’ve not seen any studies to tell us whether statin-associated diabetes is reversible, nor how quickly.

Steve Parker, M.D.

Paleolithic Diet Improved Metabolic Syndrome in Just Two Weeks

Wish I were here

Wish I were here

A Paleolithic-type diet over two weeks improves several heart disease risk factors in folks with metabolic syndrome, according to Netherlands-based researchers.

The investigators wondered if the paleo diet, independent of weight loss, would alter characteristics of the metabolic syndrome. They seem to be the first scientists to do a study like this.

“Metabolic syndrome” may be a new term for you. It’s a collection of clinical features that are associated with increased future risk of type 2 diabetes and atherosclerotic complications such as heart attack and stroke. One in six Americans has metabolic syndrome, including almost one in four of adults. The most common definition of metabolic syndrome (and there are others) is the presence of at least three of the following characteristics:

  • high blood pressure (130/85 or higher, or using a high blood pressure medication)
  • low HDL cholesterol: under 40 mg/dl (1.03 mmol/l) in a man, under 50 mg/dl (1.28 mmol/l) in a women (or either sex taking a cholesterol-lowering drug)
  • triglycerides over 150 mg/dl (1.70 mmol/l) (or taking a triglyceride-lowering drug)
  • abdominal fat: waist circumference 40 inches (102 cm) or greater in a man, 35 inches (88 cm) or greater in a woman
  • fasting blood glucose over 100 mg/dl (5.55 mmol/l)

These five criteria were identical to the ones used in the study at hand. But the study participants were required to have only two of the five, not three, for unclear reasons. I found no consensus definition elsewhere that would define metabolic syndrome as only two of the five conditions. Study participants ate either a paleo-style diet or a reference/control diet. Those eating the reference diet didn’t quite have the metabolic syndrome since they had a mean (“average”) of 2.7 metabolic syndrome characteristics. The paleo group had 3.7 characteristics.

How Was the Study Done?

Average age of the 34 study participants was 53 and they were generally healthy. None had diabetes, cardiovascular disease, or systolic pressure over 180 mmHg. Smokers were excluded. Mean body mass index was 32 (obese). Only 9 of the 34 subjects were men. Subjects were randomized to either a Paleolithic-type diet (n=18) or a “healthy reference diet based on the guidelines of the Dutch Health Council” (n=14). Efforts were made to keep body weight stable during the two-week study. Participants were nearly all caucasian.

All meals were home-delivered free of charge by a catering service.

The Paleolithic-type diet “…was based on lean meat, fish, fruit, leafy and cruciferous vegetables, root vegetables, eggs and nuts. Dairy products, cereal grains, legumes, refined fats, extra salt and sugar were not part of it.” [I like their version of the paleo diet.] Protein supplied 24% of calories while carbohydrate was 32% and fat 41%.

You can consult the full text of the published article for details of the Dutch Health Council diet. Calories were 17% from protein, 50% from carbohydrate, and 29% from fat. Alcohol isn’t mentioned at all.

Despite randomization, the paleo diet group had more metabolic syndrome characteristics than the reference diet group. For instance, 78% of the paleo group had elevated fasting glucose compared to 44% of the reference group. And 67% of the paleo group had low HDL cholesterol compared to just 13% of the reference group. These glucose and HDL differences were statistically significant. 39% of the paleo had high triglycerides compared to 19% of the others. Furthermore, the paleos’ average body weight was 98 kg (216 lb) compared to 86 kg (189 lb) in the others. The paleo group had 3.7 characteristics of the metabolic syndrome versus 2.7 in the other cohort.

Go John trail at Cave Creek Regional Park in Scottsdale, Arizona

Go John trail at Cave Creek Regional Park in Scottsdale, Arizona

Results

Compared to the reference diet, the paleo-style diet:

  • lowered systolic pressure by 9 points and diastolic by 5
  • total cholesterol fell by 0.52 mmol/l (20 mg/dl)
  • triglycerides fell by 0.89 mmol/l (79 mg/dl)
  • HDL cholesterol (good) rose by 0.15 mmol/l (6 mg/dl)
  • body weight fell by 1.32 kg (3 lb)
  • one metabolic syndrome characteristic resolved

No significant changes were seen in intestinal permeability ( by differential sugar absorption test on urine), salivary cortisol, and inflammation (hsCRP, TNFα).

Fasting plasma insulin and HOMA-IR fell in the paleo group but not the other.[Good news for folks with diabetes or prediabetes.] Yet the authors write, “Regarding glucose intolerance we did not find significant changes in our study.”

Fasting blood glucose for the group as a whole at baseline was about 1o8 mg/dl (6.0 mmol/l). Fasting glucose fell in both groups: 16 mg/dl (0.9 mmol/l) in the paleo group, 6 mg/dl (0.35 mmol/l) in the other. This was not a statistically significant difference between the groups. These numbers are from the text of the report; looking at the tables, I calculate different and less impressive reductions. The falls in fasting glucose from baseline were statistically significant for both diets.

Nearly all the statistical analysis focused on comparing the paleo diet group to the reference diet group.

My Comments

Overall, I’m not very pleased with this study. My biggest problems are 1) the unfortunate randomization that created dissimilar experimental groups,  2) the use of two diet protocols, 3) some of the study participants didn’t even have metabolic syndrome, and 4) as is typical for paleo diet studies, not many experimental subjects were involved.

The randomization led to significant differences in the metabolic syndrome patients in the two diet groups. I’m puzzled why the authors don’t comment on this. It’s a problem with clinical studies involving low numbers of participants. Ideally, you want to apply the two different diets to groups of people that are as similar as possible. These groups weren’t that similar.

The investigators’ main goal was to study whether a paleo-style diet, independent of weight loss, alters characteristics of the metabolic syndrome. Then why introduce another variable, the Dutch Health Council diet? Is it the gold standard for treating metabolic syndrome? Has it even been used to treat metabolic syndrome? The authors don’t tell us. And why not restrict participation to subjects who meet the common international definition of metabolic syndrome (at least three of the five characteristics)? Why not just take all your subjects and switch them from their standard Netherlands diet to the paleo diet? That would increase your statistical power, and would have avoided the randomization mis-match in which some in the reference diet group didn’t even have metabolic syndrome.

Here we’ve got two different experimental groups, and we’re applying a different diet to each group. The results are going to be messy and difficult to interpret. It’s always better if you can alter just one variable.

Since the paleo and reference diet cohorts were so different at baseline, why not make it easy to simply compare the paleo diet group’s “before and after numbers”? Maybe the analysis is there and I’m just not smart enough to see it.

There weren’t enough men in the study to tell us anything about the paleo diet in men with metabolic syndrome.

The statistical analysis was difficult for me to read and understand. There’s a good chance I’ve missed or misinterpreted something.

This paleo diet reduced fasting blood sugar significantly, making me think it may help in management of diabetes and prediabetes.

I estimate that as much as a quarter of the experimental subjects didn’t even have metabolic syndrome, so the study title is a bit of a misnomer.

This paleo diet did result in resolution of one metabolic syndrome characteristic, which is a good thing. So you could say the diet improves metabolic syndrome, even resolves it in some folks if it drops their metabolic syndrome characteristics from three to two. It predominantly helps lower blood pressure and triglycerides, and reduces excess weight modestly. In white women. Compared to the healthy Dutch Health Council diet.

If I had metabolic syndrome, I’d do something about it in hopes of lowering my future risk of diabetes and atherosclerotic complications. Standard physician advice is to lose excess weight and exercise regularly. There’s no consensus on diet yet. I think carbohydrate restriction is important. If the study at hand is reproducible in a larger study population, the paleo diet is a reasonable approach. Dietitian Franziska Spritzler has a great review of nutritional management of metabolic syndrome at her blog. The Mediterranean diet supplemented with nuts helps improve metabolic syndrome. The Spanish Ketogenic Mediterranean Diet may cure metabolic syndrome.

Steve Parker, M.D.

Update: I took a fresh look at this study as if it were simply a paleo diet trial involving 18 subjects who had metabolic syndrome. If I’m interpreting Table 5 correctly, and I think I am, these are the statistically significant changes after two weeks:

  • abdominal circumference decreased by 3.1 cm
  • systolic and diastolic blood pressures dropped by 8.5 and 8, respectively
  • fasting glucose dropped by 0.4 mmol/l (7 mg/dl)
  • fasting insulin fell
  • HOMA-IR decreased (less insulin resistance)
  • total cholesterol decreased from 220 to 193 mg/dl (5.7 to 5.0 mmol/l)
  • LDL-cholesterol decreased from 135 to 124 mg/dl (3.5 to 3.2 mmol/l)
  • triglycerides decreased from 168 to 89 mg/dl (1.9 to 1.0 mmol/l)

HDL cholesterol was unchanged.

The fall in AUC (area under the curve) for insulin approached but didn’t reach statistical significance (p=0.08)

Body weight fell from 98 kg (216 lb) to 95.3 kg (210 lb) but I found no p value. HDL-cholesterol was unchanged (the higher HDL I mentioned above is only in comparison to the reference diet, in which HDL fell)

All of these changes (except the lack of change in HDL-chol) would tend to promote health in someone with metabolic syndrome, prediabetes, or overweight type 2 diabetes.

Reference: Boers, Inga, et al. Favorable effects of  consuming a Palaeolithic-type diet on characteristics of the metabolic syndrome: a randomized controlled pilot-studyLipids in Health and Disease. 2014 Oct 11;13:160. doi: 10.1186/1476-511X-13-160.

Do the Drug Companies Have Too Much Influence on Diagnosis and Management of Type 2 Diabetes?

diabetic mediterranean diet, Steve Parker MD

Pharmacist counting pills

MedPageToday has recently completed a series of articles looking at socioeconomic issues related to diabetes drugs that have come onto the market in the last decade. They call it their Diabetes Drugs Investigation. I recommend the entire series to you if you have type 2 diabetes. The authors’ have five major points:

1. “Diabetes drugs improve lab tests, but not much more, particularly in pre-diabetics.” FDA drug approvals were based mostly on whether hemoglobin A1c or blood sugar levels improved, not on improvements in hard clinical endpoints such as risk of death, heart attacks, stroke, blindness, amputations, etc.

2. “Physicians and drug makers have reported diabetes drugs as the “primary suspect” in thousands of deaths and hospitalizations.”

3. “Diabetes drug makers paid physicians on influential panels millions of dollars.” The implication is that the panelists were not totally unbiased in their assessments of drug effectiveness and safety.

4. “Risk of a risk now equals disease.” This is about the latest redefinition of prediabetes which created many more “patients.” Prediabetes can progress to type 2 diabetes over a number of years: one of every four adults with prediabetes develops diabetes over the next 3 to 5 years. Some doctors are even treating prediabetes with diabetic drugs. (I recommend a “diet and exercise” approach.) The authors think the prediabetic label—one third of U.S. adults, including half of all folks over 65—is over-used and over-treated.

5. “The clinical threshold for diagnosing diabetes has crept lower and lower over the past decade.” For instance, in 1997 expert panels lowered the threshold defining diabetes from a fasting blood glucose level of 140 mg/dl (7.8 mmol/l) to 125 mg/dl (6.9 mmol/l). Four million more American adults became diabetics overnight. In 2003, they lowered the threshold for prediabetes from a fasting blood glucose from 110 mg/dl (6.1 mmol/l) to 100 mg/dl (5.6 mmol/l). Boom! 46 million more American prediabetics.

I fully agree with the authors that we don’t know which drugs for type 2 diabetes are the best in terms of prolonging life, preventing diabetes complications, and postponing heart attacks and strokes. Furthermore, we don’t know all the adverse long-term effects of most of these drugs. For instance, metformin had been on the market for over a decade before we figured out it’s linked to vitamin B12 deficiency.

That’s why I try to convince my patients to do as much as they can, when able, with diet and exercise before resorting to one or more drugs. (All type 1 diabetics and a minority of type 2 diabetics must take insulin.) Maybe it’s healthier to focus primarily on drug therapy…but I don’t think so.

RTWT.

Steve Parker, M.D.

Amanda Torres Turns Her Life Around With Paleo/Primal Lifestyle

This is the old Amanda:

In December 2009, I was 25 years old and weighed 210 lbs. I was obese for my 5’5″ frame, never felt well, and was popping handfuls of pills every day just to get by. I was taking 2 anti-depressants, anxiolytics, prescription sleeping pills, courses of Prilosec once or twice a month, acid-blocking pills or antacid tablets 1-3 times a day, anti-diarrhea pills several days a week, and I was constantly catching respiratory infections and frequently took courses of antibiotics. In fact, I was put on chronic antibiotics by a dermatologist to treat rosacea, acne, and a truly horrible condition known as hidradenitis suppurativa (acne inversa). I would take them for several weeks at a time, until everything calmed down, but inevitably within a few weeks more I would end up with another debilitatingly painful HS boil and would need to start up the antibiotics again. I also got either a yeast infection or a urinary tract infection almost once a month. In the summer of 2008 I was diagnosed as pre-diabetic with metabolic syndrome and hypertension, so by the end of 2009 I was quite probably a full-fledged type II diabetic, I just never got an official diagnosis. I was falling apart mentally and physically, and scared to death of a miserable future full of multiple chronic illness and scary prescription medications, so I decided to make some drastic changes in my lifestyle. I resolved to do  my research over the holidays, and begin in 2010 with my new way of life.

She ran across Mark Sisson’s website and the rest is history.

Read about her transformation.

 

h/t Julianne Taylor

Ryberg et al: Effects of Paleolithic Diet on Obese Postmenopausal Women

Sweden's Flag. Most of the researchers involved with this study are in Sweden

Sweden’s Flag

After menopause, body fat in women tends to accumulate more centrally than peripherally. This is reflected in a higher incidence of fatty liver disease, type 2 diabetes, and cardiovascular disease. A multinational group of researchers wondered if a modified paleo-style diet would have metabolic effects on healthy overweight and obese (BMI 28–35) postmenopausal women in Sweden, with particular attention to fat levels in liver and muscle. I’ll call this the Ryberg study because that’s the first named author.

Study Details

Curiously, they never give the age range of the 10 study participants. Were they closer to 52 or 82?

tuna, fishing, Steve Parker MD, paleo diet, tuna salad

Has anyone even bothered to ask why the tuna are eating mercury? —Jim Gaffigan

The five-week intervention diet seems to have been mostly prepared and provided by the investigators, but they allowed for home cooking by providing menus, recipes, and a food list. No limit on consumption. The goal was to obtain 30% of calories from protein, 40% from fat (mostly unsaturated), and 30% from carbohydrate “…together with 40 g nuts (walnuts and sweet almonds) on a daily basis….”

The diet included lean meat, fish, fruit, vegetables (including root vegetables), eggs and nuts. Dairy products, cereals, beans, refined fats and sugar, added salt, bakery products and soft drinks were excluded.

“They were also advised to use only rapeseed [i.e., canola] or olive oil in food preparation.”

A diet like this should reduce average saturated fat consumption, which was a stated goal, while substituting monounsaturated  and polyunsaturated fat for saturated.

These women were sedentary before and during the intervention.

Results

The ladies indeed made some major changes in their diet. Total calories consumed fell by 22% (2,400 to 1,900 cals). The average weight of participants dropped from 190 lb (86.4 kg) to 180 lb (81.8 kg).

Carbohydrates consumption as a percentage of total calories fell from 49% to 25%. Total carb  grams dropped from 281 to 118, with fiber grams unchanged. To replace some of the carbs, the women increased their protein and fat calorie percentages by about a third. The authors don’t make it clear whether the total carb grams included total fiber grams. (I could probably figure it out if I had the time and inclination, but don’t.) “Before” and “after” fiber grams were 25 and 27, respectively.

In other words, “…the ratio between energy intake from the macronutrients protein, total fat and carbohydrates expressed as E% [calorie percentages] changed significantly from 16:33:50 at baseline to 28:44:25 after five weeks.” Total daily fat grams didn’t change, but the contribution of saturated fat grams fell.

Elevated blood pressure is one component of metabolic syndrome

Elevated blood pressure is one component of metabolic syndrome

A 10-point drop in systolic blood pressure over the five weeks didn’t quite reach statistical significance (p=0.057), but the 9% drop in diastolic pressure did.

“Fasting serum levels of glucose, leptin, cholesterol, triglycerides, HDL, LDL, ApoB and apolipoprotein A1 (ApoA1) and percentage HDL also decreased significantly.”

Fat (or lipid) content of the liver dropped by half. It was measured by magnetic resonance spectroscopy. Peripheral muscle fat content didn’t change, measured in the soleus and  tibialis anterior muscles of the leg.

Urinary C-peptide excretion and HOMA indices [HOMA1-IR formula] decreased significantly, whereas whole-body insulin sensitivity, measured using the hyperinsulinaemic euglycaemic clamp technique, was not significantly changed.” See footnote labelled PPS at bottom page for confusing details.

My Comments

The intervention diet was a reasonable version of the Paleolithic diet, with one exception. From what I’ve seen from Eaton, Konner, and Cordain, I think they’d agree. Except for the rapeseed oil. It’s fallen out of favor, hasn’t it?

Here’s what the Jaminet’s wrote about canola:

Canola oil…is rapeseed oil bred and processed to remove erucic acid and glucosinolates. During processing, the oil is treated with the solvent hexane and very high temperatures; it may also be subject to caustic refinement, bleaching, and degumming. [Perfect Health Diet, p.225.]

I can’t quite see Grok doing that.

My fantasy about extra virgin olive oil is that it simply oozes out of the olives when pressure is applied. So easy a caveman could do it.

Eaton and Konner have argued that our ancestral diet would have had at least two or three times the fiber as was provided by this diet. But that would have been at a total daily calorie consumption level of at least 3,000 or 3,5oo back in the day. So this diet isn’t so far off.

10-lb Weight Loss Without Calorie Restriction? I'll Take That.

10-lb weight loss In five weeks without conscious calorie restriction? I’ll take that.

The 10 lb (4.6 kg) weight loss is impressive for an eat-all-you-want diet. Calorie intake dropped spontaneously by 500/day, assuming the numbers are accurate. The satiation from higher protein consumption may explain that. The authors admit that the women lost more weight than would be predicted by the energy balance equation (i.e., a pound of fat = 3,500 calories). They wonder about over-estimations of food intake, thermogenic effects of protein versus other macronutrients,  and loss of glycogen (and associated body water). You can’t argue with those scales, though.

While serum C-peptide didn’t fall, urinary levels did. (My sense from reviewing other literature is that 24-hr urine levels of C-peptide are more accurate indicators of insulin production, compared to a single fasting C-peptide level.) The authors interpret this as increased insulin sensitivity in the liver in combination with decreased insulin secretion by the pancreas. Fasting serum insulin levels fell from 8.35 to 6.75 mIU/l (p<0.05).

Regarding the non-significant change in overall insulin sensitivity as judged by hyperinsulinemic euglycemic clamp technique, remember that insulin sensitivity of the liver may be different from sensitivity in peripheral tissues such as muscle. These investigators think that liver insulin sensitivity was clearly improved with their diet.

Blood lipid changes were in the right direction in terms of cardiovascular disease risk, except for the drops in HDL (from 1.35 to 1.17 mmol/l) and ApoA1.

This study may or may not apply to men. Also note the small sample size. Will these results be reproducible in a larger population? In different ethnicities?

I like the reduction in blood pressure. That could help you avoid the risk, expense, and hassle of drug therapy.

From 97 to 90 mg/dl

Serum glucose fell from 96  to 90 mg/dl

I like the drop in fasting blood sugar from 96 to 90 mg/dl (5.35 to 5 mmol/l). It’s modest, but statistically significant. Was it caused by the weight loss, reduced total carb consumption, paucity of sugar and refined starches, lower total calories, higher consumption of protein and mono- and polyunsaturated fats, or a combination of factors? As with most nutritional studies, there’s a lot going on here. A small fasting blood sugar drop like this wouldn’t matter to most type 2 diabetics, but could diabetics see an even greater reduction than these non-diabetics? Only one way to tell: do the study.

I can well imagine this diet curing some cases of metabolic syndrome, prediabetes, mild type 2 diabetes, and fatty liver disease.

Most type 2 diabetics (and prediabetics, for that matter) are overweight or obese.  If a diet like this helps them lose weight, it could improve blood sugar levels. Nearly all authorities recommend that overweight and obese diabetics and prediabetics get their weight down to normal. (I admit that weight loss and improved blood sugar levels are not always in sync.) Weight loss by any standard method tends to improve insulin sensitivity.

Furthermore, the elevated fasting blood sugars that characterize so many cases of diabetes and prediabetes are usually linked to, if not caused by, insulin resistance in the liver. According to these investigators, the diet at hand improves insulin sensitivity in the liver, and even lowers fasting blood sugars in non-diabetic older women.

This modified Paleolithic-style diet doesn’t include table sugar or refined grain starches. That would help control blood sugar levels in both type 1 and type 2 diabetics and prediabetics. The authors didn’t say so, but this must be a relatively low-glcemic-index diet.

The investigators don’t mention ramifications of their diet for folks with diabetes. Their focus is on ectopic fat accumulation (in liver and muscle) and its linkage with insulin resistance and cardiovascular disease. They’ve put together a promising program to try on diabetics or prediabetics. They just need the will and funding to git’r done.

I agree with the authors that the lower calorie consumption, rather than the paleo diet per se, may have caused or contributed to the reduction in liver fat.

Stockholm Palace

Stockholm Palace

The investigators wonder if a Paleolithic-style diet like this would be beneficial over the long-term in patients with non-alcoholic fatty liver disease (NALFD) and associated metabolic disturbance (e.g., impaired sensitivity sensitivity in the liver). NAFLD tends to predict the development of diabetes and cardiovascular disease. If we can prevent or reverse fatty liver, we may prevent or reverse type 2 diabetes and cardiovascular disease, to an extent. You’ll be waiting many years for those clinical study results.

But you have to decide what to eat today.

A significant number of American women (20%?) need to lose weight, lower their blood pressures, lower their blood sugars, and decrease their liver fat. This Ryberg Paleolithic-style diet would probably do it.

A very-low-carb diet is another way to reduce liver fat, and it’s more effective than simple calorie restriction.

Steve Parker, M.D.

Reference: Ryberg, M., et al. A Palaeolithic-type diet causes strong tissue-specific effects on ectopic fat deposition in obese postmenopausal women. Journal of Internal Medicine, 2013, vol. 274(1), pp: 67-76.  doi: 10.1111/joim.12048

PS: See Carbsane Evelyn for her take on this study here and here.

PPS: Urinary C-peptide secretion reflects insulin production. HOMA is a gauge of insulin resistance, much cheaper and quicker than the purported “gold-standard” hyperinsulinemic euglycemic clamp technique. Why HOMA and the clamp technique in this study didn’t move together is unclear to me, and the authors didn’t explain it. School me in the comment section if you can. Click this HOMA link and you’ll find this statement: “HOMA and clamps yield steady-state measures of insulin secretion and insulin sensitivity in the basal and maximally stimulated states, respectively. HOMA measures basal function at the nadir of the dose-response curve, whereas clamps are an assessment of the stimulated extreme.” Maybe that means HOMA is applicable to the fasted state (no food for 8 hours), whereas the clamp technique is more applicable to the hour or two after you ate half a dozen donuts.

What’s Wrong With Type 2 Diabetics?

Type 2 diabetes and prediabetes are epidemics because of excessive consumption of refined sugars and starches, and lack of physical activity.  I can’t prove it; nevertheless that’s my impression after years of reading the nutrition science literature and thinking about it.

I could be wrong.  I reserve the option to change my mind based on evidence as it becomes available.  That’s one of the great things about science.  Accurately identifying the cause of diabetes could provide strong clues about optimal prevention and treatment strategies.

Genetics undoubtedly plays a major role in diabetes, but the gene pool hasn’t changed much over the last several decades as type 2 diabetes rates have soared.

The problem in type 2 diabetes and prediabetes is that the body cannot handle ingested carbohydrates in the normal fashion. In a way, dietary carbohydrates (carbs) have become toxic instead of nourishing. This is a critical point, so let’s take time to understand it.

NORMAL DIGESTION AND CARBOHYDRATE HANDLING

The major components of food are proteins, fats, and carbohydrates. We digest food either to get energy, or to use individual components of food in growth, maintenance, or repair of our own body parts.

We need some sugar (also called glucose) in our bloodstream at all times to supply us with immediate energy. “Energy” refers not only to a sense of muscular strength and vitality, but also to fuel for our brain, heart, and other automatic systems. Our brains especially need a reliable supply of bloodstream glucose.

In a normal, healthy state, our blood contains very little sugar—about a teaspoon (5 ml) of glucose. (We have about one and a third gallons (5 liters) of blood circulating. A normal blood sugar of 100 mg/dl (5.56 mmol/l) equates to about a teaspoon of glucose in the bloodstream.)

Our bodies have elaborate natural mechanisms for keeping blood sugar normal. They work continuously, a combination of adding and removing sugar from the bloodstream to keep it in a healthy range (70 to 140 mg/dl, or 3.9 to 7.8 mmol/l). These homeostatic mechanisms are out of balance in people with diabetes and prediabetes.

By the way, glucose in the bloodstream is commonly referred to as “blood sugar,” even though there are many other types of sugar other than glucose. In the U.S., blood sugar is measured in units of milligrams per deciliter (mg/dl), but other places measure in millimoles per liter (mmol/l).

When blood sugar levels start to rise in response to food, the pancreas gland—its beta cells, specifically—secrete insulin into the bloodstream to keep sugar levels from rising too high. The insulin drives the excess sugar out of the blood, into our tissues. Once inside the tissues’ cells, the glucose will be used as an immediate energy source or stored for later use. Excessive sugar is stored either as body fat or as glycogen in liver and muscle.

When we digest fats, we see very little direct effect on blood sugar levels. That’s because fat contains almost no carbohydrates. In fact, when fats are eaten with high-carb foods, they tend to slow the rise and peak in blood sugar you would see if you had eaten the carbs alone.

Ingested protein can and does raise blood sugar, usually to a mild degree. As proteins are digested, our bodies can make sugar (glucose) out of the breakdown products. The healthy pancreas releases some insulin to keep the blood sugar from going too high.

In contrast to fats and proteins, carbohydrates in food cause significant—often dramatic—rises in blood sugar. Our pancreas, in turn, secretes higher amounts of insulin to prevent excessive elevation of blood glucose. Carbohydrates are easily digested and converted into blood sugar. The exception is fiber, which is indigestible and passes through us unchanged.

During the course of a day, the pancreas of a healthy person produces an average of 40 to 60 units of insulin. Half of that insulin is secreted in response to meals, the other half is steady state or “basal” insulin. The exact amount of insulin depends quite heavily on the amount and timing of carbohydrates eaten. Dietary protein has much less influence. A pancreas in a healthy person eating a very-low-carb diet will release substantially less than 50 units of insulin a day.

To summarize thus far: dietary carbs are the major source of blood sugar for most people eating “normally.” Carbs are, in turn, the main cause for insulin release by the pancreas, to keep blood sugar levels in a safe, healthy range.

Hang on, because we’re almost done with the basic science!

You deserve a break

CARBOHYDRATE  HANDLING  IN  DIABETES  &  PREDIABETES

Type 2 diabetics and prediabetics absorb carbohydrates and break them down into glucose just fine. Problem is, they can’t clear the glucose out of the bloodstream normally. So blood sugar levels are often in the elevated, poisonous range, leading to many of the complications of diabetes.

Remember that insulin’s primary function is to drive blood glucose out of the bloodstream, into our tissues, for use as immediate energy or stored energy (as fat or glycogen).

In diabetes and prediabetes, this function of insulin is impaired.

The tissues have lost some of their sensitivity to insulin’s action. This critical concept is called insulin resistance. Insulin still has some effect on the tissues, but not as much as it should. Different diabetics have different degrees of insulin resistance, and you can’t tell by just looking.  (There are several other hormones involved in regulation of blood sugar.)

Did you know that people who work at garbage dumps, sewage treatment plants, and cattle feedlots get used to the noxious fumes after a while? They aren’t bothered by them as much as they were at first. Their noses are less sensitive to the fumes. You could call it fume resistance. In the same fashion, cells exposed to high insulin levels over time become resistant to insulin.

Insulin resistance occurs in most cases of type 2 diabetes and prediabetes. So what causes the insulin resistance? It’s debatable. In many cases it’s related to overweight, physical inactivity, and genetics. A high-carbohydrate diet may contribute. A few cases are caused by drugs. Some cases are a mystery.

To overcome the body tissue’s resistance to insulin’s effect, the pancreas beta cells pump even more insulin into the bloodstream, a condition called hyperinsulinemia. Some scientists believe high insulin levels alone cause some of the damage associated with diabetes. Whereas a healthy person without diabetes needs about 50 units of insulin a day, an obese non-diabetic needs about twice that to keep blood sugars in check. Eventually, in those who develop diabetes or prediabetes, the pancreas can’t keep up with the demand for more insulin to overcome insulin resistance. The pancreas beta cells get exhausted and start to “burn out.” That’s when blood sugars start to rise and diabetes and prediabetes are easily diagnosed. So, insulin resistance and high insulin production have been going on for years before diagnosis. By the time of diagnosis, 50% of beta cell function is lost.

Steve Parker, M.D.

EXTRA  CREDIT  FOR  INQUISITIVE  MINDS

You’ve learned that insulin’s main action is to lower blood sugar by transporting it into the cells of various tissues. But that’s not all insulin does. It also 1) impairs breakdown of glycogen into glucose, 2) stimulates glycogen formation, 3) inhibits formation of new glucose molecules by the body, 4) promotes storage of triglycerides in fat cells (i.e., lipogenesis, fat accumulation), 5) promotes formation of fatty acids (triglyceride building blocks) by the liver, 6) inhibits breakdown of stored triglycerides, and 7) supports body protein production.

In his fascinating book, Cheating Destiny: Living With Diabetes, America’s Biggest Epidemic, James Hirsch describes what happened to type 1 diabetics before insulin injections were available. Type 1 diabetics produce no insulin. Until Frederick Banting and Charles Best isolated and injected insulin in the 1920s, type 1 diabetes was a death sentence characterized not only by high blood sugars, but also extreme weight loss as muscle and fat tissue wasted away. The tissue wasting reflects insulin actions No. 4, 5, 6, and 7 above.

Banting and Best worked at the University of Toronto in Canada. Their “discovery” of insulin is one of the greatest medical achievements of all time.

TV’s Biggest Loser Plan Improves Prediabetes and Diabetes in Small Study

TV’s “The Biggest Loser” weight-loss program works great for overweight diabetics and prediabetics, according to an article May 30, 2012, in MedPage Today.

This isn’t directly related to the paleo diet or lifestyle, but I thought you might be interested.

Some quotes:

For example, one man with a hemoglobin A1c (HbA1c) of 9.1, a body mass index (BMI) of 51, and who needed six insulin injections a day as well as other multiple prescriptions was off all medication by week 3, said Robert Huizenga, MD, the medical advisor for the TV show.

In addition, the mean percentage of weight loss of the 35 contestants in the study was 3.7% at week 1, 14.3% at week 5, and 31.9% at week 24…

The exercise regimen for those appearing on “The Biggest Loser” comprised about 4 hours of daily exercise: 1 hour of intense resistance training, 1 hour of intense aerobics, and 2 hours of moderate aerobics.

Caloric intake was at least 70% of the estimated resting daily energy expenditure, Huizenga said.

At the end of the program, participants are told to exercise for 90 minutes a day for the rest of their lives. Huizenga said he is often told by those listening to him that a daily 90-minute exercise regimen is impossible because everyone has such busy lives.

“I have a job and I work out from 90 to 100 minutes per day,” he said. “It’s about setting priorities. Time is not the issue; priorities are the issue.”

Of the 35 participants in this study, 12 had prediabetes and six had diabetes.  This is a small pilot study, then.  I bet the results would be reproducible on a larger scale IF all conditions of the TV program are in place.  Of course, that’s not very realistic.  A chance to win $250,000 (USD) is strong motivation for lifestyle change.

Steve Parker, M.D.

PS: Although not mentioned in the article, these must have been type 2 diabetics, not type 1.