Time Restricted

Experiences with Time-Restricted Eating and Managing Chronic Disease

Diabetes

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New study adds to story on gut bacteria and diabetes

This past week, a new study was published in the November 1 issue of Cell further investigating a role of gut bacteria and amino acid metabolism and its role in impairing insulin sensitivity.  The particular branch-chained amino acid (BCAA) under study was histidine, and how the gut bacteria process it differently in diabetic versus non-diabetic individuals.

In diabetics, gut bacteria process histidine into a specific metabolite called imidazole propionate at much higher concentrations, and this metabolite is believed to impair insulin signaling.  Here’s a picture from the study that describes the mechanism:

Graphical abstract from Cell VOLUME 175, ISSUE 4, P947-961.E17, NOVEMBER 01, 2018
How histidine metabolizes and impairs glucose metabolism in diabetics

To me, what is really significant about this study is the linkage to the gut bacteria.

In the past, doctors and scientists used to blame high protein and red meat for reducing insulin sensitivity.  After all, high histidine foods include beef, lamb, cheese, pork, chicken and other high protein foods. Some examples of studies linking high protein diets to insulin resistance include:

  • A 2009 study out of Duke expanded upon this hypothesis that high levels of protein coupled with high levels of fat (“the Western diet”) led to reductions in insulin sensitivity in animal studies.
  • A 2016 study out of New Zealand also took a closer look at high protein / high fiber diets and their effect on insulin sensitivity, taking fat out of the equation.  Taking into account weight loss differences, the study observed reduction in insulin sensitivity in obese study participants with high protein, compared to high carbohydrate, low fat diets.
  • A study published in the June issue of the Journal of Hepatology drew an association of insulin resistance with consumption of red meat and high heat cooking methods.  Here is its “lay summary:”

High red and processed meat consumption is related to several diseases. In addition, cooking meat at high temperatures for a long duration forms heterocyclic amines, which have harmful health effects. Non-alcoholic fatty liver disease is a significant public health burden and its formation is strongly related to insulin resistance. In this study, both were found to be more frequent in people who consume relatively high quantities of red and processed meat. In addition, a high intake of heterocyclic amines was associated with insulin resistance.

The natural reaction many reading these studies (which I think are valid, by the way) would be to figure out how to reduce protein intake to improve insulin sensitivity.  Even with this latest study, if histidine causes increased production of a harmful metabolite in diabetics, why not reduce histidine intake by reducing protein intake?  Not so fast.

I personally believe that this most recent study about the gut bacteria metabolizing histidine differently in diabetics from non-diabetics helps fill in a missing gap.  All around us there are exceptions to people who live on high protein / high meat diets that do not have diabetes or heart disease.  Just google “Inuit paradox” or “French paradox” and you’ll get lots of hypotheses why this may be the case, ranging from the types of fats in seals and walruses to drinking wine.  All of this may be valid, but there is a lack of discussion about gut bacteria.

If you haven’t already, see my previous blog post about gut bacteria and Type II diabetes.  The association between dysbiosis (an imbalance in the gut bacteria) and diabetes has been shown to be strong, and there are numerous studies demonstrating that fasting can positively affect the gut microbiome.

Personally, I believe that repairing the gut microbiome, returning the histidine metabolism of diabetics to be more like non-diabetics, may be a more promising step toward addressing the root causes of insulin resistance, rather than simply trying to reducing protein intake without fixing the underlying problem.

 

Beef icon made by Freepik from www.flaticon.com is licensed by CC 3.0 BY

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Refeeding Days 3-4 & Departure!

We are on our way out of Buchinger Wilhelmi.

Days 3 and 4, as well as Departure Day were a breeze as our food intake increased!  We got to enjoy our last activities here.  And, we got our final blood lab results back!

Menus

Refeeding Day 3

Day 3 menu (target 1,200 calories, but I got more at lunch!)

  • Breakfast – muesli 😋, crisp bread with vegetarian spread 😋
  • Lunch – huge rice salad 😋, huge yogurt 😋, apple 😋, nuts 😋 (I was out on a 5 hour biking and hiking tour, and the tour guide tells the kitchen not to worry about lunchtime calories on tours!)
  • Dinner – celery & apple salad 😋, pumpkin soufflé with vegetables 😋

Refeeding Day 4

Day 4 menu (target 1,500 calories):

  • Breakfast – muesli 😋, crisp bread with vegetarian spread 😋
  • Lunch – beetroot and leaf salad 😋, “spicy budwig” quark and oil cream 😋, pasta with pumpkin and vegetables 😋
  • Dinner – leaf salad 😋, sauerkraut 😋, vegetarian spreads with vegetables and breads 😋

My main comment here on the menus here for Days 3 and 4 is that the breakfast feels really small and simply whets the appetite for more.  After fasting, it seems like it’d be more comfortable to simply eat the food for breakfast and lunch at the same time, extending the period of not eating.

Departure Day

On departure day, we were also served the light breakfast (same as Refeeding Day 4) and were given a box lunch to go (same as my Refeeding Day 3 lunch box, but smaller!)  My wife and I just ate the yogurt immediately after breakfast because it wouldn’t make it through airport security…

Activities

Hiking and Biking Tour

Clearly, the highlight of Refeeding Day 3 (and really of the time here!) was the 5 hour biking and hiking tour.  The route started by bicycle from the clinic, through the town, and to the edge of a forest.  We then hiked to a chapel called Maria Im Stein (“Maria in the Stone”) where we also drank the medicinal water from the well!  On the way out, we hiked barefoot in the river, stopped to have lunch, and hiked barefoot on the way back through the forest.  Then, we met our bicycles, put our shoes back on, and cycled back to the clinic!  My tour guide (Tobi) was super cool, and I had a great time!

Map to Maria Im Stein
The route for our 5 hour biking and hiking tour to Maria im Stein

My wife and I also our final set of blood tests, which we reviewed with our doctor here on Refeeding Day 4.

Our Last Walk

It’s so pretty here that we just had to get outside again on our last full day here!  My wife and I went for our final walk in Überlingen today!  Even though it looked like it was going to rain, the weather cooperated!

Final Ueberlingen Walk
Our final walk in Überlingen

Final Labs

On day 4, we also reviewed our blood test results with our doctor comparing the values from our digestive rest day (23-Aug) to refeeding day 3 (17-Sep)!  The good news is that my blood tests now show normal values for triglycerides and LDL / HDL ratio!.  All other values got better!  Some highlights for “before and after” — again all without any drugs!

Normal 23-Aug 17-Sep Comments
Glucose in serum 60-100 133 106 Better!
HbA1C < 5.7 7.5 7.0 Better!
Cholesterol Total < 200 296 262 Better!
HDL Cholesterol > 40 52 62 Good!
LDL / HDL Ratio < 3.0 3.8 2.9 Normal!
LDL Cholesterol < 155 296 181 Better!
Triglyceride < 150 215 136 Normal!

I’ve got to keep on working at this through repeated fasting, but I remain cautiously optimistic!

Results from morning nurse visits on Refeeding Days 3-4 & Departure Day

  • Blood pressure: 111/74, 106/66, 119/81 (Overall good!)
  • Blood sugar: 111, 109, 120 (So far, steady at “prediabetic” levels)
  • Weight: 64.4 kg (141.7 lbs), 64.6 kg (142.1 lbs), 64.8 kg (142.6 lbs) (gained 1.2 kg since ending the fast!)

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Mitochondrial Dysfunction & Natural Healing

Mitochondrial medicine takes a different angle on the study and treatment of chronic diseases like Type II diabetes and non-alcoholic fatty liver disease (NAFLD).  There is also some interesting work underway regarding mitochondria and the brain.

You may remember from high school biology class that mitochondria are the subunits of our cells (with the notable exception of our red blood cells), responsible for the production of chemical energy (ATP, or adenosine triphosphate) in our bodies.

A growing body of research now suggests that Type II diabetes and non-alcoholic fatty liver disease are not only strongly associated with, but are caused by, mitochondrial dysfunction.  Mitochondrial medicine may provide a “grand unifying theory” of multiple effects, including insulin resistance and the reduced pancreas beta cell production.

Maintenance of normal blood glucose levels depends on a complex interplay between the insulin responsiveness of skeletal muscle and liver and glucose-stimulated insulin secretion by pancreatic β cells. Defects in the former are responsible for insulin resistance, and defects in the latter are responsible for progression to hyperglycemia. Emerging evidence supports the potentially unifying hypothesis that both of these prominent features of type 2 diabetes are caused by mitochondrial dysfunction.

— “Mitochrondrial Dysfunction and Type 2 Diabetes,” Science, 21-Jan-2005, p. 384

In addition, “accumulating evidence indicate that hepatic mitochondrial dysfunction is crucial to the pathogenesis of NAFLD.”

The literature can get pretty technical surrounding the underlying mechanisms of the energy production, the impact on our organs, and our overall health.  However, the root of the problems seem to stem from interruptions in the flow of electrons (often caused by oxidative stress) in a chain of reactions.  I encourage any fellow geeks to read the underlying articles.

However, the purpose of this blog is to really summarize what’s happening in the observable “real world” to cause mitochondrial dysfunction and what we can do about it.

What Causes Mitochondrial Dysfunction?

Mitochondria are inherited from the mother, so if children are born with defective genes, they will generally see the onset of these symptoms in childhood.

However, it is very possible (and common) to acquire mitochondrial dysfunction in adulthood through oxidative stress.  What has mitochondrial medicine deduced about causes for this oxidative stress and resultant mitochondrial dysfunction?

The good news is that there are many mechanisms from nature that protect us from oxidative stress, including enzyme reactions involving antioxidants and that increase energy production, as well as natural substances that detoxify the body.

How can we prevent mitochondrial dysfunction?

Fasting

The “go to” treatment for mitochondrial dysfunction is fasting.  Fasting for more than 12 hours without eating starts autophagy, or reparation of cells.  It also spurs mitophagy, which is the decomposition of damaged or defective mitochondria, key to restoring proper mitochondrial function.

In addition to metabolic benefits, fasting is also beneficial for the brain.  Fasting for prolonged periods triggers ketosis.  For the brain, using ketone bodies for fuel helps to produce more energy than the glucose branch and produces less oxidative stress.  In prolonged fasting, the brain can consume 2/3 of its energy from ketone bodies and reduce its glucose consumption to 1/3 (per a 2005 study).

Prolonged fasting has been shown to help regenerate the mitochondria (and the neurotransmitters!) inside the brain.  Mark Mattson, Chief of the Laboratory of Neurosciences at the National Institute on Aging, did an informative TEDx talk on how intermittent fasting helps the brain through improving mitochondrial function.

Moderate physical exercise

Moderate physical exercise stimulates production of the body’s own antioxidants and growth of mitochrondria in skeletal and heart muscles.  Be careful, though.  Too much exercise has been shown to have the reverse effect.  For reference, see the abstract for a 2005 paper aptly titled “A half-marathon and a marathon run induce oxidative DNA damage, reduce antioxidant capacity to protect DNA against damage and modify immune function in hobby runners.“)

Relaxation techniques

Every day our brains burn 600 calories – 1/3 of our total energy expenditure!

Relaxation techniques, such as meditation, have been shown to reduce this energy expenditure, resulting in less mental stress, less oxidative stress, nitrosative stress and inflammation.  These relaxation techniques also promote regeneration of enzymes, better metabolic efficiency, and production of hormones like serotonin.

Micronutrients

There are two categories of micronutrients to take.  Academic papers (example) list many of these micronutrients that can support mitochondrial function.

  • Reduce oxidative stress
    Vitamin C, Vitamin E, Reduced Glutathione, CoQ10, Vitamin B2, Omega 3 fatty acids, Zinc, Manganese, Copper, Selenium, Curcumin (turmeric), Silymarin (milk thistle), Provitamin A Carotenoids, Reservatrol (grapes), Quercetin (apples), et al
  • Promote energy production
    Vitamin B1, Alpha Lipoid Acid, Vitamin B2 and Vitamin B3, Magnesium, CoQ10

Elimination / Detoxification

The aim of “elimination” is to absorb toxins within the gastrointestinal tract, again to improve mitochondrial function.

Some substances that have been investigated to help eliminate toxins include:

Summary

The net here is that the mechanisms and scientific foundations explained by mitochondrial medicine call for treatment using many of the same techniques as those evangelized by today’s complementary or alternative therapies — including fasting, exercise, relaxation, and detoxification supplemented with hgh quality micronutrients.  The difference now is that mitochondrial medicine is beginning to scientifically explain and study what many of the “natural healing” practitioners have already been practicing for years!

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Refeeding Days 1-2 – On the rebound

Fasting is like summiting a mountain.

Summiting a mountain may sound like the daunting prospect, but the real danger lies in coming back down again, a new study shows.

While hikers may feel they have conquered the hardest part after reaching the peak, in fact 75 per cent of falls occur on the road home.

My wife and I thought that after getting through 22 days of fasting, the hard part was over.

Actually, the hard part is the first day of refeeding.

Day 1 of refeeding is designed to be only 800 calories:

  • Breakfast: 2 prunes, spelt porridge with apple 😋
  • Lunch: chicory salad 🤮, “spicy budwig” quark & oil cream 😋, mashed potatoes & spinach 🤮
  • 2pm snack: coconut milk yogurt 😋
  • Dinner: pumpkin soup 😋😋😋, vegetables with rice balls in a saffron sauce 😋

Recall that the day before, breaking the fast was designed to be under 300 calories.

The problem is that up until now, we’ve had unlimited energy because our brains and bodies were being fueled by our ketones and fatty acids.  As we break the fast, we start to halt ketosis, forcing the brain and body to live off glucose which hasn’t yet built up in the body! We can see the progress (and resultant end) of ketosis (or fat burning) using ketone strips.

ketosis ending
Breaking the fast puts an end to ketosis
(as evidenced by morning urine samples)

So, by late afternoon (right before dinner), my wife and I were pretty exhausted.  We were warned!  Digestion takes energy, and we were also no longer accustomed to the blood flow to our stomachs to support digestion!

Fortunately, we were able to turn the corner at dinner, which was much more substantial. (Yay for rice!)

Refeeding Day 2 has been much easier with an increased caloric intake of 1,000 calories:

  • Breakfast: 2 prunes, muesli 😋😋😋
  • Lunch: leaf salad 😋, “spicy budwig” quark & oil cream 😋, quinoa soufflé 😋
  • 2pm snack: coconut milk yogurt, nuts 😋
  • Dinner: fennel salad, braised chicory with vegetable jus and bulgar wheat

So, we’re on the rebound!

Results from morning nurse visits on Refeeding Days 1-2

  • Blood pressure: 98/67, 114/80 (Overall good!)
  • Blood sugar: 122, 108 (Not concerned about the 122 because I ran before the nurse visit!)
  • Weight: 63.6 kg (139.9 lb), 64.0 kg (140.8 lb) (Weight gain expected from refilling digestive tract and absorbing more water)

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FYI – Blood sugar can RISE immediately after exercise

I was surprised to attend a lecture just three weeks ago where a doctor told diabetics to exercise to lower their immediate blood glucose readings.

After the lecture, I informed the doctor privately that this is not what I have actually observed over the last 15 years, and after some initial dispute, he expressed surprise.  Obviously, this response is what I encountered 15 years ago when I was first diagnosed with diabetes, but I was surprised that the consensus view hasn’t changed since then given that patients are readily armed with their own glucose meters.

Turns out the American Diabetes Association continues to spread this incomplete information, too, without actually talking about how exercise might work against getting a low reading in the short term.  According to their site:

There are a few ways that exercise lowers blood glucose:

  • Insulin sensitivity is increased, so your muscle cells are better able to use any available insulin to take up glucose during and after activity.
  • When your muscles contract during activity, your cells are able to take up glucose and use it for energy whether insulin is available or not.

This is how exercise can help lower blood glucose in the short term.

I actually don’t dispute the points they’re making, and I think everyone agrees that exercise is good.  The information is just incomplete and frustrates diabetics who don’t attain the immediate results that their doctors tell them they should be getting!  Fortunately, the Joslin Diabetes Center provides more complete information on the topic.

When you exercise your muscles need more glucose to supply energy. In response, your liver increases the amount of glucose it releases into your bloodstream. Remember, however, that the glucose needs insulin in order to be used by your muscles. So if you do not have enough insulin available, your blood glucose levels can actually increase right after exercise. Basically, stimulated by the demand from your exercising muscles, your body is pouring glucose into your bloodstream. If you do not have enough insulin available to “unlock the door” to your muscles, the glucose cannot get into your muscles to provide needed energy. The end result is that glucose backs-up in your bloodstream, causing higher blood glucose readings.

For the record, I went running while in Germany yesterday morning.  Here was my blood sugar reading before (108).

Blood Sugar 108
Fasting blood sugar BEFORE exercise – (108)

And here it was after (130).

Blood Sugar 130
Fasting blood sugar AFTER exercise – (130)

The takeaway here is that patients who have blood glucose meters often have more detailed information than the simplified models portrayed by the American Diabetes Association’s published materials or the simplified guidance given at the doctor’s office.  Those who are early in their journeys to manage and reverse their own diabetes should take the time to educate themselves.

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Breaking the fast!

“Every fool can fast, but only the wise man knows how to break a fast.”
– George Bernard Shaw, Nobel-prize winning playwright

Breaking our 22-day fast at Buchinger Wilhelmi

To achieve the sustainable lifestyle benefits of fasting, the methodology here is as much about breaking the fast, as the prolonged fasting itself.  The purpose of this exercise is to reintroduce food with a very low calorie (<300 calorie) menu of easy-to-digest foods.

The breaking of the fast happened in three phases today.

  • An apple compote (“mousse”) and 1-2 nuts at lunch (pictured above)
  • A whole apple at 2pm delivered to our room
  • A potato and vegetable soup at dinner where we were presented with celebratory candles and certificates documenting our accomplishment!

The compote and the soup were very tasty!  While it may seem ironic that a fasting clinic has gourmet food, the maintenance of a healthy and sustainable diet moving forward is viewed as critical.

Weight Gain

The expectation was set here that we would gain between 0.5 kg and 1.5 kg through our initial re-feeding because our digestive tracts are refilling, and our bodies are absorbing more water as protein structures get rebuilt, glycogen reserves get built up, salt intake goes up, and water requirements go up to support secretion of digestive juices.  That said, the initial low caloric intake will still be supporting fat burning in these initial days.

Lower Energy

Another expectation set here is that we will initially experience a lower amount of energy when we re-introduce food, as we’ve become used to our bodies not expending energy to support digestion.  We are also not accustomed any longer to blood flowing to our stomachs after meals.  As such, we’ve been able to exercise any time of day!  The recommendation here is to rest and to ensure waiting 2.5 hours after eating to exercise during this initial period.

General Recommendations

Through these first few days after fasting, we were told to:

  • Chew food intensively
  • Drink 2-3 liters of fluid per day (between, not during meals)
  • Drink hot water in the morning (slow sips)
  • Eat 1-3 soaked prunes in the morning on an empty stomach (part of the standard “breakfasts”)
  • Eat high-fiber foods (again, part of the standard meals served here)
  • Exercise
  • Perform stomach or colon massages
  • Stay away from meat, sugar, alcohol, and coffee (you can’t get those things here at the clinic, but we can still go into town!)
  • And, if constipated, drink 50-100ml of sauerkraut juice mixed with warm water on an empty stomach.  This is an old German remedy.

After Going Home

No surprises here, but the other part of the education here is about both intermittent fasting / time-restricted feeding, as well as the 5:2 diet.  The key is to not let the metabolic benefits experienced here just fade away after returning to our normal lifestyles.  I completely assumed this, which is why I called the blog “time-restricted” for the long term!